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Coexisting 2016 > Liver New - Done on Saturday > Flashcards

Liver New - Done on Saturday Flashcards

1
Q

The liver is the site of synthesis of all clotting factors except

A

vWF

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2
Q

CV function in patients with cirrhosis

A
  1. Hyperdynamic circulation
    • High CO and Low SVR
  2. Possible cardiomyopathy
  3. Decreased response to catecholamines
  4. Increased flow to splanchnic, pulm, muscular, cutaneous beds
  5. Decreased hepatic flow
  6. Portal HTN
  7. Arterial hypoxemia
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3
Q

S/S of cirrhosis

A
  • Fatigue /malaise
  • Anorexia/ weakness
  • Nausea/ vomiting
  • Abdominal pain
  • Jaundice /spider nevi
  • Hypoalbuminemia
  • Coagulation disorders
  • Endocrine disorders
  • Hepatic encephalopathy
  • Gastroesophageal variceal
  • Hepatomegaly /ascites
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4
Q

Many alcoholics can get cardiomyopathy. How does this affect your anesthetic?

A

Don’t give anything that depressed the myocardium

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5
Q

How do the majority of cirrhosis patients die during abdominal surgery?

A

60% die from bleeding

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6
Q

Coagulation in Cirrhosis

A

Treat bleeding with FFP, Vitamin K, Platelets

Cirrhosis patients will have:

  1. Prolonged PT/INR
  2. Vit K deficiency
  3. factors II, V, VII, IX, X deficiency
  4. Thrombocytopenia

(Bleeding accounts for 60% of deaths in abdominal surgery →surgery contraindicated if Platelets are low )

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7
Q

Pre-op considerations in cirrhosis

A
  1. Treat as full stomach →RSI
  2. Low albumin → decrease drug doses
  3. Ascites → fluid status
  4. Cardiomyopathy
  5. PaO2 60-70 (R→L pulm shunt)
  6. Hypoglycemia
  7. Pneumonia
  8. Encephalopathy
  9. Hepatorenal syndrome
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8
Q

monitoring for cirrhosis patients

A
  1. CVP, A-line, +/- PA
  2. UO → foley
  3. Blood glucose
  4. AVOID esophageal temp probe
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9
Q

Why are cirrhosis patients considered full stomachs?

A
  1. Alcohol use weakens the lower esophageal sphincter
  2. ascites
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10
Q

Liver patients tend to be (hyper/hypo)glycemic

A
  • Hypoglycemic.
    • Give fluids with glucose
  • Pts are hypoglycemic d/t decreased hepatic gluconeogenesis
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11
Q

How should we maintain anesthesia for the patient with cirrhosis?

A

IA at 1/2 MAC with N2O and opioids

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12
Q

In cirrhosis, we need a (higher/lower) dose of NMRs and why?

A

Need higher dose because Vd will be increased

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13
Q

What NMBs are best for cirrhosis

A
  • Mivacurium
  • atracurium
  • cisatracurium*
  • (the ones metabolized in blood)
  • Sux is apparently ok too
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14
Q

Reasons why liver patients are at risk for morbidities post-op

A
  • Pneumonia
  • Bleeding
  • Sepsis
  • Poor wound healing
  • Liver dysfunction
  • DT’s
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15
Q

Other comorbidities that alcoholics may have

A
  • Hypothermia
  • alcoholic poluneuropathy
  • Wernicke-Korsakoff syndrome
  • Pernicious anemia
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16
Q

Considerations for Maintenance of anesthesia in cirrhosis patients

A
  1. Balanced technique:
    • Combine Volitile anesthetics (1/2 MAC), N2O and opioids.
  2. Manitain hepatic blood flow →
    • Sevo, Iso and Des are all safe to use
    • MUST maintain an adequate BP →hypotension will decrease oxygen delivery to the hepatoytes
  3. Use NMBs that are metabolized in the blood
    • mivacurium, atracurioum, cis-atratrcurium, sux
    • Will also need larger doses → d/t larger volume of distribution, but also the doses will last longer
  4. Don’t give anything that will depress the heart!
  5. Patients will have low protein binding
  6. Bleeding risk
  7. Considered full stomachs
    • poor lower esophageal sphincter tone
  8. ​Give fluids that contain glucose → often they become hypoglycemic
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17
Q

This enzyme is deficient in porphyria

A

ALA synthetase

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18
Q

S/S of porphyria attack

A
  • abd pain
  • N/V
  • ANS instability (HTN and tachycardia)
  • electorlyte (Na, K, MG) disturbances
  • neuro psych manifestations
  • weakness
    • can progress to quadriparesis and respiratory failure
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19
Q

Regional anesthesia and porhyria

A
  1. AVOID During an acute exacerbation
  2. otherwise no absolute contraindications
  3. Pre anesthetic neuro eval
  4. Keep in mind ANS blockade may lead to cardiovascular instibility (especially with hypovolemia)
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20
Q

Why do patients have hyperdynamic circulation with liver disease?

A
  • Accumulation of vasodilating compounds like prostaglandins and interleukins
  • Reduced blood viscosity may also play a role.
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21
Q

Any IAs that decrease hepatic BF will increase serum concentrations of

A

Alpha-GST (Glutathione S-transferases)

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22
Q

Blood volume in liver disease

A
  • Decreased in
    • central circulation
  • but increase in
    • splanchnic, pulmonary, muscle, and cutaneous corcualtion.
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23
Q

GA Considerations in porphyria

A
  1. Use short acting agents
  2. Monitor for instability
  3. Induction
    • Propofol, ketamine → these are ok to use in porphyria
    • NO ETOMIDATE → trigger
  4. Maintenance
    • Nitrous, inhaled anesthetics, opioids, NDMR
  5. CP bypass is a stress → will need ICU after and VERY good post op management!
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24
Q

Is cimetidine good or bad in porphyria?

A

GOOD

It decreases heme consumption and decreases ALA synthetase activity

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25
Q

These meds can be given to treat porphyria

A

Hematin 3-4 mg/kg IV, somatostatin, plasmapheresis

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26
Q

Cholecystectomy

Induction/Maintenance

A
  1. Consider volume & electrolyte replacement
  2. RSI with cricoid pressure, cuffed tube
  3. Reverse tburg
  4. Mechanical ventilation
  5. Judicious use of opioids
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27
Q

Cholecystectomy and opioids

A
  • Sphincter of Oddi spasm occurs in 3% of the population
  • Antagonize spasm with
    • Naloxone (maybe not the best idea)
    • glucagon
    • NTG
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28
Q

Volatile anesthetics and hepatic dysfunctions

A
  • VA produce a self-limiting post-op liver dysfunction
    • transient increase in alpha-GST
  • Halothane hepatitis
    • Immune mediated 1 in 10,000-30,000
    • Only Sevo does not metabolize into trifluoroacetylated compounds
29
Q

What would you do if a patient has post-op hepatic dysfunction

A

Multi-factorial analysis

  1. Review all drugs administered
  2. Check for sepsis
  3. Check bilirubin
  4. Rule out occult hematomas → hyperbilirubinemia
  5. Review peri-operative record for
    • hypotension
    • hypoventilation
    • hypoxemia
    • hypercarbia
    • hypovolemia
30
Q

What is hepatitis

A

Inflammation of the liver parenchyma d/t

  1. Viral
  2. Autoimmune
  3. Drug-Induced

Acute

  • usually self-limiting and most often viral but can be caused by drugs/toxins

Chronic

  • Hepatic inflammation >6 months
  • Cirrhosis, hepatocellular carcinoma or liver failure (ETOH/HCV/HBV/Autoimmune)

Symptoms may be minimal (malaise/jaundice) to severe with compromise to multiple organ systems

31
Q

Common hepatitis causes

A
  • HBV, HDV, HCV, autoimmune, drug induced
  • Graded on degree of inflammation, necrosis, progression, and degree of fibrosis
32
Q

Pre-op Assessment - hepatitis

A
  1. How long has the hepatitis been present
  2. What stage is it
  3. What type/mode of transmission
  4. Signs/symptoms the pt is experiencing Is patient optimized for anesthesia (fluids, e-lytes)
  5. Does everyone have proper vaccines in place?
33
Q

Pre-op considerations in hepatitis

A

Coags? Encephalopathy?

34
Q

Induction for hepatitis

A
  • NPO?
  • Volume status (often hypovolemic)
  • Other organ system involvement
35
Q

Hepatitis

etiology, types, sxs,

A

Etiology:

  1. Inflammation of the liver parenchyma
  2. Viral
  3. Autoimmune
  4. Drug-Induced

Types:

  • Acute
    • usually self-limiting and most often viral but can be caused by drugs/toxins
  • Chronic
    • Hepatic inflammation >6 months
    • Cirrhosis, hepatocellular carcinoma or liver failure (ETOH/HCV/HBV/Autoimmune)

S/S

  • may be minimal (malaise/jaundice) to severe with compromise to multiple organ systems
  • anorexia, N/V, low grade fever, dark urine, clay colored stool, jaundice, acute liver failure
  • AST/ALT 400-4000
36
Q

Hep B Tx

A
  • Interferon
  • Lamivudine
  • Adefovir
37
Q

Hep C Tx

A
  • Interferon
  • Ribavirin
38
Q

Autoimmune hepatitis

A
  • Cellular immune response against self-antigens in the liver
  • Diagnosis confirmed with clinical findings, lab testing and histologic evaluation
  • No curative intervention
  • Goal is to induce remission with corticosteroids and immunosuppressive drugs or liver transplantation
39
Q

Cirrhosis

etiology & sxs

A

Etiology

  • Chronic, progressive parenchymal damage leads to scarring and nodular formation

Signs and Symptoms

  • Fatigue/Malaise
  • Jaundice
  • Anorexia/weakness/N/V
  • Spider angiomata
  • Hypoalbuminemia
  • Ascites/hepatomegaly
  • Coagulation disorders
  • Endocrine disorders
  • Hepatic encephalopathy
  • Gastroesophageal varices
  • Hyperdynamic circulation
  • Hepatorenal Syndrome
40
Q

Liver blood supply

A
  1. Hep. artery gives
    • 25% flow and 50% oxygen
  2. Portal vein gives
    • 75% flow and 50% oxygen
41
Q

Pre-op/Induction cirrhosis

A
  1. volume status
  2. RSI
  3. Protein binding
  4. ETOH on board? (lowers anesthetic requirements)
  5. Cardiomyopathy
  6. Consider vitamin K, FFP, Platelets
  7. Administer glucose solutions
42
Q

Post-op cirrhosis considerations

A

Increased post-op morbidity

  1. Liver dysfunction/failure = #1 cause of death post-op
  2. Pneumonia
  3. Bleeding
  4. Sepsis
  5. Poor wound healing
  6. DTs
  7. Electrolyte disturbance
  8. Renal failure
43
Q

DTs timeline

A
  • 6-8 hours of ETOH withdrawal pt may become tremulous
  • 24 hours hallucinations, grand mal seizures may occur
  • DTs within 72 hours

Treat with benzos

44
Q

What is Porphyria

A
  • Metabolic disorder that results from deficiency of specific enzyme in the heme synthetic pathway
    • ​deficiency of aminolevulinic acid (ALA)
  • Results in overproduction of porphyrins
    • Accumulation of intermediate forms of porphyrin at the site of enzyme blocked
      • ​​Any increase in heme requirements results in accumulation of pathway intermediates
  • Porphyrins essential for physiologic functions
    • Oxygen transport and storage
    • Heme most important porphyrin
    • Bound to proteins
    • Production regulated by aminolevulinic acid (ALA) synthetase
      • Controlled by endogenous concentration of heme
  • Any metabolism needs that rely on the cytochrome P - 450 isoenzymes induce ALA synthetase resulting in increased intermediates
45
Q

Porphyria Treatment

A
  1. Hematin 3-4mg/kg (drug of choice)
  2. Remove triggering agents
  3. Hydration
  4. Carbohydrates (b/c a trigger is fasting)
  5. Treat pain and N/V
  6. Beta blockers for HTN & tachycardia
  7. Benzodiazepines for seizures
  8. Fluid and electrolyte balance (10% glucose saline infusions)

(also somatostatin, plasmapheresis)

46
Q

Triggers in porphyria

A

Enzyme inducing drugs

  1. Drugs that have an Allyl group →barbs
  2. Drugs with a Steroid structure
    • Pentathol, thiamylal, methohexital, etomidate​

Hormonal fluctuations (everything we induce!)

  1. fasting
  2. dehydration
  3. stress
  4. infection
47
Q

Anesthetic management in porphyria

A
  1. Avoid known triggers
    • minimize use of multiple drugs
    • Multiple enzyme inducing agents more dangerous than exposure to any one drug
  2. Minimize stress
  3. Ensure proper hydration & carbs
    • use glucose solution
    • Fluid and electrolyte balance
      • 10% glucose saline infusion
  4. Give anxiolytics
  5. Treat pain/N/V
    • BB for HTN and tachycardia
    • Benzodiazepines for seizures
  6. Cimetidine
    • decreases heme consumption and inhibits ALA synthetase (good)
  7. ​Hematin 3-4 mg/kg IV; Somatostatin; plasmapheresis
48
Q

What labs assess Liver function?

A
  • Bilirubin
  • Aminotranferases
  • Alkaline Phosphatase
  • INR
  • Albumin
49
Q

Billirubin

A

Degradation product of hemoglobin and myoglobin

  • Unconjugated is formed in the periphery→transported to liver via albumin→conjugated into water soluble compounds (unable to cross membranes)→eliminated from body

​​Increased *UNconjugated* bilirubin

  • Increased bilirubin production (hemolysis, skeletal muscle breakdown)
  • Decreased Hepatic uptake (low albumin stores)
  • Decreased conjugation

Increased *Conjugated* Bilirubin:

  • decreased canicular transport of bilirubin (billiary tract problem)
  • Acute/chronic hepatocellular dysfunction
  • Obstruction of bile ducts
50
Q

Aminotransferase

A
  • Lacks liver specificity → found throughout the body
  • Cholestatic disorders
    • ​increased levels may indicate damage of hepatic membranes from bile salt
  • 5’NT = most specific to billiary damage
51
Q

International Normalized Ratio

A
  • Strong correlation of deteriorating hepatic function
  • Used in Child-Pough score
  • Incicates impairment of hepatic synthesis of coagulation factors and Vitamin K
  • Tests 2, 7, 9, 10 and proteins C and S
52
Q

Albumin

A
  • MOST abundant plasma protein (only made in liver)
  • Synthesized by hepatocytes
  • If levels are decreased may mean:
    • Protein manutrition
    • Loss of protein →nephrotic syndrome
    • severe reduction in synthesis from liver

(acute liver failure will have high levels of albmin → albumin half life = 21 days )

53
Q

Acute Cholecystitis

Etiology, risk factors, sxs, treatment

A
  • Etiology:
    • Gallbladder or biliary tract stone
  • Risk factors
    1. Women
    2. fair skinned
    3. increased age
    4. obesity or rapid weight loss
    5. pregnancy
  • SXS:
    1. N/V
    2. fever
    3. abdominal pain
    4. RUQ tenderness radiates to back
    5. intense pain
    6. dark urine
    7. scleral icterus
  • Treatment:
    • Surgery when condition has stabilized
      • Laparoscopic (5% convert to open)
      • ERCP (endoscopic retrograde cholangiopancreatography)
54
Q

Laparoscopic Procedures - risks

A
  • Insufflation of abdominal cavity (pneumoperitoneum) → increased intraabdominal pressure leading to:
    1. Inadequate ventilation
    2. Decreased venous return → decreased CO and increased MAP and SVR
    3. Bradycardia due to peritoneal stretching
  • Increased MAP and SVR over several minutes restores CO
    • due to increased abdominal pressure
    • neurohumoral response and
    • absorbed CO2
  • Risk for vascular injury and acute blood loss
55
Q

Laparoscopic Procedures - Considerations

A
  1. Pre-Induction/Induction
    • Consider volume and electrolyte replacement
    • RSI with cricoid pressure/cuffed ETT
  2. Watch PIP/MV and adjust ventilation accordingly
  3. Reverse Trendelenburg aids surgical access and may improve ventilation
  4. Support BP and HR
  5. NG/OG tube
  6. Avoid nitrous oxide
  7. Judicious use of opioids
    • Opioids may cause Sphincter of Oddi spasm (morphine)
    • <3% incidence
    • Antagonize spasm with IV Glucagon/Naloxone/Nitroglycerin
56
Q

Viral Hepatitis

types, diagnosis, treatment, complications

A

​Types:

  • Acute has 5 types - HAV, HBV, HCV, HDV, HEV
    • A most common in the world (50%)
    • C most common blood borne infection in US
    • D can only infect if the pt already has B
    • E for enteric transmission in Asia, Africa, Central America
  • Herpes simplex virus/ cytomegalovirus/ Epstein-Barr

Diagnosis

  • Requires serologic testing or biopsy for definitive diagnosis

Treatment

  • Treatment of acute viral hepatitis is symptomatic
    • good nutrition
    • avoid ETOH
    • avoid overexertion

​Complications

  • Development of cirrhosis and primary hepatocellular carcinoma associated with chronic HBV/HCV infection
57
Q

Autoimmune Hepatitis

etiology, diagnosis, tratment

A

Etiology

  • Cellular immune response against self-antigens in the liver

Diagnosis

  • confirmed with:
    • clinical findings
    • lab testing
    • histologic evaluation

Treatment

  • No curative intervention
  • Goal is to induce remission with corticosteroids and immunosuppressive drugs or liver transplantation
58
Q

Drug Induced Hepatitis

etiology, diagnostic, treatment

A

Etiology:

  • Analgesics, anticonvulsants, antibiotics, antihypertensives and many others
  • APAP exhausts glutathione stores leading to inability to conjugate substances
  • N-acetylcysteine within 8 hours

Diagnosis

  • Sxs Resemble acute viral hepatitis so prompt diagnosis imperative

treatment:

  • Removal of offending agent
59
Q

Halothane Hepatitis

etiology & anesthetic management

A

Etiology:​

  • Trifluoroacetyl halide metabolites from VA metabolism covalently bond with microsomal proteins on hepatocytes - changing them from “self” to “nonself”
    • IgG antibody mediated
  • All volatile anesthetics, except Sevoflurane, can elicit immune-mediated hepatitis
    • Halothane most common culprit due to high degree of liver metabolism
    • sensitized individuals may show cross-reactivity with other volatile anesthetics (except SEVO)
    • 1-10,000-30,000

Anesthetic management:

  • TIVA or Sevo great options
60
Q

Cirrhosis - assessment tool

A

Child-Pugh Score

  • Tool used specifically to predict surgical mortality with cirrhosis
  • Assesses:
    1. Total bilirubin
    2. serum albumin level
    3. INR
    4. ascites
    5. hepatic encephalopathy
  • Class A= 10% mortality rate in intraabdominal surgery
  • Class B= 30% mortality
  • Class c= 80% mortality
  • A/B with preoperative optimization ok for surgery
  • class C surgery should be delayed (unless getting liver transplant)
61
Q

Cirrhosis - Anesthetic Considerations

optimization, ecephalopathy, ascites, varices, bleeding, renal, circulation, coagulopathy, PK/PD, liver blood flow

A

I appologize in advance for this long one

  • Preoperative Optimization!
    • Improve diet with protein and caloric intake
    • Blood glucose control pre/intra/post op (infusions with glucose?)
    • Aldosterone antagonist
    • Electrolyte and fluid status!
  • Encephalopathy
    • RSI
    • Judicious use of sedatives and induction agents
  • Ascites
    • RSI
    • Mechanical ventilation - behaving like a restrictive disease
    • PFTs
    • Pulmonary artery pressures
    • Fluid status - large removal of ascities w/out replacement with 7-8 g Albumin can lead to CV collapse
  • Esophageal Varices
    • no esophageal temp probe
    • no NG/OG tube
  • Bleeding?
    • RSI
    • Octreotide (50mcg/hr)
    • Vasopressin (20 U over 5 min)
  • ​Renal Impairment
    • Euvolemia
    • Monitor and correct for acid-base and electrolyte imbalances
  • Hyperdynamic Circulation
    • Decreased SVR mostly compensated with increased CO
    • Hypoalbumemia = edema
    • Cardiomyopathy
      • Avoid myocardial depressants
    • Invasive monitors, intravascular fluid replacement and vasopressors (phenylephrine/NE/Vasopressin)
    • Impaired response to catecholamines
      • Will see a limited response to increased dose requirements
  • ​Coagulopathy
    • T/C
    • Vitamin K non emergently
    • FFP, Cryoprecipitate, platelets
      • Only factors NOT produced by the liver are factors III, IV, XII
    • PRBCs
      • Impaired ability to handle citrate loads
      • Ionized calcium monitoring and calcium administration
  • Pharmacokinetics
    • Albumin
      • Decreased protein binding and increased VD
    • Decreased clearance
      • Example: larger initial dose of NDMR to compromise for the increased VD but decreased subsequent dosing due to decreased clearance
    • Caution with drugs dependent on liver clearance (cisatra/atra/miv great options) and drugs toxic to liver
  • ​Maintain liver blood flow
    • Hepatic artery 25% blood flow with 50% oxygen delivery
    • Portal vein 75% blood flow with 50% oxygen delivery
    • Intravenous anesthetics maintain hepatic blood flow if arterial blood pressure maintained
    • All inhalational agents maintain hepatic blood flow except halothane
    • Avoid SNS stimulation
      • ​give pain meds
      • prevent N/V
      • use lidocaine
62
Q

Alcoholism

A
  • Chronic ETOH causes enzyme induction
    • increased anesthetic needs
  • Acute ETOH decreases anesthetic needs
    • due to ADDITIVE effects
  • Acute intoxicated
    • RSI
  • Heavy ETOH can lead to acute hepatitis
63
Q

Alcohol Withdrawal Syndrome

sxs, treatment

A

Signs & Symptoms

  • Increased SNS- catecholamine release
  • Agitation
  • Tachycardia
  • Delirium tremors (48-72 hours post ETOH)à medical emergency
  • Hallucinations
  • Diaphoresis
  • Cardiac dysrhythmias
  • Hemodynamic instability
  • Grand mal seizures and hypoglycemia

Treatment

  • Benzodiazepine
  • Beta antagonist (propranolol or esmolol)
  • Airway protection
  • Correct fluid/electrolyte and metabolic disturbances
  • DT’s mortality rate is 10% due to hemodynamic instability, cardiac dysrhythmias and seizures
64
Q

Porphyria

Signs and Symptoms

A
  1. Severe abdominal pain/N/V due to autonomic neuropathy
    • ​​think RSI for induction
  2. ANS instability
  3. Electrolyte imbalances (Na, K, Mg)
  4. Skeletal muscle weakness- respiratory failure
  5. Cardiovascular instability resulting in Hypertension and tachycardia (less likely hypotension)
  6. Seizures
65
Q

Porphyria

Anesthetic Management

A
  1. Pre-op prep
    • Identify and avoid triggers (www.drugs-porphyria.com)
    • Assess:
      • skeletal and CN function
      • Cardiac - HTN, tachycardia
  2. Intra-op
    • Minimize multiple drug exposure
    • Fluid/electrolyte management
    • Anticipate post-op ventilation
    • Minimize stress of preop fasting glucose-saline infusion
  3. Preop meds
    • Anxiolytics, aspiration prophylaxis
    • Cimetidine inhibits ALA synthetase activity and decreases heme consumption
66
Q

Porphyria

Regional vs General

A

Regional

  • No absolute contraindications
  • Pre anesthetic neuro eval
  • ANS blockade may lead to cardiovascular instability especially with hypovolemia
  • Avoid in acute exacerbation

General

  • Use short acting agents
  • Monitors!
    • ​they may need an a-line
  • Induction with propofol or ketamine
  • Maintenance with N20, inhaled anesthetics, opioids and NDMR
  • Cardiopulmonary bypass is a stressor
67
Q

Porphyria

Safe drugs

A
  1. Opioids
  2. Propofol
  3. Ketamine
  4. ASA/APAP
  5. PCN
  6. Glucocorticoids
  7. Insulin
  8. Atropine/Glycopyrrolate
  9. Neostigmine
  10. Locals
  11. Most cardiovascular drugs
  12. Inhalational agents
  13. NDMR
68
Q

Porphyria

Unsafe drugs

A

SEND Phil BAK

  1. Sulfonamide antibiotics
  2. Etomidate
  3. Nifedipine
  4. Diazepam
  5. Phenacetin/Phenobarb
  6. Barbiturates
  7. Alcohol
  8. Ketorolac

Coexisting 2016 (12 decks)

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