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Flashcards in Liver reduced I Deck (61)
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CV function in patients with cirrhosis

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



coagulation and treatment

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 )


Once a potentially serious vascular injury is suspected, immediate conversion to an open procedure must be considered.

Direct compression of the bleeding site is the quickest and safest way to gain initial control of blood loss, especially with a venous injury.

If the patient exhibits unstable vital signs, adequate volume replacement, while controlling the blood loss, must take place prior to attempting repair of the injury.

If the bleeding site is difficult to see, early and wide exposure of the site and the surrounding structures must be obtained.

The vessel wall must be repaired with precise intima to intima apposition without tension.

Venous injuries may be best handled by ligation rather than suture repair if the patient is unstable.

If ligation of a vessel does not lead to ischemia, definitive repair may be postponed until the patient is stable and/or when the appropriate vascular surgeon is available



Pre-op considerations in cirrhosis

  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




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


How should we maintain anesthesia for the patient with cirrhosis?

IA at 1/2 MAC with N2O and opioids


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

Need higher dose because Vd will be increased


What NMBs are best for cirrhosis

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


liver patients have higher post op morbidity

what are some causes?


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


Other comorbidities that alcoholics may have

  • Hypothermia
  • alcoholic poluneuropathy
  • Wernicke-Korsakoff syndrome
  • Pernicious anemia


Considerations for Maintenance of anesthesia in cirrhosis patients


  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


This enzyme is deficient in porphyria

ALA synthetase


S/S of porphyria attack

  • 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


Regional anesthesia and porhyria

  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)


Why do patients have hyperdynamic circulation with liver disease?

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


Any IAs that decrease hepatic BF will increase serum concentrations of

Alpha-GST (Glutathione S-transferases)


Blood volume in liver disease

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


GA Considerations in porphyria

  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!


Is cimetidine good or bad in porphyria?


It decreases heme consumption and decreases ALA synthetase activity


Acute Cholecystectomy



Procedural considerations


  1. Gallbladder or biliary tract stone
  2. Fat, fair, women, over 40,
    • ​​also rapid weight loss, and pregnancy
  3. Present with: N/V, fever, abdominal pain, RUQ tenderness radiates to back, intense pain, dark urine, scleral icterus
  4. Surgery when condition has stabilized 
    • Laparoscopic 5% convert to open
    • ERCP (endoscopic retrograde cholangiopancreatography) – done under fluro 

Laproscopic Procedures

  1. Insufflation of abdominal cavity
    • (pneumoperitoneum)→increased intra-abd pressure
    1. Inadequate ventilation
    2. Decreased venous return = decreased CO and increased MAP and SVR
      • due to increased abdominal pressure, neurohumoral response and absorbed CO2.
    3. Bradycardia due to peritoneal stretching
    4. Risk for vascular injury and acute blood loss

Considerations for Procedure

  1. Consider Volume & Electrolyte replacement (N/V)
  2. RSI with Cricoid Pressure cuffed endotracheal tube (Pain slows the gut!!!)
  3. Watch PIP/MV and adjust ventilation accordingly
  4. Reverse Trendelenburg aids surgical access and may improve ventilation
  5. Support BP and HR
  6. NG/OG tube (decompression of the stomach)
  7. Avoid nitrous oxide (it goes into the airspaces)
  8. Judicious use of opioids
    • Opioids may cause Sphincter of Oddi spasm, < 3% incidence (DO NOT use morphine and meperidine)
    1. Fentanyl has a much lower incidence
    2. Antagonize spasm with IV Glucagon 0.5 mg, Naloxone or Nitroglycerin


Cholecystectomy and opioids

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


Volatile anesthetics and hepatic dysfunctions

  • 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


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

 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


What is hepatitis

Inflammation of the liver parenchyma d/t 

  1. Viral
  2. Autoimmune
  3. Drug-Induced


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


  • 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


Common hepatitis causes

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


Pre-op Assessment - hepatitis

  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?


Pre-op considerations in hepatitis

Coags? Encephalopathy?


Induction for hepatitis

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



etiology, types, sxs, 


  1. Inflammation of the liver parenchyma
  2. Viral
  3. Autoimmune
  4. 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)


  • 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


Hep B Tx

  • Interferon
  • Lamivudine
  • Adefovir


Hep C Tx

  • Interferon
  • Ribavirin