Liver reduced I Flashcards Preview

Coags? Encephalopathy?

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

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

• Interferon
• Lamivudine
• Adefovir

• Interferon
• Ribavirin

• 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

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

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

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

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

• 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

• 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

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)

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

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 

• Bilirubin
• Aminotranferases
• Alkaline Phosphatase
• INR
• Albumin

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

• 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

• 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

• 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 )

• 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                                                       chol-angio-pancreato-graphy)

• 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

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)}
   • _{Antagonize spasm with IV Glucagon/Naloxone/Nitroglycerin}

​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

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

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

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

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)

_{*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

• 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

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

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

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

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

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

SEND Phil BAK

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