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List the causes of cirrhosis
- Primary biliary cirrhosis
- Wilson’s disease
- α 1 antitrypsin deficiency
- Nonalcoholic steatohepatitis (fatty liver)
What are the symptoms or characteristic findings of cirrhosis?
- Symptoms of fatigue or malaise are common to all acute and chronic forms of chronic liver disease.
- Other characteristic findings include: palmer erythema. Spider angionoma, gynomastia, testicular atrophy, and evidence of portal hypertension (splenomegaly and acites).
What are some abnormal lab values you would see in cirrhosis?
- ↓ Serum albumin
- ↑ PT
- ↑ Liver enzymes
- Liver biopsy will provide the dx but not the cause
What is the pathophysiology of Primary biliary cirrhosis ??
Primary biliary cirrhosis is likely d/t an immune mechanism that occurs. In this case there are antimicrobial antibodies. With primary biliary cirrhosis there is a progression and destruction of the bile ducts.
What patient population does primary biliary cirrhosis occur often in?
most often in women age 30-50years.
What is Hemochromatosis? ( a cause of cirrhosis)
inherited autosomal recessive disorder associated with iron deposits into body tissues.
Is Wilson's disease inherited?
YES, autosomal recessive
What is Alpha antitrypsin deficiency?
: associated with rare form or cirrhosis and often adult patients have emphysema with it. With this there is an accumulation of abnormal antitripysin in the liver
What are the complications of cirrhosis?
- Portal HTN
- Gastroesophageal varices
- Bacterial peritonitis
- Hepatorenal syndrome
- Hyperdynamic circulation
- Arterial hypoxemia
- Impaired immunity
- Hepatic encephalopathy
- Primary hepatocellular carcinoma
What causes the ascites seen in cirrhosis?
Ascites is the presence of intra-abdominal fluid that develops as a result of portal HTN If the pressure in the portal vein exceeds that normal 10mmHg, the fluid will leak from the capsule of the liver from the lymphatics into the capillaries because of blocked outflow. So our starling forces. High hydrostatic pressure but also low colloid osmotic pressure because of low levels of plasma albumin.
Hepatorenal syndrome has a very poor prognosis and this is why renal failure is associated w/liver disease. Most pt die within a few weeks of development of ischemia. What causes this?
Increased bilirubin correlate with potential for post-op renal failure. Acute kidney injury may be d/t endotoxins from infection and hypovolemia from decreased renal blood flow.
Portal HTN is caused by increased resistance from damaged liver cells. There is a back flow or shunting to organs with low resistance & collateral circulation relieves the pressure by essentially redirecting the blood flow. Where does the blood redirect that causes esophageal varices?
between the esophageal veins draining into either the azygous vein of the systemic system or the left gastric vein of the portal system. When these dilate they become esophageal varices
Portal HTN is caused by increased resistance from damaged liver cells. There is a back flow or shunting to organs with low resistance & collateral circulation relieves the pressure by essentially redirecting the blood flow. Where does the blood redirect that causes hemorrhoids?
between the rectal veins. The middle and inferior rectal veins draining into the IVC in the systemic and the superior rectal vein as continuing into the mesenteric vein in the portal vein in the portal system. When these dilate they become hemorrhoids.
Portal HTN is caused by increased resistance from damaged liver cells. There is a back flow or shunting to organs with low resistance & collateral circulation relieves the pressure by essentially redirecting the blood flow. Where does the blood redirect that causes kappamedusae?
- between the paraumbilical veins in the portal system anastomose with the small epigastric vein of the anterior abdominal wall in the systemic.
- These can produce what’s called kappamedusae seen on the abdominal wall where the periumbilical vein radiate under the skin around the umbilicus
What is a portacaval shunt or anastomosis?
- that blood can be diverted from the portal vein to the systemic vasculature by creating a communication between the portal vein and the IVC
- It will decrease the pressure in the portal vein
What is the transjuglarportosystemic shunt.
This can be inserted under fluroscopy by the internal jugular vein. Then provides a conduit for portal vein blood to flow directly into the hepatic vein while bypassing the liver parenchymas.
In cirrhosis, Hyperdynamic circulation is common with a CO of_______, how does this happen?
- C.O. > 14 L/min not uncommon
- SVR decreases, possibly from circulating vasodilating endotoxins. So all this contributes to a hyperdynamic circulation and the heart just doesn’t do well w/changes of preload and afterload
What are the respiratory complications of cirrhosis?
- PaO2 levels of 50-70mmHg are common in pt w/cirrhosis.
- Presence of ascites will limit diaphragmatic movement and HTN causes R to L shunting.
- Smoking and COPD also contribute to hypoxemia.
- ↓ PaCO2 d/t hyperventilation. Probably d/t elevated ammonia levels so respiratory alkalosis develops.
- Hyperventilation is contraindicated because this shifts ammonia ion to ammonia which worsens encephalopathy.
- HPV is impaired.
- Aspiration may also be d/t excessive alcohol consumption and elevated ammonia is frequent in alcoholics.
What is the cause of Hepaticencephalopathy?
- Hepatic encephalopathy results from elevated levels of ammonia, bilirubin, a build of GABA (remember the liver is needed to bring down GABA). May reverse w/flumazanil.
- Hepatoencephalopathy maybe precipitated by hemorrhage or anemia or actually CNS depressant meds, hypovolemia, infection, stress, alkalosis, hypoxemia, and hypothermia. It can also occur after a paracentesis.
What is the coagulopathy seen in cirrhosis?
- Platelets - ↓ number & impaired function
- Clotting factors - ↓ synthesis & ↓ half-life
- ↓ vitamin K synthesis & storage
- Thrombocytopenia from hypersplenism.
What causes the hypoglycemia seen in cirrhosis?
- ↓ glycogen stores
- Impaired gluconeogenesis
- ↑ insulin
Describe the lab evaluation for cirrhosis and ascites
- Liver evaluation: LFTs, coags, basic hematology, Abdominal U/S & CT, Upper endoscopy (varices), & Biopsy
- Renal & circulatory evaluation: Serum creatinine & lytes. Urine sodium & protein. BP
- Ascitic fluid eval: Cell count, Bacterial culture,, Total protein? Other testing
What is a way we can remove ascitic fluid?
- Removed by diuresis w/an aldosterone antagonist (Spironlactone).
- Remember Aldactone because it’s potassium sparing and aldosterone antagonist, if the patient has renal disease then at risk for hyperkalemia and that could present a problem
What is the goal for diuresis when removing ascitic fluid?
Meds for diuresis goal is 1L/day because if it’s removed more rapidly it can cause hypovolemia and azotemia
For Ascites, if diuresis doesn’t decrease the fluid then a leveen shunt can be inserted. What does this do?
- This will divert ascites subcutaneously from the peritoneal cavity to the IJ via a one way valve.
- This technique may result in a low grade DIC and infection both of which have limitations on its use.
- Finally, removing acites fluid for testing and acutely would be done by paracentesis.
Perioperative Risk: Child- Turcotte-Pugh (CTP) Score. Bilirubin (mg/dl):
- 1 Point: < 2
- 2 Points: 2-3
- 3 Points: > 3
Perioperative Risk: Child- Turcotte-Pugh (CTP) Score. Albumin (g/dl)
- 1 point: > 3.5
- 2 points: 2.8– 3.5
- 3 points: < 2.8
Perioperative Risk: Child- Turcotte-Pugh (CTP) Score. INR
- 1 point: < 1.7
- 2 points: 1.7 – 2.3
- 3 points: > 2.3
Perioperative Risk: Child- Turcotte-Pugh (CTP) Score. Encephalopathy
- 1 point: None
- 2 points: Grade I - II
- 3 points: Grade III - IV
Perioperative Risk: Child- Turcotte-Pugh (CTP) Score. Nutrition
- 1 point: Excellent
- 2 points: Good
- 3 points: Poor
Perioperative Risk: Child- Turcotte-Pugh (CTP) Score. Ascites
- 1 point: None
- 2 points: Moderate
- 3 points: Marked/Tense
Perioperative Risk: Child- Turcotte-Pugh (CTP) Score, total points = what risk...
- A is low risk. Total score of 5-6points on this scale. B is medium risk 7-9points.
- C is high risk, 10-15points
Perioperative Risk: Child- Turcotte-Pugh (CTP) Score has shown 1M mortality ranges of....
- Class A:of 5-10%
- Class B: 14-30%
- Class C: 51-80%
- Essentially non-cardiac elective surgery is not recommended for patients w/class C cirrhosis
What is the MELD (model for end-stage liver disease)
- created w/the objective system for assessing perioperative risk in patients w/cirrhosis.
- Rating is based on INR, total bilirubin, serum Cr.
- Also say MELD score of less than 10, 10-14, and greater than 14 correlate well with A, B, & C of the CTP score.
- But also say that this score is a superior predictor of peri-op risk.
What % of patients have portal pulmonary HTN?
- Portal pulmonary HTN is defined as a mean PA pressure of greater than 25mmHg.
- Seen in2-4% of pt w/cirrhosis.
- Severe portal pulmonary HTN is a contraindication to transplantation.
Ruptured esophageal varices and the bleeding that results will account for about ___ of the mortality of pt w/cirrhosis
Treatment of varices includes...
The tx of varices can include sclerotherapy and esophagial ligation. Beta blockade can help, vasopressin, Somatostatin and TIPS procedure
Renal dysfunction is almost always the result of ________
- It appears as either acute kidney injury or hepatorenal syndrome.
- It can be due to general hypoperfusion or bleeding from varices. Also can be d/t blood sequestration, acites, or overall dehydration.
- If volume is corrected quickly, it can be reversed but it can also progress to ATN.
Hepatorenal syndrome is defined as a plasma Cr greater than ____ in the absence of other causes of renal disease.
Name the two types of hepatorenal syndrome
- 1) progresses rapidly and requires hemodialysis and liver transplant.
- 2) is more stable and responsive to conservative treatment like vasopressin and betablockade and TIPs procedure
What are the drugs that can cause chronic hepatitis?
drug-induced chronic hepatitis can be seen with methyldopa, trazadone, isoniazids (anti-TB), as well as the sulfonamides, acetaminophen, ASA, phenytoin
What autoimmune disorders are associated with primary biliary cirrhosis?
- Rheumatoid arthritis
- CREST syndrome (limited cutaneous form of scleroderma).
- Pernicious anemia
- Sjorens syndrome
- Renal tubular acidosis
What is CREST syndrome
CREST is acronym for the 5 main features which are calcinosis, Raynaud's syndrome, esophageal dismotility, scerlodactily, and telangiesctasia
What should we test the ascitic fluid for??
The ascitic fluid itself should be sent to the lab for a cell count and culture Along with total protein, albumin, glucose, an acid-fast smear looking for TB and cytology
What types of hematologic disorders might we see in cirrhosis?
- anemia might be d/t bleeding, malnutrition or bone marrow suppression.
- BMS can also cause thrombocytopenia which could also be caused by sequestration of platelets in the spleen or some sort of immune mediated destruction of platelets.
- Coagulopathy can be d/t decreased synthesis of vitamins for clotting factors and accelerated fibrinolysis.
- Cirrhotic patients often present in a chronic form of DIC
Pt w/acute hepatitis or a child Type C or MELD ___ cirhosis should have elective surgery cancelled whereas child A (MELD __) can safely undergo elective surgery
MELD >14 ; MELD <10
For major surgery INR____and plt count of ____ and fibringoen ______ is preferred.
- INR <1.5
- Plt >100,000
- Fibrinogen >100mg/dl
Pre-op,if serum Na is low, correct slowly with an increase of not more than _mEq in 24hrs
Can jaundice cause erroneous reading on the pulse oximeter?
What is the main goal of anesthesia in a patient w/cirrhosis?
- Preserve hepatic blood flow
- Maintain liver function
What should we know about the volatiles for the patient w/cirrhosis?
- all the volatiles will decrease hepatic blood flow because it decreases SVR.
- Isoflurane actually dilates the hepatic artery and so it preserves reciprocity of hepatic blood flow.
- It’s possible Des has a similar effect
What should we remember about neuraxial blockade and cirrhosis?
- Regional may be ok if coags are normal but it’s generally is contraindicated because they aren’t normal.
- do a neuraxial block: impt to remember it also decreases SVR and so hepatic blood flow.
Which anesthetic technqiue will decrease Hepatic blood flow the least?? How much will it decrease?
- Barb/N2O/narcotic technique will decrease blood flow the least.
- About 15%.
What should we remember about hyperventilation and hepatic disease?
- See increased intrathoracic pressure and decreased hepatic blood flow decreased PaCO2.
- Decreased portal venous flow and increased ammonia levels.
- Converting over from the ammonium ion.
- Also increased K+ excretion because of respiratory alkalosis
How much will Positive Pressure Ventilation decrease hepatic blood flow?
So PPV has effect of decreasing hepatic blood flow by about 20%.
PEEP will have an effect such that 5cm of PEEP will decrease hepatic blood flow by about __% and 10cm by about __% so overall, if possible it might be best to avoid post-op ventilation.
What should we remember about Succinylcholine in cirrhosis?
- Pseudocholinesterase levels may be decreased but clinically prolonged effect of Succinylcholine isn’t usually significant.
- And Succinylcholine is generally the NMB of choice because these patients are at high risk of aspiration so an RSI is mandatory
What is the best intermediate acting NMB?
Intermediate acting drugs (Vecuronium and Rocuronium) are prolonged in liver disease and so Cisatracurium is probably the best choice
Which meds undergo Phase 1 metabolism?
- Diazepam, midazolam
- Amide local anesthetics
Which meds undergo Phase 2 metabolism??
- Most opioids
Why can we see altered drug responses, not just pharmacokinetic changes in cirrhosis?
One thing is the patient w/cirrhosis may have an abnormal BBB so there can be altered drug responses because of that in addition to the pharmacokinetic changes
What is the equation for 1/2 life?
- 1/2 life = Vd/Cl
- So as Vd is increased and clearance decreases (in liver failure) the 1/2 life increases,
What things cause enzyme induction?
occurs w/barbiturates, steroids, benzos, phenytoin, anti-histamine and of course, alcohol
Where should we monitor patients post-op in liver disease?
All pt should be monitored for 24hr in step down or ICU if pre-existing liver disease since morbidity and mortality is very high
Post-op: Class C (MELD > 14) cirrhosis, 1 month mortality = __ – ___%
What are the common complications post-op in patients with cirrhosis??
- New onset ascites
- Volume overload
- Worsening hepatic encephalopathy
- Upper GI bleed
- Renal failure
- Decreased liver function with coagulopathy
What are the s/s in acute liver failure?
- Mental status changes → coma
- Hallmarks: mental status, elevated PTT and INR
What are the anesthesia considerations in acute renal failure?
- Correct abnormal coags
- Usual caution with meds & liver disease
- Monitor for hypoglycemia, lytes, acid-base
- Transfuse slowly (citrate intoxication)
- Maintain hepatic blood flow & oxygenation
- Aseptic technique essential (risk of infection is substantial)
What % of Liver transplants are d/t Hep C?
40% due to HCV related liver disease
What are the 1 and 5 year survival rates for liver transplants?
- 1 year survival 85%
- 5 year survival 70%
What % of liver transplants are cadaver donors?
90% cadaver donors
Describe the effect of size on liver transplantation.
- Live donors are done in adults but it’s limitations of size substantially….if donor lobe is too small then liver dysfunction will develop within the 1st week after transplant.
- In general cirrhotic patients need a donor liver at least as large if not larger than their native liver.
What are the contraindications for liver transplant?
- Incurable malignancy
- Advanced age
- Active systemic or incurable infection (Hep C)
- Current ETOH abuse
- Major systemic disease
- Morbid obesity
List the common problems in the pre-anhepatic stage of liver transplant
- Blood loss (portal HTN)
Describe what happens during the pre-anhepatic phase of liver transplantation
- Dissection phase: involves mobilizing vascular structures around the liver, hepatic arteries, the portal vein, supra and inferior hepatic vena cava.
- Also isolating the common bile duct and then removing the native liver.
Why is veno-venous bypass helpful in liver transplantation
- ↓ blood loss during phase 1
- Manages complications of cross-clamping of portal vein & IVC
- This bypasses blood from lower to upper part of body and helps to maintain HD stability and decrease bleeding from the engorged portal system.
- Veno-venous bypass can have the result of improving HD, delaying onset of metabolic acidosis and decrease blood loss and maintain renal function
What are the problems with veno-venous cannulation during liver transplantation
can cause air embolism or thromboembolism & inadvertant decannulation
Describe how/where the veno-venous cannula is placed in liver transplantation
- Veno-venus bypass cannulas are placed in the common iliac and portal vein and the portal vein.
- The common iliac vein drains blood from the LE and the transected portal vein cannula drains blood from the viscera.
- Cannulas then get joined at a Y connection and blood gets drained at a pump then returned to the body through a central venous cannula to the axillary or jugular vein.
Do we need to heparinize in veno-venous cannulation for liver transplantation?
NO, Patient isn’t heparinized there is heparin in the tubing and no additional heparin is needed. Pt can’t metabolized heparin because liver isn't functioning so no additional heparin is given.
What is the flow rate for the veno-venous cannulation
Flow rate of the bypass is low, it’s like 1Lmin
What types of blood products might we give during the pre-anhepatic phase?
Packed cells, FFP, but avoid platelets and cryo during VVB
What kind of complications from massive transfusion should we watch out for in the pre-anhepatic phase?
How would we manage acid base balance and u/o during the pre-anhepatic phase?
- NaBicarb for metabolic acidosis
- Maintain u/o with fluids, mannitol, low dose Dopamine(+/-)
What is the anhepatic phase for liver transplantation??
- Clamping of hepatic vessels & VC → reperfusion of new liver
- Begins when blood supply to the native liver is stopped by clamping hepatic artery and portal vein. This is when the liver is removed. During this phase the pt essentially has no liver
- The donor liver is implanted by an anastomosis of the super hepatic vein to the hepatic vena cava and that’s followed by an anastomosis of hepatic artery.
What are the common problems during the anhepatic phase?
- Blood loss
- More coagulopathy & fibrinolysis
- ↓ renal function
- Can’t metabolize drugs, etc. (get citrate intoxication
What abnormalities would you NOT treat during the anhepatic phase?
Treated acidosis, electrolyte and glucose abnormalities but not coagulopathies again until Veno-venous bypass is removed.
How do we prepare for reperfusion during liver transplantation?
- In order to prepare for reperfusion we give steroids, usually methylprednisolone, Ca+ chloride and Na Bicarbonate.
- Can also put patient on 100% oxygen.
- Have emergency drugs and equip available. Atropine, epinephrine, defibrillation, rapid transfuser.
- Need to ensure patient has adequate IV volume before flushing the portal vein.
What is the reperfusion (Neohepatic phase) of liver transplantation?
- Unclamping of portal vein (first), hepatic artery, & IVC with perfusion of donor liver
- Liver gets flushed w/blood to remove air, debris, and any preservative solution and the clamps on the VC are removed.
What are some common problems during the reperfusion (Neohepatic phase)?
- ↓ HR
- Lactic acidosis
Patient is likely to become HD unstable various dysrhythmias, severe bradycardia, hypotension and hyperkalemia. What can we do???
- Want to correct acidosis, iCa should be normal w/K less than 4
- Anticipate pulmonary edema, 100% oxygen.
- D/C volatiles about 5min before unclamping.
- Plan for coagulopathy and lab tests TEG (thromboelastogram) to guide management
What happens after reperfusion (What surgical steps)
- As graft begins to function patient will stabilize. Reperfusion of hepatic artery and blood flow is restored and then hemostasis is achieved w/administration of clotting factors (now bypass is off) coags will normalize.
- Donor and recipients common bile duct is anastomosed and the gall bladder is also removed. Again bypass is d/c and abdomen is closed
After reperfusion, where should we maintain the BP?
IMPT to maintain pressure about 70 to prevent hepatic artery thrombosis but again don’t want it to be high because it will cause bleeding.
Name the problems associated w/Reperfusion
- Volume overload
- Hemodynamic instability
- Pulmonary emboli
- Profuse bleeding/coagulopathy
- Pulmonary edema
- Pulmonary HTN
- Hyperkalemia (want K les than 4 before reperfusion)
When will the K+ level normalize after reperfusion, what can we do to treat it?
If K elevated will normally go back to normal after 10-20 min after reperfusion. Tx by CaCl or bicarb if needed
What are the types of hemodynamic instability seen during reperfusion?
- Hypotension (MAP < 70% baseline)
- Bradycardia, conduction defects
- ↓ SVR with acutely ↑ RV pressures → pulmonary HTN
- Cardiac arrest
Fibrinolysis is at peak after reperfusion. Why is this and how do you treat it?
Driven by an abrupt increase in tissue plasminogen activator levels. Which get released from endothelial cells of the liver. Antifibrinolytic agents (Amicar and Cryoprecipitate) may be needed to counteract the fibrinolysis.
Describe the pre-op assessment in liver transplantation?
- Labs & tests
- Type & X for 2-4 units + FFP
- Anticipate ascites, peripheral edema portal HTN and hepatomegaly
- CV hyperdynamic w/increase CO and low SVR. Cardiomyopathy is also possible, watch for arrhythmias.
- Up to 80% of may have cerebral edema and increased ICP encephaolopathy.
- Hepatorenal syndrome increased BUN and Cr. Pulmonary HTN and V/Q mismatch. Atelectasis pleural effusions, if they have excessive pulmonary HTN might have gotten prostaglandins infusion pre-op for treatment.
- They might also have massive hepatopulmonary syndrome which is type of oxygen resistance hypoxemia which means they need to be intubated post-op.
Describe the monitoring used in liver transplantation
- Monitoring includes everything from thermoregulation & invasive monitors
- An a line is essential. Want to check w/surgeon, if using VV bypass using axillary vein, don’t want to go in the wrong spot.
- CVP, a line is essential. TEE may be helpful, but if pt has varices, check w/surgeon!!
Describe the lab monitoring
- Want the K low again, because it will elevate w/reperfusion.
- Check labs Q30min if patient is unstable, Q1hr if they are stable (dictated by what’s going on)
- Maintain Na within 10mEq of normal values.
- Because patients are at high risk for citrate toxicity, want to check their iCa levels frequently.
For liver transplantation. Rapid transfuser is essential ___-_____ml/min. 2 dedicated volume lines (1 being a 7fr to handle that transfuser)
What lab test will help guide blood product administration?
- Thromboelastogram (TEG) will help guide blood
- product administration.
What medications will we use intra-op for liver transplantation?
- Vasoactive agents: not just boluses but by infusion. maybe phenylephrine, certainly epi, maybe norepi, nitro, dopamine, dobutamine, amiodorone. Also antiarrhythmics like lidocaine.
- Bolus agents: ephedrine, esmolol, CaCl, atropine, bicarb, heparin. Amicar.
What should we keep in mind w/phenylephrine and liver transplantation?
- be mindful our goal is to perfuse liver.
- Don’t want to vasoconstrict.
- We already said the alpha 1 receptors are there so when we stimulate the alpha 1 receptors we’ll effect the liver.
VAM is sometimes used in liver transplantation?
Parental systemic alkalinizer, includes replenisher and acts as an osmotic diuretic to tx acidosis. Along w/bicarbonate. Doesn’t contain Na+.
Vasopressin and also methylene blue can scavenge free radicals and solumedrol
What kind of vasoactive medications should we avoid for liver transplantation?
Avoid direct acting vasopressors
Describe immediate and acute rejection, after liver transplantation
- Immediate: hyperacute. D/t preformed antibodies and there are microvacular clots and thrombosis that result
- Acute: happens after 5 days post-op.
How can we tell if the liver is working post-transplant?
iCa (citrate metabolism) correction of acidosis, correction of blood glucose from release of glycogen, bile formation, the reduced need for HD support, and the metabolism of MR and any other drugs
Pt will continue to get immunosuppressant drugs after liver or cadaver donor. Given 1st in OR. 1st __hr are critical even if the liver looks like it’s functioning at time of transplant. Within __-__hr the surgeon will know if the liver is functioning properly.