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50 Cards in this Set
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preop |
preop |
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what is the MELD score? |
model for end-stage liver disease tool for stratifying the severity of liver disease to prioritize organ allocation ranges from 6-40 uses: Cr bilirubin INR high the score the higher the short term mortality most transplant pts have 11-20 |
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is the MELD used for patients with fulminant hepatic failure of with life expectancy of <7 days? |
no these patients are designated status 1 and given the highest priority |
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what do you think of this patients dyspnea? |
she has a history of smoking, alcohol abuse, and liver disease, so it could be secondary to: 1. smoking/COPD 2. alcoholic CM 3. cirrhotic CM 4. ascites 5. pleural effusions 6. hepatopulmonary syndrome 7. or any combination of the above the patients worsening dyspnea in the upright position, platypnea, is consistent with hepatopulmonary syndrome, so i would look for other signs of this |
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what other signs of HPS would you look for? |
1. hypoxia (PaO2 < 70 on room air) 2. fatigue 3. digital clubbing 4. spider angiomata 5. deoxygenation in the upright position (orthodexia) HPS is defined by the triad of liver disease, dec oxygenation, and intrapulmonary vascular dilation as diagnosed on echo, perfusion lung scanning, or pulm arteriography |
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what is the tx for HPS? |
unless completely unresponsive to supplemental oxygen, it is an idication for liver transplant (is unresponsive this indicates unacceptable perioperative risk of graft hypoxia and failure) |
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what do you think of the abdominal exam findings? |
a tense distended abdomen with a fluid wave in a patient for a liver tx is consistent with marked ascites, which could be contributing to the dyspnea |
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what causes ascites in cirrhosis? |
its likely multifactorial: portal HTN and the renal retention of sodium and water result in transudation of fluid into the peritoneal cavity |
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what does this fluid cause? |
it can put pressure on the diaphragm and stomach, resulting in compromised pulmonary gas exchange and risk of aspiration respectively |
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would you perform preop paracentesis? |
i would consider preop therapeutic paracentesis which may have several benefits, including: 1. inc CO from dec pressure on the IVC 2. improved pulm gas exchage (inc compliance and reduced V/Q mismatch) 3. dec risk of aspiration 4. there is some evidence that paracent may transiently reduce renin and aldosterone levels, serum Cr and BUN, and portal pressures |
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what would you be sure to do if you did a paracentesis? |
ensure adequate volume expansion with colloids to prevent circulatory collapse due to the progressive reaccumulation of ascitic fluid some evidence supports giving 50% of the plasma expander right after the paracentesis, and then the other half 6 hrs later (when removing 5L of fluid, some recommend albumin 6-8 g/dL of ascites drained to prevent renal decompression) |
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are you concerned about hepatorenal syndrome? |
yes i am given his elevated Cr (>1.5) and recognizing that up to 10% of pts with advanced liver dz and ascites develop this life-threatening renal failure caharcterized by constriction of the renal vasculature, dec GFR, preserved renal tubular function, hyperosmolar urine, urinary Na excretion <10 mEq/L, azotemia, and normal renal histology but there are other reasons for renal failure in a cirrhotic pt, including prerenal, ATN, and drug toxicity, so i would perform additional labs to ID the cause of elevated cr |
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how would you determine whether his elevated Cr was due to HRS? |
in determining the cause of his azotemia, i would: 1. evaluate response to a fluid bolus 2. review meds and history looking for nephrotoxic drugs or contrast agents 3. check urine Na levels, osmolality, urine-to-plasma cr ratio, and urinary sedimentation level if renal function improved with fluid bolus, id consider it prerenal if urinary Na >10 or there were casts in the urine sediment, this is ATN i would also consider the criteria for HRS |
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criteria for HRS |
major criteria: 1. presence of advanced liver dz and portal HTN 2. a low GFR (cr >1.5 of cr cl <40) 3. the absence of shock, infection, fluid losses, or treatment with nephrotoxic agents 4. no improvement in renal function in response to 1.5L fluid challenge 5. absence of proteinuria (<500 mg/day), urinary obstruction, or parenchymal renal disease minor criteria 1. oliguria (<500 ml/24 hrs) 2. a low urinary sodium concentration (<10 mEq/L) 3. a urine osmolality that exceeds plasma osmolality by at least 100 4. spont dilutional hyponatremia (serum Na<130) 5. absence of RBCs in the urine |
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assuming this is HRS, what is the pathophysiology of it? |
the inc level of endothelial (prostacycline and no) and nonendothelial (glucagon) vasodilators assoc with severe liver disease, causes splanchnic vasodilation, which leads to dec in the effective volume sensed by the kidney, which leads to compensatory activation of the renin-a-a system and sympathetic nervous system, which although leads to systemic and renal vasoconstriction, but these effects are not sufficient to counteract the splanchnic vasodilation, and persistent splanchnic dilation and dec renal perfusion result in profound intrarenal arterial vasoconstriction and eventually HRS |
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types of HRS |
**PIC** |
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platelets= 76 PT/PTT= 16/30 s INR= 1.4 would you give blood products prior to sx? |
given the urgency i would not try to normalize the coagulation status as long as platelets >50-60 and INR < 1.5, and there were no signs of active bleeding the complete correct of coagulation abnormalities would be difficult if not impossible, and the definitive tx is liver transplant and should not be delayed unless absolutely necessary, however coag status needs to be taken into account when placing lines, monitors, esp PAC, TEE if esophageal varices, or ICP |
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whats the cause of coagulation abnormalities in liver dz? |
1. dec production of coagulation and inhibition factors (all are made by the liver except 8 and vWF) 2. quantitative and qualitative platelet defects (due primarily to portal HTN-induced splenic sequestration) 3. vit K def 4. hyperfibrinolysis 5. dec clearance of activated clotting factors 6. DIC |
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echo estimates the PA P is 46. does this concern you? |
yes it does bc patients with PAP >35 and PVR >250 are at inc risk of perioperative death from RHF or hepatic failure and since liver transplant is contraindicated if PA P >50, id consider RH cath to confirm the echo pressure, and if the pressure showed moderate elevation of 35-45 id consider placing a PA cath prior to induction, recognizing this may be difficult if there is encephalopathy |
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what would you do while placing the lines? |
given his coagulation status id consider giving FFP and using US guideance to reduce significant bleeding |
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why wouldnt you give platelets? |
i would consider it, but theres some evidence that giving them may prove detrimental to graft and pt survival |
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portopulmonary HTN |
***PIC*** |
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couldnt you just use TEE and avoid placing a PAC? |
TEE could be used but id be reluctant due to inc risk of bleeding associated with its placement and esophageal varices, which is a relative contraindication as always i would weight the risks and benefits |
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the patient seems mildly confused, does this concern you? |
he is taking neomycin and lactulose, which are used to dec the production of ammonia by intestinal bacteria, which suggests hes been having hepatic encephalopathy, so this mild confusion does not concern me because it is likely related to this |
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how does hepatic encephalopathy result? |
impaired liver function leads to the accumulation of neurotoxins like ammonia, GABA, mercaptans, short chain aftty acids, and manganese other contributing factors: altered cerebral energy homeostasis astrocyte swelling disruption of the BBB |
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how would you treat it? |
if i ruled out other causes, such as chronic subdural, psychoactive drugs, or Wernickes enceph from alcohol, i would try to ID and tx any inciting factors (GI bleed, infection, hypotension, anemia, hypovolemia, azotemia, oaracentesis, recent TIPS, diarrhea and vomiting, and diuretics) i would also evaluate for signs of inc ICP, avoid hypokalemia which can inc renal production of ammonia, avoid alkalemia since it can inc diffusion of ammonia across the BBB, correct any hypovolemia or anemia, and be cautious about benzos or other psychoactive drugs |
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intraop |
intraop |
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which lines and monitors would you require? |
this is based on the potential for sig HD instability and blood loss, the complications of ESLD, PPH, and HRS, so in addition to ASA standard i would want: 1. A line for close HD monitoring and frequent blood draws 2. central line and PAC for intraop monitoring of PA pressures and to give vasoactive drugs 3. foley to closely monitor urine output in a pt with HRS and a case associated with large fluid shifts 4. i would avoid TEE or NGT given the varices to avoid massive bleeding potential 5. id want a couple of large bore IVs for high volume infusion, and rapid infusion equipment 6. consider venovenous bypass, and if so avoid placing any lines in the arm selected for the procedure??? |
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what is veno-venous bypass? |
the femoral and portal veins are cannulates to reroute flow from below the diaphragm to the suprahepatic vena cava when caval flow is interrupted during the anhepatic phase of the sx |
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what are the advantages of VVBP? |
1. improved HD stability 2. better organ perfusion during the anhepatic phase 3. improved cardiac filling 4. dec blood and fluid requirements 5. splanchnic decompression 6. preserved drainage of the renal veins 7. limited metabolic impairment 8. imprved cardiac filling 9. improved surgical field 10. dec pulm edema |
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disadvantages? |
inc risk of air embolism thromboembolism arm lyphedema hematoma vascular or nerve injury |
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would you place an epidural? |
given the thrombocytopenia and possible thrombocytopathia, elevated PT, PTT and INR, and the potential for prolonged significant coagulopathy i would avoid neuraxial for concern of an increased risk of epidural hematoma formation i would consider other methods of pain control, like opioids, nonopioids, and PCA |
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how would you induce? |
given his ascites, the emergent nature of the case and preumed full stomach, and the gastroparesis which often accompanied ESLD, i would want perform a RSI to reduce the risk of aspiration therefore assuming a reassuring airway and that he was HD stable, I would make sure the appropriate monitors and IV access was obtained, give aspiration prophylaxis, place in reverse tberg, preoxygenate with 100% oxygen for 5 min, give lidocaine, propofol, and sux, and rapidly securing the airway |
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what would you remember about sux? |
the potential for prolonged effect due to reduced pseudocholinesterase |
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would you place an OG to reduce the risk of aspiration? |
while it would decompress the stomach to dec the risk of aspiration and improve surgical exposure, i would avoid it due to the risk of significant bleeding in a patient with esophageal varices |
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esophageal varices |
increasing portal pressures (>12 mmHg) result in dilation of the superficial veins of the esophageal mucosa, which are thin walled and prone to bleeding from trauma |
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would you use sux for RSI? |
given the inc risk of aspiration i would use sux to facilitate intubation as rapidly as possible, understanding there may be a prolonged effect, but that the length of this case will allow for adequate metabolism |
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the surgeon is planning infracaval interposition of the new liver. briefly describe the 3 stages of liver transplant? |
1. dissection (preanhepatic): liver is dissected and mobilized 2. anhepatic: starts with clamping of the hepatic artery and goes through removal of the old liver and implantation of the donor liver 3. reperfusion (neohepatic) completion of the anastomosis, ensuring adequate hemostasis, and completion of sx |
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at the start of the anhepatic phase, the surgeon clamps the IVC. the BP drops to 78/44. what will you do? |
1. i would ask the surgeon to release the clamp, since the timing suggests that the reduced preload from clamping is responsible bc there are other causes, id: 2. switch to 100% O2 3. confirm the measurement 4. verify proper ETT placement 5. auscultate the lungs 6. give fluids and pressors 7. discuss VVBP with the surgeon 8. if VVB was not reasonable for whatever reason, id volume load to a target CVP of 10-20, and ensure presence of vasopressors to replace the clamp |
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during the anhepatic phase the patients EKG starts to show peaked T waves and a widening QRS. what do you think is going on? |
this is consistent with significant hyperkalemia, he is at risk of this from acidosis during the anhepatic phase, his dec UOP from HRS, and high K levels in stored blood, and the washout of the K containing preservative solution |
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what would you do? |
i would: 1. give Ca to depress cardiac membrane excitability 2. ensure immediate access to a defibrillator and be prepared to immediately treat arrhythmias or HD instability 3. try to correct anything exacerbating cardiac hyperexcitability, such as acidosis, hyponatremia, and hypocalcemia 4. give insulin and glucose, B2 agonist, and sodium bicarb to facilitate intracellular movement of K 5. hyperventilate to promote alkalosis and intracellular movement of K 6. give consideration to HD |
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could these EKG findings represent citrate tox? |
while the widened QRS could, the peaked T waves are more consistent with hyperkalemia however given the likely rapid admin of blood products combined with the dec clearance of citrate from the liver, i would look for other signs |
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other signs of citrate tox |
signs of hypocalcemia in a patient under GA: 1. hypotension 2. narrow pulse P 3. prolonged QT 4. elevated intraventricular EDP 5. elevated CVP 6. flattened T waves |
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tx of citrate tox |
if at any point it developed, id give CaCl (3-5ml of 10% solution) or gluconate (10-20ml of a 10% solution), correct hypothermia, optimize perfusion to the liver, monitor serum Ca levels, repeat Ca as needed, and prepare to treat significant hypotension or arrhythmias |
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you treat the hyperK and proceed through the anhepatic phase without further difficulty. at the beginning of the reperfusion phase the patients BP drops from 112/78 to 64/37. what do you think is going on? |
hypotension at the start of this phase is likely due to the removal of clamps and development of postinfusion syndrome, which is hypotension, bradycardia, arrhythmias, and elevated PA pressures but i would also consider: hemorrhage, tension pneumo, CHF, hyperkalemia |
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what causes reperfusion syndrome? |
several mechanisms are proposed: 1. excessive K load with flushing of the graft into the systemic circulation 2. release of vasoactive substances and acid metabolites from the LE 3. deleterious effects of cold blood on the heart 4. release of cytokines things that worsen this condition: metabolic acidosis, hypovolemia, hypocalcemia, hyperkalemia, hypothermia |
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what can be done to reduce the incidence? |
carefully flush the graft prior to reperfusion give bicarb or THAM prior correct metabolic abnorms give Ca (500mg CaCl) can give pressors or inotropes to correct any preexisting hypotension before reperfusion |
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postop |
postop |
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would you extubate this patient immediately after the case? |
while many are after liver tx, in this case i would not extubate due to preop ascites, PPH, HRS, and hepatic encephalopathy, i would transport him to the ICU and delay extubation until all criteria are met and a mor ethorough eval of his condition can be performed |
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what potential post-op complications should be anticipated following liver tx? |
1. bleeding esophageal varices 2. vascular anastomotic leak or failure 3. coagulopathy 4. renal dysfucntion 5. CHF 6. TRALI 7. pulm edema 8. biliary complications 9. hepatic or portal vessel thrombosis 10. encephalopathy 11. peripheral nerve injury 12. diaphragmatic or phrenic nerve injury 13. systemic infection 14. acute graft failure or rejection 15. metabolic abnormalities |
