A 57-year-old, 72 kg male is scheduled for a liver transplant.
History of present illness: The patient suffers from chronic hepatic cirrhosis.
Patient medical history: hypertension (HTN), hypercholesterolemia.
Medications: He is currently on spironolactone, propranolol, metronidazole, and lactulose.
Physical exam: Vital signs: BP 126/80 mmHg, pulse 104 bpm, RR 28, oxygen 92% on RA. Mallampati score is 2 with a full range of motion. Dentition is normal. Auscultation reveals a systolic murmur due to a systolic anterior motion (SAM) of the mitral valve. There is a fluid-filled abdomen on exam. The rest of the exam is unremarkable.
Labs: Hb = 11.3 g/dL, white blood cell count (WBC) 11,000, Na = 132 mEq/L, K = 4.0 mEq/L.
A. Preoperative Evaluation
First, a complete medical history and physical examination should be performed. From the history, I would want to know if he has had any episodes of chest pain, shortness of breath, or lightheadedness. I would also inquire about his baseline exercise tolerance by determining how many stairs he can climb comfortably. From the physical, I would listen to the heart sounds and assess for signs of congestive heart failure, such as jugular venous distention (JVD), pedal edema, and pulmonary edema, while keeping in mind that fluid overload can also be seen in cirrhosis. Finally, I would look at studies, specifically an EKG, and an echocardiogram because these patients are at high risk for pulmonary hypertension. If available, I would want to know the results of a stress test.
Liver Function Status
I would ensure the patient has large-bore PIV access, a preinduction arterial line, and a central line to allow adequate fluid resuscitation. In terms of induction, this patient most likely has ascites and so must be considered to have a full stomach. Since he could be volume depleted, it would be prudent to use cardiac stable agents for the induction. Higher than normal minimum alveolar concentration (MAC) values may be needed for maintenance because patients with cirrhosis often have a history of alcoholism. Finally, I would avoid using drugs that undergo significant hepatic metabolism.
What are the factors associated with liver disease that lead to the accumulation of ascites?
The factors that lead to ascites are hypoalbuminemia, portal hypertension, and water retention (secondary to secretion of antinatriuretic factors and antidiuretic hormone [ADH]).
Hepatorenal syndrome is an often fatal condition that is associated with rapid functional renal failure secondary to fulminate liver disease and cirrhosis.
Your resident informs you that there is no recent echocardiogram on file. Would you delay the case?
Yes, I would delay it because I want to fully understand the severity and symptomology associated with the systolic murmur, because this would affect my anesthetic management. I also want to know if this patient has pulmonary HTN, because severe pulmonary HTN (>50 mmHg) is a contraindication to a transplant.
In addition to the standard ASA monitors (pulse oximeter, noninvasive blood pressure [NIBP], EKG, EtCO2, and temperature) I would place an arterial line, a central line catheter (large 12 Fr), and transesophageal echocardiography (TEE).
Yes. The use of TEE may cause rupture and bleeding of esophageal varices. However, if extreme caution is exercised during the insertion and manipulation of the TEE probe, the likelihood of this complication has been found to be very low. In this case with the history of SAM and the high hemodynamic variations expected on a liver transplant procedure, I consider the use of TEE to be essential.
Assuming the patient is medically optimized, would you perform an intrathecal morphine injection for perioperative pain control in this patient?
No. Liver dysfunction is associated with multiple coagulation derangements (prolonged prothrombin time [PT], elevated international normalized ratio [INR], thrombocytopenia, platelet dysfunction). Regional anesthesia is an unacceptable high-risk procedure for this patient.
Because this patient likely has increased intra-abdominal pressure from ascites, I would treat him as I would for a full stomach. Thus, I would premedicate with sodium citrate, metoclopramide, and an H2 antagonist. Then, I would place the patient in reverse Trendelenburg position to reduce the risk of any passive regurgitation. Assuming a normal airway, I would perform a rapid sequence induction (RSI) with cricoid pressure using etomidate, and succinylcholine after adequate prehydration and placement of a preinduction arterial line.
Immediately after induction, the BP rapidly decreases to 75/40 mmHg, and HR is 80 bpm. What are you going to do?
I would immediately place the patient on 100% oxygen, look at the monitors to rule out a malignant arrhythmia, and pulse oximeter to rule out hypoxia, hypercarbia while feeling for a carotid pulse. Assuming all of these parameters were normal, I would open the fluids and administer a low dose of phenylephrine to improve the BP.
1. Preanhepatic phase: Period when the native liver is mobilized and dissected
2. Anhepatic phase: Period when the native liver is removed
3. Reperfusion phase: Period during which the new donor liver is anastomosed
Shortly after the surgeon has made the incision, you notice a very active suctioning sound. The patient starts turning gradually hypotensive although no significant blood loss has occurred. How would you assess this? What is your differential diagnosis? How would you manage the patient?
I would immediately look at the vitals and ensure the patient is not hypoxic, hypo- or hypercarbic, or in a malignant rhythm. Assuming all of these were normal, the most common initial cause of hypotension at the early stages of liver transplantation is hypovolemia due to the combination of the vasodilatory effects of the induction agents and the drainage of ascites. Thus, I would administer a bolus of a colloid-containing solution and continue giving boluses according to the central venous pressure (CVP) values and the appearance of the heart cavities on the TEE.
Twenty-five minutes into the anhepatic phase you notice a sustained period of hypotension, with no significant increases in blood loss. CVP = 11 mmHg, hemoglobin/hematocrit (H/H) = 10 g/dL/L, 30%. How would you evaluate this situation?
First, I would look at the patient’s other vitals to make sure they are stable. During the anhepatic stage, blood loss is not the typical cause of hypotension, especially after having a normal CVP value. After ruling out a mechanical cause of the problem by looking over the surgical field and asking the surgical team to check for sponges and evaluating suction containers, I would focus on contractility issues. First, I would review the electrocardiogram tracing, looking for prolongation of the QT interval (hypocalcemia) and ST interval (changes during acute ischemic events). I would also look at the trans esophageal echocardiogram (TEE) to evaluate for regional wall motion abnormalities +/-, global hypokinesia.
What is the difference between the “traditional technique” and the “piggyback” technique during the anhepatic phase? How do they affect your anesthetic management?
In the traditional technique, the surgeon performs a complete vascular occlusion by clamping the inferior vena cava (IVC), suprahepatic vena cava, hepatic artery, and the portal vein. As a result, venous return decreases by 50–60% and severe hypotension with a compensatory tachycardia may occur from the low CO. To prevent this, veno-venous bypass (VVBP) would have to be initiated and the complications associated with VVBP, such as arm edema, air embolism, and vascular injury, would have to be treated. The alternative is for me to volume load the patient with a target CVP of 10–20 mmHg and administer vasopressor boluses prior to clamping of the vessels. In the piggyback technique, the vena cava is partially occluded, making the surgery more challenging but eliminating the need for VVBP or the hemodynamic fluctuations encountered with the traditional technique.
The surgeon notifies you that he or she is about to “reperfuse.” How would you prepare for this?
Reperfusing the transplanted liver is one of the most critical moments of the operation, because the recipient’s blood will flush through the new liver and force multiple metabolic products into the main circulation. This will lead to a decrease in cardiac contractility, CO, systemic vascular resistance (SVR), and abrupt rises in pulmonary vascular resistance and serum hydrogen and potassium ion concentrations.
I would prepare by keeping the patient’s intravascular volume optimized, checking the ABG and H/H to correct any acid–base electrolyte disorder, and transfuse according to hemodynamic and H/H levels. I would have pressors, calcium, insulin, sodium bicarbonate, and blood products in line ready for use. Once the patient’s status was optimized, I would notify the surgeon to start the reperfusion process.
Reperfusion syndrome is hemodynamic instability, of unknown mechanism usually occurring during the first 5 minutes of reperfusion, that is associated with hyperkalemia and hemodynamic fluctuations such as hypotension, bradycardia, elevated pulmonary artery pressure (PAP), and supraventricular tachycardia.
C. Postoperative Care
You are paged to the surgical intensive care unit (SICU) because the nurse has just noticed that the drains from the abdominal cavity have been filling up rapidly. What should you do at this point?
I would immediately go to the patient’s bedside and evaluate his vital signs to make sure they are stable while asking the nurse to notify the surgeon. I would send for an ABG, H&H, and thromboelastography (TEG) samples. If hypotension was present I would give a bolus of 500 mL of lactated Ringer’s (LR) immediately, as well as a dose of phenylephrine to recover the BP.
While you are administering the first bolus of fluids, the laboratory calls to inform you that the TEG maximum amplitude (MA) value is below the normal values. An ABG shows: Hb = 9.2 g/dL, pH = 7.32, PaCO2 = 53 mmHg, BE = −2. CVP = 4 cm H2O, BP = 98/54 mmHg. What would you do?
The low MA value suggests to me an issue related to the platelet component. Thus, I would start transfusing two bags of platelets, watching closely the CVP value since a high CVP may lead to congestion of the new liver and trigger further bleeding and/or graft dysfunction. The other results suggest anemia, which can be worsened by the transfusion of non–red blood cells containing fluids. Therefore, I would prepare the patient for blood transfusion, making sure of the availability of five units of blood. The ABG result suggests the presence of mild respiratory acidosis, so I would adjust the mechanical ventilation by increasing the respiratory rate or tidal volume as tolerated.
After the transfusion of two units of platelets the patient’s nurse calls you to tell you the patient’s bleeding had initially improved but is now worsening again. How do you respond?
I would immediately evaluate the patient at the bedside. I will check vital signs to verify stability. Based on the clinical presentation of recurring hemorrhage and the findings from the TEG results, the diagnosis of fibrinolysis is more clear. At this point, I would order a dose of intravenous aminocaproic acid and check the level of fibrinogen to determine if a transfusion of cryoprecipitate is required.
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