Friday, September 27, 2013

Liver Transplant III

A gentleman with hepatitis C cirrhosis is scheduled for an orthotopic liver transplant. Though he has no other major medical conditions, his liver disease is fairly severe; his MELD score, a measure initially used to estimate 3 month mortality and now used to determine liver transplant priority, is 36, suggesting over 50% mortality in the next 90 days. He has significant ascites, leg swelling, esophageal varices, coagulopathy, portal hypertension, and hepatic encephalopathy. He needed a new liver.

We waited to induce anesthesia until the donor organ arrived. Until the transplant surgeon examines the organ fully, there is always the possibility that the surgeon may cancel the procedure. Though this was highly unlikely, we also did not want to put the patient at risk unnecessarily. Once we got the green light, we induced anesthesia, struggling with hypotension as liver disease severely impairs normal cardiovascular responses. We placed multiple lines including single lumen central line placeholders that could be converted to bypass cannulae if necessary. The transesophageal echocardiogram showed a hyperdynamic heart, commonly seen in patients with liver disease. We began reversing the patient's coagulopathy as his INR was five times normal. We began the patient on octreotide and some vasopressin, and the surgeons began.

To expose all the abdominal organs, major vessels, and the cirrhotic liver, the surgeons make a large "Chevron" incision below the ribcage about two feet long. He also makes an incision from the bottom of the breastbone down to the bellybutton. When he does so, several liters of ascites, fluid that accumulates in the abdomen as a result of liver dysfunction, spilled out. The dissection is meticulous, especially since the patient had gallbladder surgery in the past and had some scarring and adhesions. Through this time, we struggled with the blood pressure; cirrhotics are in a chronically vasodilated state, and general anesthesia doesn't help. This was a rare surgery in which we ran a very light anesthetic with heavy paralysis. With the level of liver dysfunction, the patient was confused and disoriented to start and would not be able to metabolize anesthetics easily. Thus, we expected our midazolam to linger longer than normal and provide adequate amnesia.

As the surgeons prepared to remove the old liver and connect the new one, they placed vascular clamps along the inferior vena cava. The clamp time was less than half an hour, but during this time, the normal blood return from the intestines and lower legs was impaired and portal venous pressures began to increase. The old liver came out, scarred, battle-ridden, even with the remnant of a TIPS catheter. The surgeons worked furiously to reconnect the inferior vena cava "cuff" of the new liver to the severed vena cava of the patient. Similarly, they reconnected the hepatic artery and portal vein. Meanwhile, we began optimizing the patient to the tenuous moment that the cross-clamps would be removed. We replaced electrolytes, warmed the patient, and decreased the anesthetic to almost nothing. Since the patient is anhepatic - liverless - the circulating medications were not being metabolized.

With the removal of the vascular clamp, blood flow began circulating through the new liver. However, this meant that all the toxins that built up while the donor liver was out of the body and being prepared are now released into the body. Cold potassium, preservation solution, cytokines, inflammatory mediators, and cellular debris floods into the heart. This is then followed by the venous blood draining from the intestines and lower extremities that could not be cleared during the cross-clamp. This blood is no better for the heart. To prepare for this hit, we gave calcium, glucose, insulin, and bicarbonate. Nevertheless, the patient's heart rate plummeted to 30 and the blood pressure halved, then halved again.The surgeons could not palpate the carotid or femoral pulses. This is the rollercoaster of the liver transplant. Fortunately, we anticipated this. I bolused atropine, escalating doses of epinephrine, and additional calcium chloride with appropriate responses. We shot a cardiac output with our pulmonary artery catheter and it showed a markedly stunned heart and a completely vasoplegic vascular system.

The anesthesia is challenging. We sent off blood gases every 20 minutes, adjusted our drips, fixed electrolytes, and gave blood products. The patient bled and bled and bled, and we found ourselves spiking bag after bag of blood, plasma, platelets, and cryoprecipitate. Eventually, we were able to achieve hemostasis and as the new liver began to work, we weaned the patient completely off drips. The heart began to squeeze vigorously, and we knew we had weathered the patient through.

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