# Liver Transplantation: Anesthetic Management by Surgical Phase

## Introduction

Orthotopic liver transplantation (OLT) is one of the most physiologically demanding procedures in anesthesia. The operation is characterized by massive fluid shifts, coagulopathy, hemodynamic instability, metabolic derangements, and the potential for rapid cardiovascular collapse. The anesthetic management is organized around three distinct surgical phases, each with unique challenges: the dissection (pre-anhepatic) phase, the anhepatic phase, and the neohepatic (reperfusion) phase.

## Preoperative Considerations

### Recipient Assessment

The MELD score determines transplant priority and reflects the severity of hepatic dysfunction. Cardiovascular evaluation includes echocardiography to assess for cirrhotic cardiomyopathy and portopulmonary hypertension, with dobutamine stress testing or cardiac catheterization added as indicated. Portopulmonary hypertension with a mean pulmonary artery pressure greater than 35 mmHg is a relative contraindication to transplantation, while a pressure exceeding 50 mmHg is an absolute contraindication. Hepatopulmonary syndrome, in which intrapulmonary shunting causes hypoxemia, may worsen with positive-pressure ventilation. Renal function must be assessed because hepatorenal syndrome is common, and the need for intraoperative renal replacement therapy should be anticipated. Coagulation status is evaluated with baseline INR, fibrinogen, and platelet count, keeping in mind that the rebalanced hemostasis concept applies. Electrolyte abnormalities including hyponatremia, hypokalemia or hyperkalemia, hypocalcemia, and hypomagnesemia are frequently present.

### Preparation and Setup

Vascular access requires two large-bore peripheral IVs (14-gauge or rapid infusion catheter introducers), large-bore multilumen central venous access, and arterial line placement at the radial and/or femoral artery. A rapid infusion device capable of delivering warmed fluids at 500 to 1500 mL per minute (such as a Belmont or Level 1 system) is essential, along with a cell salvage device for autotransfusion. Viscoelastic monitoring with TEG or ROTEM should be available at the bedside. Blood products must be immediately available, typically including 10 units of packed red blood cells, 10 units of FFP, 2 units of pooled platelets, and cryoprecipitate. Point-of-care testing for arterial blood gases, electrolytes, lactate, ionized calcium, and glucose is required. Transesophageal echocardiography is essential for real-time hemodynamic assessment, though it carries a relative contraindication in patients with grade 3 varices.

## Phase 1: Dissection (Pre-Anhepatic) Phase

### Surgical Activity

This phase involves mobilization of the native liver and dissection of the hilar structures, including the hepatic artery, portal vein, and bile duct. Lysis of adhesions may be extensive, especially in re-transplantation cases. The duration is typically 1 to 3 hours but is highly variable.

### Anesthetic Challenges

Hemorrhage during this phase can be significant, driven by portal hypertension, collateral vessel formation, underlying coagulopathy, and adhesions. Large-volume ascites drainage during laparotomy causes intravascular volume depletion. Hemodynamic instability results from the combination of hemorrhage, third-spacing, and vasodilation. Coagulopathy management should be guided by viscoelastic testing, with targets of fibrinogen greater than 150 mg/dL and platelets greater than 50,000 per microliter.

### Management Goals

Euvolemia is maintained with crystalloid, colloid, and blood products guided by hemodynamics and point-of-care testing. Vasopressors such as norepinephrine and vasopressin are used for persistent hypotension despite volume resuscitation. Ionized calcium must be corrected aggressively because citrate from blood products causes hypocalcemia, with a target of ionized calcium greater than 1.0 mmol/L. Correction of coagulopathy should begin early, while avoiding excessive FFP administration that could lead to volume overload. Normothermia is maintained with forced-air warming and fluid warmers.

![Illustration of the three surgical phases of liver transplantation showing the vascular anatomy at each stage](images/olt-surgical-phases.png)

## Phase 2: Anhepatic Phase

### Surgical Activity

The anhepatic phase encompasses native hepatectomy and vascular clamping of the IVC and/or portal vein, followed by implantation of the donor liver with vascular anastomoses. Two surgical techniques are available: the classic approach with venovenous bypass, and the piggyback technique in which the IVC is partially preserved.

### Anesthetic Challenges

Hemodynamic compromise from IVC clamping is the dominant challenge, with decreased venous return causing up to a 50% drop in cardiac output. The piggyback technique, which involves side-clamping the IVC, produces less hemodynamic compromise than classic total IVC cross-clamping. Venovenous bypass diverts portal and femoral venous blood to the axillary or jugular vein to maintain preload, though it is used less frequently now that the piggyback technique has become standard.

The absence of hepatic function during this phase means there is no drug metabolism, no lactate clearance, no coagulation factor synthesis, and no glucose production. Progressive lactic acidosis develops from absent hepatic clearance and tissue hypoperfusion. Hypocalcemia worsens because citrate from transfused blood is not metabolized, requiring aggressive calcium replacement. Hypothermia results from the cold donor organ, open abdomen, and massive transfusion. Hypoglycemia occurs due to absent hepatic gluconeogenesis, necessitating frequent glucose monitoring and dextrose infusion as needed. Hyperkalemia develops from transfused blood, metabolic acidosis, and absent hepatic potassium uptake.

### Management Goals

Volume loading before IVC clamping and vasopressors to maintain MAP greater than 65 mmHg are essential. Frequent ABG and electrolyte monitoring every 15 to 30 minutes guides management. Aggressive calcium replacement with calcium chloride 1 g IV boluses counteracts citrate toxicity. Sodium bicarbonate is administered for pH less than 7.20, with THAM as an alternative. Hyperkalemia is managed with insulin and glucose along with calcium administration. Potassium-containing fluids are minimized, using normal saline or Plasmalyte judiciously.

## Phase 3: Neohepatic (Reperfusion) Phase

### Surgical Activity

This phase begins with unclamping of the portal vein and hepatic artery and reperfusion of the donor graft. Biliary anastomosis and surgical hemostasis follow.

| Surgical Phase | Duration | Key Challenge | Hemodynamic Concerns | Critical Monitoring |
|---|---|---|---|---|
| Phase 1: Dissection (Pre-anhepatic) | 1–3 hours | Hemorrhage from portal HTN and collaterals | Hypovolemia, vasodilation, coagulopathy | Viscoelastic testing, iCa2+, ABG |
| Phase 2: Anhepatic | 1–2 hours | Absent hepatic function; IVC clamping | ↓ CO (up to 50%), lactic acidosis, hyperkalemia | ABG/electrolytes q15–30 min, glucose |
| Phase 3: Neohepatic (Reperfusion) | Variable | Post-reperfusion syndrome; graft assessment | Profound hypotension, bradycardia/asystole, arrhythmias | TEE, serial labs, urine output |

### Post-Reperfusion Syndrome (PRS)

Post-reperfusion syndrome is defined as a decrease in MAP greater than 30% lasting more than 1 minute within 5 minutes of reperfusion. It occurs in 25 to 40% of liver transplants. The mechanism involves the release of cold, acidotic, hyperkalemic preservation fluid and vasoactive mediators including potassium, hydrogen ions, cytokines, and air from the graft into the systemic circulation. Clinical features include profound hypotension, bradycardia that can progress to asystole, arrhythmias (especially from hyperkalemia), pulmonary hypertension, decreased cardiac output, and fibrinolysis.

### Management of PRS

Anticipation and preparation are paramount: calcium chloride, epinephrine, and vasopressin should be drawn up and ready before reperfusion. Some centers administer calcium chloride (1 to 2 g) and sodium bicarbonate prophylactically before unclamping. Treatment includes epinephrine (10 to 100 mcg boluses), vasopressin, and atropine for bradycardia, along with calcium for hyperkalemia and CPR if cardiac arrest occurs. TEE monitoring is invaluable for assessing RV function during acute RV failure from pulmonary hypertension and for detecting air embolism. Fibrinolysis, if confirmed on TEG or ROTEM, may be treated with tranexamic acid (1 to 2 g) or aminocaproic acid.

### Graft Function Assessment

Evidence of functioning graft includes clearing of acidosis with improving lactate and pH normalization, improving coagulation parameters with decreasing INR and improving TEG/ROTEM tracings, bile production, hemodynamic stabilization, and correction of hypoglycemia.

![Graph showing typical hemodynamic changes across the three phases of liver transplantation with markers for IVC clamping and reperfusion events](images/olt-hemodynamic-timeline.png)

## Postoperative Management

ICU admission is universal, with plans for 24 to 72 or more hours of mechanical ventilation. Assessment for primary graft non-function includes monitoring for persistent coagulopathy, acidosis, absent bile output, and rising transaminases. Immunosuppression protocols with tacrolimus, mycophenolate, and corticosteroids begin immediately. Monitoring for hepatic artery thrombosis with Doppler ultrasound, bleeding requiring re-exploration, and renal dysfunction is essential. Extubation proceeds when the patient is hemodynamically stable, alert, and meeting ventilatory criteria.

![Photo of a liver transplant operating room setup showing the rapid infusion device, multiple IV pumps, TEE probe, and point-of-care testing equipment](images/olt-or-setup.png)

## Key Clinical Pearls

Post-reperfusion syndrome is the most immediately life-threatening event during liver transplantation, and epinephrine and calcium must be drawn up before unclamping. Ionized calcium must be monitored and replaced aggressively throughout the case because citrate toxicity from massive transfusion is the most common cause of hypocalcemia. TEG and ROTEM are essential for transfusion guidance; treating an INR number rather than viscoelastic data leads to over-transfusion. The piggyback technique has largely replaced the classic technique, reducing hemodynamic instability and eliminating the need for venovenous bypass in most cases. Communication with the surgical team about the timing of clamping and unclamping is critical for anesthetic preparedness.

## References

1. Walia A, Schumann R. The evolution of liver transplantation practices. *Curr Opin Organ Transplant*. 2018;23(2):178-184.
2. Hilmi I, Planinsic RM. Anesthesia for liver transplantation. In: Miller's Anesthesia. 9th ed. Elsevier; 2020:2099-2132.
3. Aggarwal S, Kang Y, Freeman JA, et al. Postreperfusion syndrome: cardiovascular collapse following hepatic reperfusion during liver transplantation. *Transplant Proc*. 1987;19(4):54-55.
4. Roullet S, Freyburger G, Cruc M, et al. Management of bleeding and transfusion during liver transplantation before and after the introduction of a rotational thromboelastometry-based algorithm. *Liver Transpl*. 2015;21(5):714-722.