Liver Transplant Phases + Reperfusion Syndrome

End-stage liver disease recipients are uniquely deranged: hyperdynamic circulation (high CO, low SVR — cirrhotic cardiomyopathy may mask underlying LV dysfunction), portopulmonary hypertension (PAH from chronic shunting — mPAP >35 mmHg may contraindicate transplant), hepatopulmonary syndrome (intrapulmonary shunts → hypoxemia that paradoxically improves AFTER transplant), coagulopathy (decreased synthesis of factors II, VII, IX, X + thrombocytopenia from splenic sequestration — BUT also decreased protein C/S so balanced; TEG/ROTEM more useful than INR), hyperammonemia + hepatic encephalopathy, renal dysfunction (hepatorenal syndrome), massive ascites, varices (avoid TEE in known severe esophageal varices — consider TTE or epicardial echo).

Large-bore access (rapid-infuser, two 8.5 Fr introducers), arterial line, central line + PA catheter or TEE.

Hemodynamic challenges: blood loss from collaterals and varices (5-15 L baseline; massive transfusion ratio 1:1:1 PRBC:FFP:platelets), ongoing coagulopathy correction (TEG-guided — fibrinogen <150 → cryo, platelet count <50 → platelets, prolonged R-time → FFP), ascites drainage causing sudden CV shifts.

Antifibrinolytic (TXA 1 g, or epsilon-aminocaproic acid) routinely used; thromboelastography mandatory.

Calcium administration must keep up with citrate from massive transfusion — check ionized Ca q15-30 min.

Two surgical techniques: CLASSICAL — IVC + portal vein cross-clamped (40-60% drop in venous return → marked hypotension; venovenous bypass historically used to maintain return).

The donor liver is anastomosed and the portal vein + IVC are unclamped — cold, acidic, hyperkalemic preservation effluent (UW or HTK solution) washes from the graft into the systemic circulation.

POSTREPERFUSION SYNDROME (PRS): bradycardia + hypotension + decreased SVR + arrhythmia (often VF) within 5 min of reperfusion, occurring in ~30% of cases.

Pre-treatment: empirically administer calcium chloride 1 g IV + sodium bicarbonate 50 mEq + epinephrine 10-50 mcg bolus AT the moment of unclamping; have epi infusion ready at 0.05-0.2 mcg/kg/min.

Recognize early VF — defibrillate, continue ACLS, more calcium + bicarb.

Watch K closely (often >6 transiently — usually self-resolves as graft starts metabolizing).

Signs of GOOD graft function: bile production (surgeon will report yellow-gold bile within 30-60 min), lactate clearance (lactate trending down by end of case), correction of coagulopathy (INR normalizes — paradoxically may become HYPER-coagulable transiently; thrombosis risk for hepatic artery + portal vein), glucose normalization, core temperature recovers with active warming.

Hepatic artery anastomosis is created during this phase + assessed with Doppler.

Signs of POOR graft function ('primary non-function'): persistent acidosis, no bile, rising lactate, persistent coagulopathy, no glucose recovery — may require emergent re-transplant.

Close vasopressor down as graft function returns.

Massive transfusion ratio 1:1:1 (PRBC:FFP:platelet) as baseline; modify by TEG/ROTEM.

Cell-saver IS used routinely (concerns about malignancy with hepatocellular carcinoma have largely been settled — leukocyte-depletion filter makes it safe).

Maintain ionized Ca >1.0 (citrate toxicity from massive transfusion — give CaCl 1 g per 4-6 units PRBC), K <5.5, glucose 120-180, normothermia.

Avoid PCCs in the absence of guided coagulopathy — thrombosis risk in immediate post-transplant period.

Post-op: extubate on table if stable (early extubation improves outcomes per ERAS pathways) or transfer ventilated to ICU; continue close glucose + lactate + coag monitoring.