Intraoperative hypotension during major liver resection in a patient with cirrhosis
A 58-year-old man with Child-Pugh B cirrhosis and a MELD score of 14 undergoes a right hepatectomy for hepatocellular carcinoma. He weighs 82 kg. After induction and before the liver is mobilised, blood pressure falls to 82/44 mmHg with a heart rate of 96. Central venous pressure is 6 mmHg, and stroke volume variation on the arterial line is 18%. The surgeon has just begun the hilar dissection and warns that bleeding may increase. Baseline creatinine is 130 micromol/L, and platelet count is 88 x 10^9/L with an INR of 1.5. The team is using a low central venous pressure strategy to reduce hepatic bleeding.
1. How do you interpret the hypotension and stroke volume variation in the context of a low central venous pressure strategy, and what is your fluid and vasopressor strategy?
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Interpretation:
- Stroke volume variation of 18% suggests fluid responsiveness, but it is only reliable in a patient who is mechanically ventilated with a regular rhythm and adequate tidal volume. In cirrhosis, portal hypertension and splanchnic pooling can make dynamic indices less reliable.
- The low central venous pressure strategy aims for a CVP of 5 mmHg or less to reduce hepatic venous bleeding, but a CVP of 6 mmHg with a mean arterial pressure of 57 mmHg is inadequate for renal and cerebral perfusion, especially with pre-existing renal impairment.
Strategy:
- Exclude other causes: Check for bleeding (haemoglobin, surgical field), anaphylaxis, and myocardial depression. Confirm the arterial trace is accurate.
- Cautious fluid challenge: Give 250 mL of balanced crystalloid or 5% albumin over 10-15 minutes and reassess stroke volume variation and blood pressure. Avoid large crystalloid loads because of the risk of ascites, oedema, and dilutional coagulopathy. Aim for a CVP of around 5-7 mmHg, not zero.
- Vasopressor: Start norepinephrine at 0.05-0.1 micrograms/kg/min to maintain a mean arterial pressure of at least 65 mmHg (higher, around 70 mmHg, in cirrhosis with renal impairment). Vasopressin can be added if norepinephrine requirements escalate, because it does not increase portal pressure as much as norepinephrine alone.
- Avoid: Avoid excessive fluid and avoid drugs that reduce renal perfusion. Maintain urine output above 0.5 mL/kg/h.
- Reassess: If hypotension persists despite fluids and vasopressors, consider a transoesophageal echocardiogram to assess filling and contractility, and communicate with the surgeon about the bleeding risk.
2. The surgeon reports increased bleeding and the haemoglobin falls from 105 to 72 g/L. What is your transfusion and coagulation management plan, and how does cirrhosis change it?
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Transfusion plan:
- Transfuse red cells to maintain haemoglobin above 70-80 g/L, using a restrictive threshold appropriate for a patient with coronary risk factors. Each unit should be given with reassessment.
- Platelets: transfuse if the count falls below 50 x 10^9/L in the setting of active bleeding, or below 75-100 x 10^9/L if there is ongoing surgical bleeding. Do not transfuse prophylactically for a count of 88 x 10^9/L without bleeding.
- Fresh frozen plasma: give for active bleeding with a prolonged prothrombin time, but avoid large volumes that cause volume overload. Consider prothrombin complex concentrate if urgent reversal is needed, with awareness of thrombotic risk.
- Fibrinogen: maintain above 1.5-2.0 g/L with cryoprecipitate or fibrinogen concentrate.
How cirrhosis changes it:
- Cirrhosis is a rebalanced haemostasis state, so the INR of 1.5 does not reliably predict bleeding, and routine correction of abnormal tests is not indicated. Use viscoelastic testing (thromboelastography or rotational thromboelastometry) to guide product use.
- Avoid over-transfusion, which raises portal pressure and worsens bleeding.
- Correct calcium and temperature, and consider tranexamic acid.
- Monitor for dilutional coagulopathy and hyperkalaemia from stored blood. After resection, anticipate a further fall in platelets and fibrinogen as the remnant liver synthetic function is reduced.