Coagulopathy in liver disease

Surgical approach (context: liver surgery / transplantation / bleeding procedures in cirrhosis)

• Control source of bleeding early: direct pressure, packing, Pringle manoeuvre (temporary hepatic inflow occlusion), topical haemostats, suture/clip ligation
  • Damage control strategy if unstable: pack, temporary closure, ICU resuscitation, return to theatre
• Minimise blood loss: low CVP strategy during parenchymal transection (balanced against renal perfusion/air embolism risk), cell salvage where appropriate, meticulous haemostasis
  • Consider portal hypertension: varices/collaterals increase bleeding risk, careful dissection
• If liver transplantation: hepatectomy phase (often major bleeding), anhepatic phase (no hepatic clearance/synthesis), reperfusion phase (post-reperfusion syndrome, fibrinolysis, hyperkalaemia)
  • Surgical vascular clamps/anastomoses, potential venovenous bypass depending on centre

Anaesthetic management (typical for major liver surgery / transplant / high-risk bleeding in cirrhosis)

• Type of anaesthesia: General anaesthesia with invasive monitoring, regional techniques often limited by coagulopathy (consider only if coagulation status acceptable and benefits outweigh risks)
  • Neuraxial blocks: avoid if INR/platelets abnormal or dynamic coagulopathy, follow national guidance and local policy, consider peripheral/field blocks with ultrasound if safe
• Airway: ETT usually required (aspiration risk, long duration, major haemorrhage, need for controlled ventilation), SGA generally inappropriate
  • RSI may be indicated (ascites, delayed gastric emptying, variceal bleed, encephalopathy)
• Duration: variable—minor procedures 1–3 h, major hepatectomy 4–8 h, liver transplant often 6–12+ h
• Analgesia: moderate–severe (major upper abdominal), multimodal opioid-sparing, consider TAP/rectus sheath/QL blocks if coagulation allows, epidural often avoided in significant coagulopathy
  • Avoid NSAIDs if renal dysfunction/variceal bleed risk, paracetamol dose-reduce in severe liver disease
• Monitoring/lines: arterial line, large-bore IV access, consider rapid infuser, central access for vasoactive drugs, temperature monitoring, urinary catheter, consider cardiac output monitoring
  • Point-of-care coagulation testing (TEG/ROTEM) to guide targeted blood product therapy
• Haemostasis strategy: treat bleeding patient not numbers, use goal-directed transfusion, early fibrinogen replacement, correct hypothermia, acidosis, hypocalcaemia
  • Transfusion triggers depend on procedure/bleeding, avoid prophylactic over-correction (thrombosis/volume overload)

Why coagulopathy occurs in liver disease (mechanisms)

• Reduced synthesis of procoagulant factors: II, V, VII, IX, X, XI, fibrinogen may be low or dysfunctional (dysfibrinogenaemia)
  • Factor VII short half-life → PT/INR rises early
• Reduced synthesis of anticoagulants: protein C, protein S, antithrombin → prothrombotic tendency despite raised INR
• Thrombocytopenia: hypersplenism (portal HTN), reduced thrombopoietin, marrow suppression (alcohol/viral), consumption/sepsis
• Platelet dysfunction: uraemia, sepsis, alcohol, endothelial dysfunction, abnormal vWF/ADAMTS13 balance may partially compensate
• Fibrinolysis abnormalities: hyperfibrinolysis (reduced clearance of tPA, low α2-antiplasmin) or hypofibrinolysis, dynamic changes esp. during transplantation/reperfusion
• Vitamin K deficiency (cholestasis, malnutrition, antibiotics) → reduced II, VII, IX, X (correctable)
• DIC-like picture can occur with sepsis/acute liver failure, differentiate from primary liver-related changes

Key concept: rebalanced haemostasis

• Cirrhosis produces simultaneous reductions in pro- and anticoagulant pathways → haemostasis may be “rebalanced” but fragile and easily tipped to bleeding or thrombosis
• INR/PT and APTT reflect only procoagulant factor deficiency and do not measure anticoagulant deficits or platelet-endothelial interactions → poor predictors of bleeding risk in cirrhosis
  • INR was designed for warfarin monitoring, in liver disease it does not equate to “auto-anticoagulation”
• Patients remain at risk of thrombosis: portal vein thrombosis, DVT/PE, catheter thrombosis, consider VTE prophylaxis on individual risk/bleeding balance

Assessment and investigations (preop and periop)

• History: previous procedural bleeding, variceal bleed, easy bruising, menorrhagia, family history, anticoagulants/antiplatelets, alcohol, sepsis, renal failure
• Examination: stigmata of chronic liver disease, ascites, encephalopathy, sepsis, signs of portal hypertension/splenomegaly
• Baseline labs: FBC (platelets), PT/INR, APTT, fibrinogen, LFTs, U&amp,E/creatinine, calcium, lactate/ABG, group &amp, screen/crossmatch
• Viscoelastic testing (TEG/ROTEM): assesses clot initiation, strength, fibrinogen contribution, fibrinolysis, useful for targeted therapy in bleeding or high-risk surgery
  • Interpret alongside clinical bleeding and surgical field, avoid treating traces in a non-bleeding patient
• Risk stratification: Child–Pugh and MELD predict perioperative mortality, not direct bleeding scores but correlate with severity and complications

When to correct coagulation abnormalities (principles)

• Do not correct INR/platelets “to normal” routinely, correct for active bleeding, high-risk procedures, or before neuraxial techniques (if ever considered)
• Optimise physiology first: temperature &gt, 36°C, pH &gt, 7.2, ionised calcium normal, Hb appropriate, avoid dilutional coagulopathy
  • Hypocalcaemia from citrate in transfused blood impairs coagulation and contractility
• Use goal-directed therapy guided by TEG/ROTEM where available, otherwise use fibrinogen/platelets and clinical bleeding

Blood products and haemostatic drugs (what to use, key points)

• Packed red cells: maintain oxygen delivery, avoid excessive haemodilution, consider restrictive strategy unless massive bleeding/ACS/brain injury
• Fibrinogen replacement: cryoprecipitate or fibrinogen concentrate, often early target in liver-related bleeding (low fibrinogen predicts bleeding better than INR)
  • Practical targets vary by context, commonly aim fibrinogen &gt, 1.5–2.0 g/L in major bleeding/high-risk surgery (local protocol)
• Platelets: consider if active bleeding or high-risk procedure with thrombocytopenia, platelet function may be impaired even with adequate count
  • Common procedural thresholds used clinically: &gt,50 x10^9/L for many major procedures, higher for neurosurgery/critical sites (institution-dependent)
• FFP: replaces multiple factors but requires large volumes, limited effect on INR in cirrhosis, risks include TACO/TRALI, consider in active bleeding with prolonged PT/APTT or guided by viscoelastic tests
• Prothrombin complex concentrate (PCC): concentrated vitamin K–dependent factors, rapid effect with small volume, consider for urgent reversal of warfarin or severe bleeding with evidence of factor deficiency, thrombosis risk
  • In liver disease without warfarin, use only with specialist input/TEG guidance due to thrombotic potential
• Vitamin K: give if deficiency likely (cholestasis, malnutrition, prolonged antibiotics), effect takes hours, safe and often reasonable empirically
• Tranexamic acid (TXA): consider if hyperfibrinolysis suspected/confirmed (TEG/ROTEM) or major haemorrhage, balance against thrombosis risk
  • In liver transplantation, hyperfibrinolysis may occur around reperfusion, many centres use TXA selectively rather than routinely
• Desmopressin (DDAVP): may improve platelet function (e.g., uraemia), limited evidence in cirrhosis, consider case-by-case
• Recombinant factor VIIa: rescue therapy for life-threatening bleeding refractory to conventional measures, high thrombotic risk, specialist decision

Regional/neuraxial anaesthesia considerations

• Neuraxial techniques carry risk of spinal/epidural haematoma, liver disease coagulopathy is dynamic and poorly captured by INR alone
• If considering neuraxial: require stable coagulation, adequate platelets, no active bleeding, no sepsis, and a clear plan for postoperative monitoring and catheter removal timing
  • Catheter removal can be higher risk than insertion if coagulation worsens postoperatively
• Prefer alternatives: multimodal systemic analgesia, wound infiltration, TAP/QL blocks (still consider bleeding risk with deep blocks), IV lidocaine/ketamine where appropriate

Perioperative plan for a bleeding cirrhotic patient (structured approach)

• Call for help early: senior anaesthetist, haematology, blood bank, activate major haemorrhage protocol if needed
• Resuscitation priorities: ABC, haemorrhage control, permissive hypotension only if appropriate and short-lived, maintain end-organ perfusion
• Laboratory and point-of-care: repeat Hb, fibrinogen, PT/APTT, platelets, ABG (pH, lactate), ionised Ca, use TEG/ROTEM to target therapy
• Transfusion strategy: early fibrinogen + platelets as indicated, PRBC to maintain oxygen delivery, avoid large-volume FFP unless indicated, correct Ca/temperature/acidosis
• Consider TXA if hyperfibrinolysis, consider PCC in selected scenarios, avoid overcorrection (thrombosis/portal vein thrombosis)
• Postop: HDU/ICU, ongoing bleeding surveillance, repeat coagulation, VTE prophylaxis decision, manage encephalopathy/renal dysfunction, careful fluid balance

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