Treatment of Flu-Induced DIC or Hemolytic Anemia
For flu-induced DIC, prioritize early antimicrobial therapy within 1 hour, implement supportive care with transfusion support as needed, and consider anticoagulant therapy (heparin, antithrombin, or recombinant thrombomodulin) based on regional availability; for flu-induced hemolytic anemia, withhold the triggering agent if possible, initiate corticosteroids (prednisone 1-2 mg/kg/day), and provide IVIG with transfusion support as required. 1, 2
Flu-Induced Disseminated Intravascular Coagulation (DIC)
Diagnostic Approach
Screen all septic patients with thrombocytopenia (platelet count <150 × 10⁹/L) using Sepsis-Induced Coagulopathy (SIC) criteria first, then progress to overt DIC criteria if SIC is present. 1, 2 This two-step approach facilitates early recognition when anticoagulant intervention is most beneficial. 1
Obtain at least 2 sets of blood cultures (aerobic and anaerobic) before starting antimicrobials. 2
Complete SIC evaluation including platelet count, PT-INR, and SOFA score. 2, 3
Immediate Treatment Protocol
Antimicrobial Therapy:
Administer effective intravenous antimicrobials within the first hour of recognition. 2 This is critical as delayed antibiotic therapy increases mortality. 3
Use broad-spectrum antimicrobials covering all likely pathogens, including anaerobes when appropriate. 2
Anticoagulant Therapy: The choice depends on regional availability and specific clinical context:
Unfractionated heparin (UFH) or low-molecular-weight heparin (LMWH) can be used, though evidence for mortality benefit in septic DIC remains limited. 1, 2
Antithrombin supplementation should be considered in patients with decreased antithrombin activity, particularly those not receiving concomitant heparin. 1, 2 The Japanese Clinical Practice Guidelines recommend this approach, though it's not universally adopted. 1 Note that the KyberSept trial showed increased bleeding with high-dose antithrombin, but subanalysis demonstrated benefit in septic patients with coagulopathy not receiving heparin. 1
Recombinant soluble thrombomodulin (rsTM) may be used where licensed, showing improvements in coagulation markers and platelet counts without increased bleeding. 1, 2 Meta-analysis suggests approximately 13% mortality reduction, though not statistically significant. 1
Supportive Care:
Provide transfusion support as required for bleeding. 1
Target mean arterial pressure ≥65 mmHg with vasopressors. 2
Maintain adequate urine output ≥0.5 mL/kg/h. 2
Critical Complication: Symmetrical Peripheral Gangrene (SPG)
Monitor for acral limb loss due to microvascular thrombosis, particularly in patients with acute hepatic dysfunction ("shock liver"). 1, 2
Timely administration of heparin and antithrombin may reduce microthrombosis risk in at-risk patients. 2 However, rsTM may be ineffective if protein C levels are severely reduced due to hepatic dysfunction. 1
Flu-Induced Hemolytic Anemia
Treatment Algorithm
First-Line Therapy:
Withhold the triggering agent (influenza infection treatment with antivirals). 1
Initiate corticosteroids: prednisone 1-2 mg/kg/day (oral or IV depending on symptom severity). 1 This is the cornerstone of treatment for autoimmune hemolytic anemia. 1
Provide IVIG (intravenous immunoglobulin). 1
Transfusion support as required for symptomatic anemia. 1, 4
Second-Line Therapy (if worsening or no improvement):
Add rituximab (375 mg/m² weekly for 4 weeks) and/or cyclophosphamide (1-2 mg/kg/day). 1
Consider cyclosporine or immunosuppression/immunoadsorption if still refractory. 1
Important Caveats
Avoid early platelet transfusion if thrombotic thrombocytopenic purpura (TTP) is in the differential diagnosis, as this can worsen outcomes. 4
Evaluate for autoantibodies (direct and indirect Coombs' tests) to confirm autoimmune hemolytic anemia. 5
If multiple cell lines are affected or pancytopenia develops, evaluate for pure red cell aplasia, aplastic anemia, or myelodysplastic syndrome. 1
Flu-induced autoimmune hemolytic anemia is rare but documented, particularly in patients with underlying liver disease. 5 These patients may have worse outcomes due to impaired hepatic synthesis of natural anticoagulants. 1