VA morning report 1.16 – Stroke and clotting on anticoagulation

Case Summary

Thanks to Arielle for presenting a fascinating case of a 65M with multiple prior stokes who presented with AMS, hypernatremia and then found to have new multifocal strokes.

Top pearls

  1. Head imaging [CT non-contrast] is not necessary in patients presenting with altered mental status [without trauma] after an obvious cause [e.g. hypernatremia] is uncovered on routine labs.
  2. Multiple trials have previously shown that PFO closure does not reduce the incidence of recurrent stroke(CLOSURE-I, PC, and RESPECT). However, two recent meta-analyses showed potential benefit in patients with recurrent cryptogenic strokes at the cost of an increases risk of Afib/flutter . Link 1      Link 2
  3. While a thrombosis on anti-coagulation raises concern for a number of hypercoaguable conditions [see below] the first step is to clarify whether the patient was receiving adequate anticoagulation [e.g. under-dosing].


Initial evaluation of a stoke
  • Is this a stoke? [DDx: Seizure, hypoglycemia, syncope, other]
    • If so, what kind?
      • Ischemic
      • Hemorrhagic
        • Where in the skull?
  • Last known normal?
  • NIH stroke scale?
  • contraindications to tPA?
    •  Benefits
      • <90 min —> NNT for functional independence = 3.6
      • <180 min —> NNT = 4.3
    •  Risk
      • 6% of any bleed
      • 1-2% of significant bleed
  • Embolectomy?
    • More evidence to suggest benefit up to 24h
    • NNT 2-3
Work up
Initial treatment
  • Aspirin 325 x1 —> 81
    • Give in ED if no tPA
    • Give 24h later if tPA given
  • Statin
    • Atorvastatin 80
  • BP management
    • Permissive HTN up to 220, usually < 1 week
  • See above for tPA or embolectomy

Clotting on anticoagulation

  • An important part of the management of  VTE is the reversal of any underlying trigger.
    • Easier when the DVT is provoked [e.g. surgery]
  • In cases with unprovoked VTE either:
    • provoking factor was not recognized OR
    • There is a genetic disruption [e.g anti-thrombin 3] in the control of the coagulation cascade.
      • These disruptions are usually related to a protein deficiency in the regulation of the cascade [e.g., protein C deficiency]
      • The urge to uncover this disorder is tempered by the fact that it rarely changes management [life long anticoagulation]
      • Down-regulation of the pro-coagulant factors [e.g. Factor 2] with lifelong anticoagulation is usually sufficient for these conditions.
  • In some acquired causes, the driver for the hypercoaguability exists outside the coagulation cascade  [e.g. heparin-induced thrombocytopenia].
    • Syndrome specific features may offer clues to the Dx [e.g. recent receipt of heparin –> thrombocytopenia], but other features include
      • Clotting in atypical locations – e.g. Budd Chiari/venous sinus thrombosis
      • Multiple simultaneous thrombi
      • Clotting while on full dose anticoagulation.

Here’s one approach to this scenario

Step 1: Is the patient taking/on the right dose of anticoagulation?
Step 2:  Consider embolic disease
Step 3:  Consider thrombotic disease

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