Is anyone starting empiric therapeutic anticoagulation on your patients? Are you using a specific marker (such as d-dimer) to determine when to start or stop anticoagulation? Are you using heparin or lovenox? There’s a lot of conflicting information out there so am interested to see what everyone is doing. Thanks!
Initial admission gets the following labs: D-dimer, PT, PTT, fibrinogen and CBC with differential and then q48h
Our institute has started prophylactic enoxaparin for ALL adults and escalation to therapeutic based on clinical examination for DVT/PE (since US techs not coming in for routine dvt rule outs due to risk of exposure).
Switch to heparin if there is renal function deterioration like rising creatinine/bun. Hope this helps.
I think the real question is, given the pathology of disease progression suggests widespread micro-thrombi as a major factor in organ damage/failure, will anti-thrombotic therapy help. If so when and how much?
Can we discontinue therapeutic anticoagulation if D- dimer comes negative??
Agee with Neilnf, in our institution we are initiating DVT prophylaxis with Lovenox or Heparin SQ. We trend D-dimer, ferritin, CRP and fibrinogen.
Therapeutic dosing is initiated upon clinical progression and progressive increase in previously stated markers.
Therapeutic dosing is reduced back to prophylaxis when markers trend down and patient’s oxygenation improves
Thank you so much, it is helpful.
We do the same here at our center .
in our ICU we are following this protocol
D-DIMER less than 1 and boy wight less 100 kg Enoxaparin 40mg sc daily
D-DIMER MORE THAN 1 AND BODY WIGHT LESS 100 KG ENOXAPARIN 40 MG BID
we start w prophylactic lovenox–but follow d dimer and use TEG if the pt becomes hypercoagulable with dec r values and inc ma we use full anticoag and asa if ma is indicting ply hypercoagulability. I beleive the TEG may be helpful in defining hyper or hypocoagulability–much better than d dimer alone
I would recommend thrombolytics and repeat until clinical improvement or noted excessive bleeding. There is so much massive clotting that it is reasonable to assume it will take more than treatment for stroke or heart attack.
I recommend the use of the TEG to guide therapy and gauge risk of clotting and bleeding–this helps guide us in anti coagulation decisions–I also think anti plt agents may be needed depending on teg
We have had several patients with severe thrombocytosis (> 900). We have initiated 81 mg ASA for anyone who’s plt count is greater than 800. We have done TEGs on these people and the MA and angle were wnl. Any thoughts?