Special thanks to all FOAMEd folks who I am learning from: Anton Helman, Amal Mattu, Anand Swaminathan, Walter Himmel, Justin Morgenstern, Martin Fandler, Philipp Gotthardt, Scott Weingart, Reuben Strayer, Chris Nickson, Sarah Gray, Joshua Farkas, Adam Thomas, Mike Cadogan, Oliver Flower, Salim Rezaie, Rob Orman, Joel Topf, Andrew Davies, Christina Shenvi,Alex Yartsev, Sergey Motov, Stephanie Sherman, Robert "Uncle Bob" Centor, Shreya Trivedi, Matthew Watto, Paul Williams, Stuart Brigham, Hannah Abrams, Avi Cooper, Tony Breu, Sharmin Shekarchian, Rabih Geha, Reza Manesh, Arsalan Derakhshan, Gurpreet Dhaliwal, Cindy Fang, Anand Viswanathan, John Hwang, Zaven Sargsyan, Mike Winters, Nick Mark, Lauren Westafer, Jeremy Faust, Greg Katz, Evan Harmon, Todd Villines, Sohah Iqbal, Michael Ragosta, Vickie Kassapidis, Brandon Oto, Bryan Boling, Alison Lai, Zahra Merali, Laiya Carayannopoulos, Emily Gutowski, Walker Redd, Navin Kumar, Joyce Zhou, Haney Mallemat, Matt Siuba, David Carr, Sebastian Casu, Michael Bernhard, Mike Cadogan, Ed Burns, Neil Long, Jacob Avila, Ben Smith, Björn Hossfeld, Sara Crager, Tim Horeczko, Simon Carley, Rick Body, Sarah Foohey, Peter DeBlieux, John Greenwood, Robert Rodriguez, Ronak Mistry, Vivek Patel, Dan Hausrath, Ryan Stanton, Ingmar Finkenzeller, Christine Whitten, Nick "OnePager" Mark, Sergio Zanotti, Kristina “Monty” Montemayor, Dave “Furf” Furfaro, Charlie Wiener, Cathy Handy, Cyrus Askin
Role of plasma, fresh frozen plasma (FFP), coagulation factors, and platelets
2013
Recommendations:
The transfusion of platelets is recommended in DIC patients with active bleeding and a platelet count of <50 × 109 L−1 or in those with a high risk of bleeding and a platelet count of <20 × 109 L−1 (low quality).
The administration of FFP may be useful in patients with active bleeding with either prolonged PT/APTT (>1.5 times normal) or decreased fibrinogen (<1.5 g dL−1). It should be considered in DIC patients requiring an invasive procedure with similar laboratory abnormalities (low quality).
The administration of fibrinogen concentrate or cryoprecipitate may be recommended in actively bleeding patients with persisting severe hypofibrinogenemia (<1.5 g L−1) despite FFP replacement (low quality).
Prothrombin complex concentrate (PCC) may be considered in actively bleeding patients if FFP transfusion is not possible.
The threshold for transfusing platelets depends on the clinical state of the patient. In general, platelet transfusions are administered to patients who are actively bleeding and who have a platelet count of <50 × 109 L−1. A much lower threshold of 10–20 × 109 L−1 is adopted in non-bleeding patients, on the basis of RCTs in patients with thrombocytopenia following chemotherapy. Platelets may be administered at higher levels than this in patients perceived to be at high risk of bleeding on the basis of other clinical and laboratory features.
It may be necessary to use large volumes of plasma to correct the coagulation defects shown by prolonged APTT or PT, or a decreased fibrinogen level. Initial doses of 15 mL kg−1 of FFP are suggested, although there is evidence that a dose of 30 mL kg−1 produces more complete correction of coagulation factor levels. In this regard, the consequences of volume overload may have to be considered.
Smaller volumes of PCC may be useful in this setting, although these products lack certain essential coagulation factors, such as factor V. Specific deficiencies in fibrinogen can be corrected by administration of purified fibrinogen concentrates or cryoprecipitate.
The response to component therapy should be monitored both clinically and by repeating platelet counts and coagulation tests following administration of these components.
The efficacy and safety of recombinant FVIIa in DIC with life-threatening bleeding are unknown, and it should be used with caution, or as part of a clinical trial.
HOA hypertrophic osteoarthropathy PPP syndrome: pancreatitis (+ pancreatic cancer), panniculitis (subcutaneous fat necrosis), polyarthritis with peri-arthritis (often oligoarthritis) due to fat necrosis with high lipase. Eosinophilia possible (Schmid triad in pancreatic cancer: subcutaneous fat necrosis („erythema nodosum-like“), polyarthritis, eosinophilia).
Reply