Warfarin (Coumadin) therapy should be discontinued two weeks prior and heparin therapy two days prior to sample collection.

 Lt blue Sodium citrate (Na Cit) - 2.7mL

If the patient has a hematocrit >55, a specially prepared Lt blue Sodium citrate (NaCit) tube must be used in place of the standard Lt blue Sodium citrate (NaCit) tube.

Hematocrit-Anticoagulant adjustments

• Do not draw from an arm with a heparin lock or heparinized catheter
• Do not over or under fill tube as the ratio of anticoagulant to whole blood is critical

Coag – tube fill guidelines

• Immediately following collection, mix sample thoroughly by gently inverting 8 - 10 times to prevent clotting

• Process Platelet Poor Plasma (P.P.P)

  • Coag – how to prepare a specimen for special coagulation testing

• Transfer plasma into an aliquot tube using a spot label "NaCit Plasma P.P.P" to label as platelet poor plasma
• Freeze immediately

Microcentrifuge vial/tube in a Snap cap conical vial/tube and cap (Beaker sites)

Coagulation specimen transport vial/tube  (all other sites)

Frozen (strict)

Refrigerated - NO

• Greiner tubes are not acceptable
• Improper labeling (unlabeled or mislabeled)
• Improper anticoagulant
• Improperly filled tube
• Hemolysis
• Clotted specimen
• Delay in transport
• Improper storage/transport temperature
• Patient on heparin > 1.0 IU/mL

Protein S, free – Immuno-turbidometric

Protein S, free (Antigenic):

Female: 55-124%

Male: 74-126%

Guidance for the evaluation and treatment of hereditary and acquired thrombophilia

The three subtypes of heritable protein S deficiencies include both qualitative and quantitative defects. Type I is a quantitative defect resulting in decreased plasma antigen levels of both free and total protein S antigen. Type II is a qualitative defect with decreased protein S activity and normal levels of free and total protein S antigen. Type III is characterized by decreased free protein S antigen and protein S activity with normal levels of total protein S antigen. Type I and III protein S deficiency are much more common than type II (dysfunctional) protein S deficiency.

Acquired free protein S deficiency may be seen in certain inflammatory conditions and will most often have decreased levels of free protein S antigen and protein S activity, but normal to elevated total protein S antigen. The hemostatic implications for patients with acquired protein S deficiency are of unclear clinical significance.

Reference:

Quality in Laboratory Hemostasis and Thrombosis. Kitchen, Steve, Olson, John D., and Preston, F. Eric. 2009 Blackwell Publishing Ltd, Sussex, UK. pg. 152.