Abnormal bleeding or bleeding tests:

• clinical comments: Be alert when patient history indicates a notable bleeding tendency spontaneously and/or after challenges such as shaving nicks, dental work, or with menses (or as family history). 

• HUS/TTP information

• tests:

  • global: bleeding time, activated clotting time, Lee-White clotting time, thromboelastography.

  • plasma factors: PT, APTT (PTT can be shortened as an acute phase reaction, especially in cases of CNS stroke); about the PT INR.

  • fibrinogen: fibrinogen (when low, look for DIC), split products, d-dimer

  • platelets: bleeding time & see lab letter, below. (remember that medications can affect tests without neccessarily having presented as clinical problems [e. g., discovering on pre-op screening]; dysproteinemias can "coat" platelets). We have had for years some platelet function tests. as of about 2005, we now have a more global PFA screen. Plavix deactivates platelets via the ADP pathway and aspirin via acetylation. Plavix is stored in fat and released for days after cessation of therapy. Therefore, skipping a dayly dose for a day or two will not be reflected as any significant change in PFA results. Forensic pathologists have noted increased liability to CNS hematoma following blows (often seeming to be somewhat trivial blows) to the head in persons on Plavix.

  • Fletcher factor deficiency or dysfunction: elevated PTT but no bleeding or bleeding history

  • inhibitor screening ("mixing studies"): to globally screen for plasma factor deficiencies or inhibitors.

  • isolated Factor X deficiency: prolonged PT & APTT & may be associated with amyloidosis (amyloid of a type poorly portrayed in special stains adsorbs the factor X out of plasma) acting as a "factor sponge"...which can do similarly with factors V, VII, & IX [CP-04-34] ¹.

  • Factor activities: as any might become elevated by such as acute phase reactions, it is unrealistic to closely follow for resolution toward normal because the CVs for "activity testing" are so large. If a factor activity is low, then the factor antigen might be low, and, if not, then there is a qualitative defect (dysfunction) in the factor being produced.

  • Gene mutation tests by molecular assay: As of 2007/8, we have some molecular testing for two Factor V Leiden mutations and a MTHFR mutation.

  • reference lab tests/testing:  via Quest-thrombophilia, Quest-bleeding, and ARUP (interpretative data with each test) as of 2008.

Hypercoagulation:

• clinical comments: Be alert when patient condition, historical details, or family history indicates a notable hypercoagulation tendency...personal or family history of spontaneous abortions or miscarriages; stroke; phlebitis cases; pulmonary emboli cases; malignant case; inflammatory (pneumonia) cases; prolonged immobility situations; obesity; hormone replacement therapy; cigarette smoking; pregnancy. "Sticky platelet syndrome". And, in routine surgical pathology specimens, be alert to venous or arterial thromboses that "don't make sense": (right tube & ovary & arterial thrombosis noted [L-05-6350]). A person on prolonged heparin therapy may carry low levels of AT III and thrombose with sudden cessation of heparin coverage. This situation may show up initially as shortened PT or APTT.

• tests:
  1. global:
  2. plasma procoagulants:
     • molecular tests:
       1. "coumadin sensitivity profile": a website with dosing formulae for each genotype HERE.
       2. AT III deficiency, inherited (either as low levels or as poorly functioning molecular variants): prevelance from about 1/500-1/5000.
  3. lupus anticoagulant:
  4. fibrinogen:
  5. platelets: 
     • platelet function analysis (PFA)
     • urinary 11-dehydrothromboxane B2 levels...this chemical is reduced if platelet activity is reduced and increased with increased "stickiness"/activity (a website)

• Laboratory Letters:

  • Nov. 2002 platelet function testing

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References:

1. Rochman H, et. al., textbook: Clinical Pathology in the Elderly...,, 1988, 222 pages.

(posted 14 December 2002; latest addition 2 December 2008)