Coagulation Testing - Revision history

Admin: /* Causes of Abnormal Results + Followup Testing */

2024-07-03T02:04:44Z

Causes of Abnormal Results + Followup Testing

← Older revision		Revision as of 22:04, 2 July 2024
Line 7:		Line 7:
	\|Factors Affected		\|Factors Affected
	\|I, II, V, VII, X		\|I, II, V, VII, X

			* Most sensitive to VII (shortest half life)
	\|All '''except''' VII - Congenital def. of VIII, IX, or XI - VWF disease → low VIII		\|All '''except''' VII - Congenital def. of VIII, IX, or XI - VWF disease → low VIII
	\|-		\|-
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	\|D-Dimer		\|D-Dimer
	\|Measures fibrin clot breakdown products from plasmin Elevated D-dimer alone is non-specific except in VTE - Can be associated with a variety of diseases or inflammatory states		\|Measures fibrin clot breakdown products from plasmin Elevated D-dimer alone is non-specific except in VTE - Can be associated with a variety of diseases or inflammatory states

			* Negative: normal, rules out DIC, PE, DVT
			* Positive: may be associated with DIC, PE, or DVT
	\|		\|
	\|		\|
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	\|Mixing Studies		\|Mixing Studies
	\|		\|
			\|
			\|
			\|-
			\|dRVVT
			\|Assesses
	\|		\|
	\|		\|
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	\|		\|
	\|		\|
			* Factor assays
	\|-		\|-
	\| rowspan="3" \|Multiple factor deficiency in intrinsic '''AND''' extrinsic pathways		\| rowspan="3" \|Multiple factor deficiency in intrinsic '''AND''' extrinsic pathways
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	\|		\|
	\|		\|
			* Factor V assay (decreased in liver disease but not Vit K deficiency)
	\|-		\|-
	\|Disseminated intravascular coagulation		\|Disseminated intravascular coagulation
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	\|		\|
	\|		\|
			* '''CBC (low platelets)'''
			* '''RBC morph (appears as MAHA - schistocytes)'''
			* Thrombin time (prolonged)
			* '''Fibrinogen (low)'''
			* '''D-Dimer (increased)'''
			* Protein C, S, AT activity assays (<50%)
			* Serum FDP (increased)
			* Plasminogen, TPA, Plasminogen activator inhibitor-1 assay (decreased)
	\|-		\|-
	\| colspan="2" \|Specific inhibitor to common pathway factor		\| colspan="2" \|Specific inhibitor to common pathway factor
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	\|		\|
	\|		\|
			* Fibrinogen assay (reduced)
			* Thrombin time (prolonged)
	\|-		\|-
	\| rowspan="5" \|PT '''only'''		\| rowspan="5" \|PT '''only'''
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	\|-		\|-
	\|Early coumadin therapy/initial dose		\|Early coumadin therapy/initial dose
	\|		\| colspan="3" \|Normal when on coumadin
	\|
	\|
	\|-		\|-
	\|Specific inhibitor to VIII (rare)		\|Specific inhibitor to VIII (rare)
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	\|		\|
	\|-		\|-
	\| rowspan="6" \|APTT '''only'''		\| rowspan="7" \|APTT '''only'''
	\|		\|
	\|VWF disease		\|VWF disease
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	* VWF:RCo Ristocetin co-factor qualitative analysis		* VWF:RCo Ristocetin co-factor qualitative analysis
	* Factor VIII activity assay (FVIII:C)		* Factor VIII activity assay (FVIII:C)
			* PAGE
	\|-		\|-
	\|		\|
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	\|		\|
	\|		\|
			* Factor assays
	\|-		\|-
			\| rowspan="3" \|Non-specific inhibitor
			\|Lupus Anticoagulant/Antiphospholipid Syndrome (Autoimmune disease)
	\|		\|
	~~\|Non-specific inhibitor~~		* Female patient
	\|		* Recurrent miscarriages (3+ unexplained)
			* Possibly mild hemolytic anemia (but may be normal)
			* Thrombosis
	\|		\|
			* Antibodies directed against phospholipids
			* Promote coagulation in the body (but act as anticoagulant in vitro)
	\|		\|
			* Mixing studies
			* dRVVT (prolonged; corrected when test is performed with high phospholipid)
			* Anti-nuclear antibody test or other immunoassays
			\|-
			\|Heparin therapy
			\| colspan="3" \|Normal when patient is on heparin. Can also be caused by specimen contamination with heparin.
	\|-		\|-
	\|		\|Other drugs
	\|~~Specific inhibitor against intrinsic factors~~		\| colspan="3" \|Rivaroxaban, apixaban, edoxaban
	\|
	\|
	\|
	\|-		\|-
			\| colspan="2" \|Specific inhibitor against intrinsic factors
	\|		\|
	~~\|Heparin therapy~~		* Usually against Factor VIII
	\|
	\|		\|
	\|		\|
	\|}		\|}
			Other disorders that may not affect PT/APTT include:

			* Deficiencies
			** Antithrombin
			** Protein C
			** Free PS
			** TPA
			* Mutations
			** Factor V (Factor V Leiden APCR)
			** Prothrombin (G20210A)
			** Fibrinogen (dysfribrinogenemia)
			** Plasminogen
			** PAI-1 (elevation)

	== Investigating Abnormal Results ==		== Investigating Abnormal Results ==

	# Check specimen integrity and HCT >55% (recollect ~~and/or dilute~~)		# Check specimen integrity and HCT
			## Correct anticoagulant (sodium citrate)
			## Proper tube filling (9:1 ratio, within 10% of fill volume)
			## If HCT >55% (recollect sample using calculated dilution)
	# Check patient history for any conditions affecting coagulation. If present, report results:		# Check patient history for any conditions affecting coagulation. If present, report results:
	## Anticoagulant therapy: warfarin/coumadin, heparin, direct oral anticoagulants (DOACs)		## Anticoagulant therapy: warfarin/coumadin, heparin, direct oral anticoagulants (DOACs)

Admin: 1 revision imported

2024-02-20T16:12:16Z

1 revision imported

← Older revision	Revision as of 12:12, 20 February 2024
(No difference)

MedLabWIki>Admin: /* PT/APTT */

2023-04-18T01:37:43Z

PT/APTT

New page

== PT/APTT ==
{| class="wikitable"
|
|PT
|APTT
|-
|Factors Affected
|I, II, V, VII, X
|All '''except''' VII - Congenital def. of VIII, IX, or XI - VWF disease → low VIII
|-
|Pathways Affected
|Extrinsic and common
|Intrinsic and common
|-
|Drugs Monitored
|Coumadin (warfarin)
|Heparin (unfractionated)
|-
|Conditions
|
|
* Specific factor antibodies
* Non-specific inhibitors
* Coagulation factor deficiencies
* Unexplained bleeding/bruising
* Recurrent miscarriages
* Disseminated intravascular coagulation (DIC)
* Recurrent thrombosis
* Prior to surgery when increased risk of blood loss or history of bleeding
|-
|Interfering Factors
|
|
* Drugs (antihistamines, ascorbic acid - Vitamin C, chlorpromazine, heparin, salicylates)
* Incorrect anticoagulant
* Hematocrit (increased/decreased)
* Sample from heparin lock or heparinized catheter
|-
|RI
|
* PT: 9.5-13.5 s
* INR: 0.9 - 1.2
* INR (warfarin): 2.0-3.0
* INR (warfarin + cardiac condition OR LA): 2.5-3.5
|
* APTT: 25-35s
* APTT (heparin): 1.5-2.5x mean)
|}
Reflex/Follow-up Testing
{| class="wikitable"
|Test (RI)
|Info
|Ordered When
|
|-
|Thrombin Time (15-20s)
|Assesses deficiencies or dysfunction of fibrinogen (Factor I) or thrombin (Factor II) inhibitor Less fibrinogen available → longer clot time
|
* Bleeding or thrombotic episodes
* Recurrent miscarriages
* '''BOTH''' PT and APTT unexpectedly prolonged
|
* Congenital fibrinogen deficiency
* Heparin therapy
* Direct thrombin inhibitor therapy
* Contamination
* Presences of thrombin or fibrinogen inhibitors (rare)
* Acquired hypofibrinogenemia from liver disease or massive hemorrhage
* Abnormal fibrinolysis
* Increased products of clot breakdown interfering with fibrin polymerization (e.g., DIC)
|-
|Fibrinogen
(2.2-5.0 g/L)
(Critical: <1.0g/L with increased PT, APTT, TT)
|Modified TT assay that estimates concentration of functional fibrinogen Clotting time correlates with active fibrinogen
|
* Acquired hypofibrinogenemia
* Assess inflammatory conditions
* Recurrent miscarriages
* Suspected congenital fibrinogen deficiency or abnormality
* '''BOTH''' PT and APTT unexpectedly prolonged
|
|-
|D-Dimer
|Measures fibrin clot breakdown products from plasmin Elevated D-dimer alone is non-specific except in VTE - Can be associated with a variety of diseases or inflammatory states
|
|
* Deep vein thrombosis
* Pulmonary embolism
* Recent surgery/trauma
* Some cancers
* Acute/chronic infections or inflammatory diseases
* DIC
* Very heavy menstruation
* Normal pregnancy (high levels associated with complications)
* Healthy elderly patient Negative result can be used to exclude venousthromboembolism (VTE) in some populations
|-
|Mixing Studies
|
|
|
|-
|Inhibitor Testing
|
|
|
|-
|Factor Assays
|
|
|
|}

== Abnormal Results ==

==== If PT/INR and APTT both prolonged ====
* Multiple factors in intrinsic and extrinsic pathways affected OR single factor deficiency in common pathway (I, II, V, or X [I if severe])
* Congenital:
** Single factor deficiency for factor I, II, V, or X
* Acquired:
** Multiple factor deficiency in intrinsic AND extrinsic pathways
*** Severe liver disease
*** Severe Vitamin K deficiency
*** DIC
** Specific inhibitor directed to common pathway factor
** Hypofibrinogenemia/dysfibrinogenemia
*** Massive hemmorage
*** Congenital
*** Fibrinolysis

==== If PT/INR is prolonged, but APTT is normal ====
* Probably related to factor VII
** Congenital single factor VII deficiency
** Acquired
*** Early liver disease
*** Early vitamin K deficiency
*** Early coumadin therapy or initial dose
*** Specific inhibitor to VII (rare)

==== If APTT is prolonged, but PT/INR is normal ====
* Probably related to intrinsic pathway factors VIII, IX, XI, or contact factors
** Congenital
*** Single factor deficiency of VIII, IX, XI with bleeding (hemophilia A, B, or C respectively)
*** VWD (can lead to factor VIII deficiency)
*** Deficiency of factor XII, pre-K, HMWK (contact factors)
**** Prolongs APTT but doesn’t result in clinically significant bleeding
** Acquired
*** Non-specific inhibitor (e.g., antiphospholipid antibodies)
**** Lupus anticoagulant in SLE patients
*** Specific inhibitor against intrinsic factors
**** Hemophilia patients may develop anti-FVIII or IX due to treatment
**** Acquired hemophilia or acquired VWD
*** Heparin therapy

=== Causes of Abnormal Results + Followup Testing ===
{| class="wikitable"
|+
!Test Affected
!Cause
!Disease States
!Symptoms/Patient History
!Pathways Affected
!Followup Testing
|-
| rowspan="6" |'''BOTH''' PT and APTT
| colspan="2" |Single factor deficiency for I, II, V, or X
|
|
|
|-
| rowspan="3" |Multiple factor deficiency in intrinsic '''AND''' extrinsic pathways
|Severe liver disease
|Jaundice, abdominal pain or tenderness
|
|
* CBC (platelet count)
* RBC morphology (macrocytes and targets)
* Thrombin time/fibrinogen
* D-Dimer
* Factor V assay (decreased in liver disease but not Vit K deficiency)
* Factor VII assay (most sensitive factor)
* Mixing studies
* Liver enzyme panel
* Total and indirect bilirubin
|-
|Severe Vitamin K deficiency
|
|
|
|-
|Disseminated intravascular coagulation
|
|
|
|-
| colspan="2" |Specific inhibitor to common pathway factor
|
|
|
|-
| colspan="2" |Hypofibrinogenemia/dysfibrinogenemia
|
|
|
|-
| rowspan="5" |PT '''only'''
| rowspan="5" |Factor VIII deficiency
|Congenital single factor VII deficiency
|
|
|
|-
|Early liver disease
|
|
|
|-
|Early Vitamin K deficiency
|
|
|
|-
|Early coumadin therapy/initial dose
|
|
|
|-
|Specific inhibitor to VIII (rare)
|
|
|
|-
| rowspan="6" |APTT '''only'''
|
|VWF disease
|
* Young patient of any gender
* Mucocutaneous bleeding (nosebleeds, menorrhagia, etc.)
|Factor VIII
|
* CBC (PLT count to rule out thrombocytopenia)
* PT/APTT (to rule out other coagulation issues)
* VWF:Ag quantitative analysis immunoassay
* VWF:RCo Ristocetin co-factor qualitative analysis
* Factor VIII activity assay (FVIII:C)
|-
|
|Hemophilia A, B, or C (single factor deficiency)
|
* Male patient
* Anatomic soft tissue bleeding (deep bleeding in muscles, joints, organs)
* Wound oozing after trauma or surgery
|
* Factor VIII (Hemophilia A - 85%)
* Factor IX (Hemophilia B - 14%)
* Factor XI or other factors (Hemophilia C - 1%)
|
* Mixing studies (should be corrected)
* Factor assays (decrease in specific factor relevant to Hemophilia)
|-
|
|Other congenital factor deficiencies
|
|
|
|-
|
|Non-specific inhibitor
|
|
|
|-
|
|Specific inhibitor against intrinsic factors
|
|
|
|-
|
|Heparin therapy
|
|
|
|}

== Investigating Abnormal Results ==

# Check specimen integrity and HCT >55% (recollect and/or dilute)
# Check patient history for any conditions affecting coagulation. If present, report results:
## Anticoagulant therapy: warfarin/coumadin, heparin, direct oral anticoagulants (DOACs)
## Liver disease (early: PT, late: both PT/APTT)
## Vitamin K deficiency
## Known factor deficiency (single or multiple)
#Look for other causes and perform reflex testing
##Decreased fibrinogen → Thrombin time or fibrinogen assay
##Specific single or multiple factor deficiency
##Inhibitor or antibody to factors
##Inhibitor or antibody interfering with test