NAME: PARDILLO, MELODY JANE B.

SECTION: BMLS 10-3C

CHAPTER 38
HEMORRAGIC DISORDERS AND LABORATORY
ASSESSMENT

HEMORRAGIC DISORDER
Normal clot formation and lysis depend on
1. Intact blood vessels
2. an adequate number of functioning platelets
3. sufficient amounts of the 12 clotting factors (I to XIII; VI is no longer used)
4. a well-controlled fibrinolytic system
Four basic problems underlying hemorrhagic disorders
 weak, damaged vessels that rupture easily or spontaneously
 platelet deficiency (thrombocytopenia) resulting from:
o hypoproliferation
o excessive pooling of platelets in the spleen
o excessive platelet destruction
 deficiency or total lack of one of the clotting factors
 excessive or insufficient fibrinolysis
A. Immune Thrombocytopenic Purpura (ITP)
 Most common thrombocytopenic disorder
 2 forms
o Acute
▪ Appears 1-6 weeks after a viral illness; self-limiting; remission occurs
within 6 months
▪ Occurs predominantly in children
o Chronic
▪ Other causes of thrombocytopenia
 Was previously called Idiopathic Thrombocytopenic Purpura (cause was unknown)
 Now considered an autoimmune disease that results in the destruction of
platelets RISK FACTORS
 Viral infections
 Sulfa-containing drugs,
quinine ETIOLOGY
 Acquired disorder in which circulating platelets are destroyed by autoantibodies that
bind with antigens on the plaletet membrane
 Platelets normal lifespan (7-10 days); with ITP  1-3 days
DX
 PLT < 100,000/mm3
 Prolonged bleeding time with normal coagulation time (all coagulation factors are
present & normal)
 Increased capillary fragility as demonstrated by the tourniquet test
 Positive platelet antibody screening
 Bone marrow aspirate containing normal or increased number of megakaryocytes
(platelet precursors)
S/S/X
 Petechiae (tiny hemorrhagic spots caused by intradermal or submucosal bleeding)
 Ecchymosis (large, blotchy subcutaneous hemorrhagic areas)
 Epistaxis
 Bleeding from gums
 Easy bruising
 Heavy menses
COMPLICATIONS
 Spontaneous cerebral hemorrhage
 Severe hemorrhages from the nose, GIT & urinary system

 Bleeding into the diaphragm

 Nerve pain resulting from pressure of hematomas on
nerves MX MNGT
 High doses of corticosteroids  inhibit the macrophage ingestion of the antibody-
coated platelets
 Plasmapheresis  used as a short-term therapy until steroid therapy takes effect
 If client is actively bleeding/requires surgery  IV gammaglobulin to increase the
platelet count
 Splenectomy
 Immunosuppressive therapy blocks the binding receptors on macrophages so
that the platelets are not destroyed
o Vincristine, vinblastine, azathioprine, cyclophosphamide
NX MNGT
 Avoid constipation, valsalva maneuver
 Avoid flossing of the teeth
 Use of soft-bristled toothbrush & electric razors
 Refrain from vigorous sexual intercourse when PLT is < 10,000/mm3
COAGULATION DISORDERS
A. Disseminated Intravascular Coagulation
 Complex syndrome of activated coagulation that results in bleeding and thrombosis
simultaneously.
 BASICALLY a loss of balance between the clotting & lysing systems in the body
caused by the simultaneous presence of THROMBIN & PLASMIN
 ↑THROMBIN  tips the balance toward the prothrombin state resulting in
thrombosis’
 ↑PLASMIN  triggers excessive clot lysis (fibrinolysis) in which clotting factors are
consumed are consumed to such an extent that generalized bleeding occurs
RISK FACTORS
 Cancer (especially prostate cancer and leukemia)
 Obstetric complications
 Acute hemolysis; Allergic reactions
 Trauma
 Shock; Sepsis
ETIOLOGY (Four categories of causative factors)
 Infection  leading cause
 Tissue coagulation factors traveling into the circulation
 Damage to the vascular endothelium
 Stagnant blood flow
DX
 Prolonged PT & PTT
 ↓PLT (<100,000/mm3)
 Fibrinogen degradation product (FDP)  elevated (75%-100%)
 D-dimer test
S/SX
 Hemorrhagic manifestations:
o Purpura, ecchymosis & Petechiae on the skin, mucous membrane, heart
lining & lungs
 o Prolonged bleeding from venipucture
o Severe, uncontrolled hemorrhage during surgery or childbirth
o Excessive bleeding from gums & nose
o Intracerebral & GI bleeding
o Renal hematuria
o Tachycardia & hypotension
o Dyspnea, hemoptysis & respiratory congestion
 Microvascular thrombosis manifestations
o Oliguria & ARF
o Pulmonary emboli
o ARDS
o Delirium, convulsion & coma
o Tissue necrosis
TEST FUNCTION EVALUATED NORMAL RANGE CHANGES IN DIC
Platelet count Platelet number 150,000- ↓
450000/mm3
PT Extrinsic pathway 11-12.5 sec ↑
PTT Intrinsic pathway 23-35 sec ↑
TT Clot formation 8-11 sec ↑
Fibrinogen Amount available for 170-340 mg/dl ↓
coagulation
D-dimer Local fibrinolysis 0-250 ng/ml ↑
Fibrin Fibrinolysis 0-5ug/ml ↑
degradation
products (FDPs)

Goals
o Identification & correction of the precipitating cause
▪ Antibiotics  for infection
o Reestablishing hemostasis by replacing missing blood components
o Supportive therapy to control hemorrhage & thrombosis
▪ Avoid injections when possible
▪ Apply pressure to bleeding sites
▪ Turn & reposition client frequently & gently
B. Hemophilia
 X-linked genetic disorder that results in a deficiency of coagulation factors
 2 major forms
o Hemophilia A (classic form) deficiency of factor VIII; X-linked
o Hemophilia B (Christmas disease)  deficiency of factor IX; X-linked
o Von Willebrand’s disease  deficiency of factor VIII & defective platelet
dysfunction; autosomal dominant trait
S/SX
 Hemarthrosis  hallmark of the disease
 Slow, persistent bleeding from cuts, trauma
 Severe hemorrhaging from the gums after dental extraction
 Epistaxis
 GI bleeding
 Hematoma
 Hematuria
 Intracranial bleeding
MNGT
 Goals
o Stop topical bleeding as quickly as possible
▪ Apply pressure or ice to the injured site
▪ Packing the area with fibrin foam
▪ Applying topical hemostatic agents such as thrombin
o Supply the missing factor causing hemorrhage
▪ Blood transfusion
o Prevent complications leading to & caused by bleeding
▪ Hemarthrosis
 Joint immobilization
 Ice pack
 If pain is severe  may aspirate blood from joints
 Once bleeding stops
o Perform active ROM without weight-bearing
 Pharmacological tx
o Aminocaproic acid (EACA, Amicar)  fibrinolytic enzyme inhibitor that can
slow the dissolution of blood clots; useful in treating mucosal bleeding
o Desmopressin (DDVAP)  induces a transient rise in factor VIII levels
 NAME: PARDILLO, MELODY JANE B. SECTION: BMLS 10-3C
CHAPTER 39
THROMBOTIC DISORDER AND LABORATORY ASSESSMENT
Thrombosis is a multifaceted disorder resulting from
abnor
malities in blood flow, such as stasis, and abnormalities
in the
coagulation system, platelet function, leukocyte
activation
molecules, and the blood vessel wall.
Thrombophilia (once called hypercoagulability) is
defined as
the predisposition to thrombosis secondary to a
congenital or
acquired disorder.
• Thrombosis is the most prevalent condition in
developed countries
and accounts for most illnesses and premature death.
• Thrombosis may be arterial, causing peripheral artery
disease,
heart disease, and stroke, or venous, causing deep vein
thrombo
sis and pulmonary emboli.
• Most thrombosis occurs as a result of lifestyle habits
and aging, but
many thrombotic disorders are related to congenital
risk factors.
• Thrombosis risk profiles may be offered to clinicians
for screening
purposes in high-risk populations.
• The main hemostasis predictors of arterial thrombotic
disease
are elevated levels of CRP (measured by high-
sensitivity assay),
homocysteine, fibrinogen, lipoprotein (a), and
coagulation factors.
• The main hemostasis predictors of venous
thromboembolic dis
ease are APL antibodies, antithrombin, PC, and PS
deficiency, FVL
mutation, and prothrombin G20210A.
• APL antibody testing requires a series of essential
hemostasis
laboratory assays clot-based tests and immunoassays.
• Antithrombin may be assayed using chromogenic
substrate and
enzyme immunoassay analyses.
• The tests for evaluating the protein C pathway
include protein C
and protein S activity and concentration, APC
resistance, FVL
assay, and C4bBP assay.
• The molecular test for the prothrombin G20210A
mutation predicts
the risk of venous thrombosis.
• DIC is a clinical diagnosis confirmed by a series of
assays in the
acute care facility.
• Chronic thrombosis may be identified using the PF
112, TAT
complex, and quantitative D-dimer assays.
• The laboratory provides confirmatory tests for HIT
with thrombosis.
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