Disorders of Hemostasis Flashcards
(197 cards)
1
Q
What is hemostasis?
A
Hemostasis is a dynamic process that is geared to preventing blood from escaping the boundaries of the vessel.
2
Q
What are the phases of hemostasis?
A
The phases of hemostasis are:
* Maintenance of vessel integrity
* Formation of a platelet plug
* Propagation of the coagulation cascade
* Clot development
* Fibrinolysis and clot disintegration
3
Q
What are the two types of hemostasis?
A
The two types of hemostasis are:
* Primary hemostasis (platelet plug formation)
* Secondary hemostasis (coagulation process)
4
Q
What maintains vascular integrity?
A
Vascular integrity is maintained by a lining of overlapping endothelial cells supported by a basement membrane, connective tissue, and smooth muscle.
5
Q
What substances do endothelial cells secrete to regulate clot formation?
A
Endothelial cells secrete:
* Tissue factor pathway inhibitor (TFPI)
* Heparin sulfate
* Prostacyclin
* Nitric oxide
6
Q
What role does CD39 play in hemostasis?
A
CD39 degrades ATP and ADP to AMP and adenosine, which are potent antiplatelet and antithrombotic agents.
7
Q
How does von Willebrand factor (vWF) contribute to hemostasis?
A
vWF links to platelet glycoprotein Ib (gpIb) receptors allowing platelet adhesion to the intravascular surface.
8
Q
What are platelets and their role in hemostasis?
A
Platelets are complex cytoplasmic fragments released from bone marrow megakaryocytes, playing roles in adhesion and aggregation.
Largely regulated by Thrombopoeitin
9
Q
What is the coagulation cascade?
A
The coagulation cascade is a complex system that results in controlled formation of a fibrin clot.
10
Q
What are the two traditional pathways of the coagulation cascade?
A
The two traditional pathways are:
* Intrinsic pathway
* Extrinsic pathway
11
Q
What initiates the clot process in the coagulation pathway?
A
The extrinsic pathway initiates the clot process through exposed tissue factor at the site of vessel injury.
12
Q
What is the role of tissue factor in hemostasis?
A
Tissue factor is a critical cofactor required for activation of factor VII.
13
Q
What is the most commonly encountered disorder of hemostasis?
A
The most commonly encountered disorder of hemostasis is antithrombotic drug administration.
14
Q
Fill in the blank: Hemostasis is dependent on normal functioning and integration of the ______, platelets, and coagulation pathway.
A
[vasculature]
15
Q
Endothelium
A
16
Q
Role of Platelets in Hemostasis
A
- Adhesion to subendothelial connective tissue: Collagen, basement membrane, and noncollagenous microfibrils; serum factor VIII and von Willebrand factor (vWF) permit this function; adhesion creates the initial bleeding arrest plug
- Release of adenosine diphosphate, the primary mediator and amplifier of
aggregation; release of thromboxane A, another aggregator and potent
vasoconstrictor; release of calcium, serotonin, epinephrine, and trace thrombin - Platelet aggregation over the area of endothelial injury
- Stabilization of the hemostatic plug by interaction with the coagulation system:
* Platelet factor 3, a phospholipid that helps accelerate certain steps in the coagulation system
* Platelet factor 4, a protein that neutralizes heparin
* Pathway initiation and acceleration by thrombin production
* Secretion of active forms of coagulation proteins - Stimulation of limiting reactions of platelet activity
17
Q
Coagulation Factors
A
Factor I. Fibrinogen
Factor II. Prothrombin
Factor III. Tissue thromboplastin
Factor IV. Calcium
Factor V. Labile factor (proaccelerin)
Factor VI. Not assigned
Factor VII. Proconvertin
Factor VIII. Antihemophilic A factor
Factor IX. Antihemophilic B factor (plasma thromboplastin component, Christmas factor)
Factor X. Stuart-Prower factor
Factor XI. Plasma thromboplastin antecedent
Factor XII. Hageman factor (contact factor)
Factor XIII. Fibrin-stabilizing factor
18
Q
Normal Controls of Coagulation
A
- Removal and dilution of activated clotting factors through blood flow, which also mechanically opposes growth of the hemostatic plug
- Alteration of platelet activity by endothelium-generated nitric oxide and prostacyclin
- Removal of activated coagulation components by the reticuloendothelial system
- Regulation of the clotting cascade by antithrombin III, protein C, protein S, and tissue factor pathway inhibitor (TFPI)
- Activation of the fibrinolytic system
19
Q
Coagulation Cascade
A
20
Q
Clinical evaluation of bleeding patient
A
21
Q
Features of Coagulation disorders that differentiate from platelet disorders
A
22
Q
DDx of Platelet Disorders
A
23
Q
DDx of Vascular disorders
A
24
Q
DDx of Coagulation Disorders
A
25
Diagnostic Hemostasis tests
26
What initial assessment is required when a bleeding disorder is diagnosed?
Stabilization, which may include intravenous fluids, RBC transfusion, or factor replacement
27
What are common initial symptoms of platelet disorders?
Epistaxis, menorrhagia, gastrointestinal bleeding
28
How are platelet disorders typically manifested?
Acquired petechiae, purpura, or mucosal bleeding
29
What distinguishes purpura associated with platelet disorders from that associated with vasculitis?
Purpura in platelet disorders is usually asymptomatic and not palpable; vasculitis purpura can burn or itch and is palpable.
30
What types of bleeding are characteristic of coagulation disorders?
Delayed deep muscle or joint bleeding
31
What are the key laboratory tests for diagnosing hemostatic disorders?
Complete Blood Count, Blood Smear, Platelet Count, Bleeding Time, Prothrombin Time, Partial Thromboplastin Time, Anti-Xa Assay, Fibrinogen, Thrombin Time, Clot Solubility, Factor Level Assays
32
What does a complete blood count assess in the context of bleeding episodes?
Degree of anemia
33
What is defined as thrombocytopenia?
Platelet count of less than 100,000/mm3
34
What is the normal bleeding time range?
8 minutes
35
What does the Prothrombin Time (PT) test?
Factors of the extrinsic and common coagulation pathways
36
What can cause a prolonged Prothrombin Time?
Vitamin K deficiency, warfarin use, liver disease
37
What factors does the Partial Thromboplastin Time (PTT) test exclude?
Factor VII and factor XIII
38
What are the two groups of inherited disorders that manifest as isolated elevation in PTT?
* Deficiencies of contact factors (e.g., factor XII)
* Deficiencies of intrinsic coagulation factors (e.g., factors VIII, IX, XI)
39
What is the role of the anti-Xa assay?
Monitoring unfractionated and low-molecular-weight heparin levels, quantifying direct factor Xa inhibitors
40
What does fibrinogen reflect in the coagulation process?
Balance between production and consumption
41
What does the thrombin time measure?
Conversion of soluble fibrinogen to insoluble fibrin
42
What is a key feature of disorders involving factor XIII deficiency?
Clot solubility testing may show abnormal results
43
How are factor levels determined in laboratory tests?
* Bioassay
* Immunologic assay
44
What do inhibitor screening tests reveal?
Antibodies in plasma that prolong the normal plasma clotting time
45
What is thrombocytopenia defined as?
A platelet count of less than 100,000 micro/mm3
46
What are the two main causes of thrombocytopenia?
* Decreased production
* Increased destruction
47
What conditions can lead to decreased bone marrow production causing thrombocytopenia?
* Chemotherapeutic drugs
* Myelophthisic disease
* Alcohol
* Thiazides
48
What is splenic sequestration in relation to thrombocytopenia?
A rare cause seen primarily with hypersplenism due to malignant hematologic disease, portal hypertension, or increased splenic RBC destruction
49
In what scenarios are platelet transfusions commonly indicated?
* Primary bone marrow disorders (e.g., aplastic anemia, acute leukemia)
50
At what platelet count is spontaneous bleeding more likely to occur?
Below 10,000/mm3
51
What is the risk of hemorrhage attributed to platelet deficiency at counts higher than 50,000 mm3?
Unlikely
52
What is immune thrombocytopenia (ITP)?
An acquired condition resulting from autoantibodies against platelet antigens
53
What are the categories of immune thrombocytopenia?
* Primary ITP
* Secondary ITP
* Drug-induced thrombocytopenia (DITP)
54
What characterizes severe ITP?
A platelet count of less than 20,000 micro/mm3
55
What age group is most commonly affected by acute ITP?
Children aged 2 to 6 years old
56
What is the typical outcome for acute ITP in children?
Greater than 90% rate of spontaneous remission
57
What are common manifestations of chronic ITP in adults?
* Easy bruising
* Prolonged menses
* Mucosal bleeding
58
What is secondary ITP associated with?
* Autoimmune diseases
* Infectious diseases
* Malignancies
59
Which drug is an important cause of drug-induced thrombocytopenia in hospitalized patients?
Heparin
60
What is the recommended treatment for newly diagnosed adult patients with ITP and platelet counts less than 30,000/mm3?
Corticosteroids
61
What is the preferred glucocorticoid for ITP treatment?
Dexamethasone, 40 mg PO or IV daily for 4 days
62
What treatment should be considered for patients with platelet counts less than 10,000/mm3 or significant bleeding?
IVIG in addition to corticosteroids
63
What is a thrombopoietin receptor agonist (TPO-RA) used for?
Life threatening bleeding in inadequate response to corticosteroids, IVIG, and platelet transfusion
64
What are the common drugs associated with drug-induced thrombocytopenia?
Quinine
Phenytoin / carbamazepine / VPA
Heparin
ASA
Digoxin
Sulfa / vanco
## Footnote
QPHADS
65
What is the mechanism by which quinine and quinidine cause thrombocytopenia?
Through an 'innocent bystander' mechanism
## Footnote
The platelet is coated with a drug-antibody complex, complement is
fixed, and intravascular platelet lysis occurs.
66
What characterizes heparin-induced thrombocytopenia (HIT)?
An immune-mediated process associated with unfractionated heparin and low-molecular-weight heparin.
Heparin is thought to pair with platelet factor 4 (PF4), a procoagulant substance found in platelet granules.
This paired complex results in rapid generation of antibodies, which coat platelets resulting in thrombocytopenia
67
What is the 4Ts Score used for?
Differentiating patients with HIT from those with alternative causes of thrombocytopenia
68
What should be done if HIT is clinically suspected?
Immediate cessation of heparin
69
What is the most widely utilized anticoagulant for the treatment of HIT?
Argatroban
70
What is the initial dose of argatroban for patients with normal hepatic function?
2 mcg/kg/min IV
71
What are alternative treatments for HIT aside from argatroban?
* Bivalirudin
* Danaparoid
* Fondaparinux
* Direct oral anticoagulants (DOAC)
72
What is the risk of HIT related to?
* Drug and dosage factors
* Duration of exposure(risk greatest after 5 days of Rx)
* Heparin type(UFH higher risk than LMWH)
* Patient gender(Females twice at risk)
* Surgical and Trauma patients
## Footnote
Can occcur a median of 14 days to upto 40 days post initiation of heparin
73
True or False: HIT can occur in the absence of exposure to heparin.
True
74
Immune Thrombocytopenia Chronicity
75
Describe 4Ts scoring system
76
4Ts Point Risk Stratification
77
What is HITT
Heparin Induced Thrombocytopenia with Thrombosis develops in 33% to 50% of patients with HIT.
## Footnote
The antibodies crated in HIT also activate platelets, creating hypercoagulable state.
78
What is post-transfusion purpura (PTP)?
A rare disorder causing a precipitous fall in platelets approximately one week following transfusion.
79
What antigen is frequently linked to post-transfusion purpura?
Human platelet antigen 1 (HPA1).
## Footnote
When an HPA1 antigen–negative patient receives a platelet transfusion, the platelets with attached HPA1
antibodies provoke an anamnestic response, though the actual mechanism of platelet destruction is uncertain. Patients are usually middle aged women with a history of prior pregnancy, during which they may have been previously sensitized to the HPA1 antigen.
80
What is the typical platelet count in patients with post-transfusion purpura?
Often falls below 10,000/mm3.
81
What is the first-line treatment for severe thrombocytopenia in post-transfusion purpura?
High-dose IVIG, 1g/kg IV.
## Footnote
Glucocorticoids may be given with IVIG. Plasma exchange therapy is no longer
considered a preferred therapy
82
True or False: Platelet transfusion is generally recommended for post-transfusion purpura.
False.
## Footnote
Transfused platelets are often rapidly destroyed, thus platelet transfusion is generally not recommended
except in the setting of severe thrombocytopenia and life-threatening bleeding, preferably with HPA1-negative blood products
83
What are thrombotic microangiopathies (TMA) characterized by?
Microangiopathic hemolytic anemia (MAHA) and thrombocytopenia.
84
What are the most common primary TMA disorders?
* Thrombotic thrombocytopenic purpura (TTP)-most common
* Hemolytic Uremic Syndrome(HUS)
85
What causes TTP?
Autoantibodies to ADAMTS13, an endothelial protein.
86
What are the classic symptoms of TTP?
F ever
A nemia
T hrombocytopenia
R enal failure (more kids, HUS)
N eurologic (more adults, TTP)
## Footnote
Petechiae and purpura 50% but overt bleeding rare
87
What is the standard treatment for TTP?
90% mortality if not treated
** Plasma exchange**( Standard)
Glucocorticoids- Prednisone 1 mg/kg PO daily
Rituximab- consider if refratory to standard Rx
Caplacizumab- 11 mg IV followed by 11 mg sc x 10 days
Eculizumab (HUS)
Avoid platelets if no life-threatening bleeding
(may increase microthrombi)
## Footnote
Plasma contains ADAMTS13
Avoid platelets if no life-threatening bleeding (may increase microthrombi)
88
What is dilutional thrombocytopenia?
A complication of massive transfusion, exchange transfusion, or fluid resuscitation.
## Footnote
Current guidelines for 1 :1 : 1 ratio of fresh frozen plasma (FFP), platelets, and RBCs may assist
in alleviating dilutional thrombocytopenia in the setting of massive transfusion.
89
What is the significance of hereditary thrombocytopenia?
As many as 1 in 7 patients initially diagnosed with ITP may have a hereditary thrombocytopenic syndrome.
90
What is Bernard-Soulier Syndrome (BSS)?
A defect in the platelet gpIb complex affecting platelet adhesion to vWF.
91
What is Glanzmann thrombasthenia (GT)?
An autosomal-recessive disorder due to a defect in the glycoprotein IIb/IIIa complex.
92
What are secretory defects in thrombocytopathy?
Defective platelet granule formation or secretory machinery.
93
What medication blocks thromboxane A2 formation?
Aspirin.
94
What is thrombocytosis?
Defined as a platelet count of greater than 600,000/mm3.
95
What are common causes of secondary thrombocytosis?
* Infection
* Iron deficiency.
96
What is primary thrombocytosis associated with?
* Polycythemia vera
* Myelofibrosis
* Chronic myelogenous leukemia.
97
What is the recommended evaluation for primary thrombocytosis?
A thorough hematologic evaluation.
98
Describe Plasmic Score?
99
What are six potential treatments for ITP?
1. Corticosteroids : (can be PO or IV, often high dose and pulse requiring admission)
2. Immunosuppression: IVIG, rituximab
3. RhoGAM/WinRho (must be Rh+ to work; spleen has less ability to destroy platelets covered in RhIG)
4. Thrombopoeitin receptor agonist (TPO-RA – romiplastim, eltrombopag)
5. Emergency splenectomy
6. Platelet transfusion for life-threatening bleeding, target >50
## Footnote
Pediatric: Mild bleeding typically no medication, even with platelets <20
Consult for workup (rule out sepsis/HUS-TTP, malignancy ie leukemia)
100
When should thrombocytopenia be treated in the ED?
* 100 : SAH/ICH, neurosurgery
* 50 : LP, Active bleeding (GIB, intraabdominal) , ITP with life-threatening bleeding
* 30 : Paracentesis
* 20 : Large laceration, central line
## Footnote
“A platelet count of >10 usually provides adequate hemostasis…”
101
List 5 adverse effects of platelet transfusion
102
What causes Hemophilia A?
A deficiency of factor VIII.
## Footnote
Hemophilia A is primarily sex-linked recessive as it is carried on the X chromosome.
103
What is the prevalence of Hemophilia A in males?
Approximately 17 cases per 100,000 males.
## Footnote
This translates to around 1,125,000 affected individuals worldwide.
104
How many people in the United States have Hemophilia A?
Approximately 13,500 people.
## Footnote
X linked recessive, only males will have clinical disease
105
How is the severity of Hemophilia A categorized?
By factor VIII activity level:
* Severe: less than 1%
* Moderate: 1% to 5%
* Mild: 5% to 40%.
106
What percentage of Hemophilia A cases are considered severe?
Approximately 42%.
107
What is the risk associated with severe Hemophilia A patients?
Increased risk to develop alloantibodies, termed inhibitors, that may inactivate factor VIII.
108
What is the primary source of factor VIII for replacement therapy?
Recombinant DNA technology.
109
What is Emicizumab?
A recombinant immunoglobulin that substitutes for part of the function of activated factor VIII.
110
How does Emicizumab function?
By bridging activated factor IX and factor X to restore the function of missing activated factor VIII.
111
What is the typical concentration of factor VIII in plasma?
Circulates in low concentrations bound to vWF.
112
What are common sites of bleeding in Hemophilia A?
Deep muscles, joints, urinary tract, and intracranial sites.
113
What are major causes of morbidity in Hemophilia A?
Recurrent hemarthrosis and progressive joint destruction.
114
What is the probability of intracranial hemorrhage (ICH) in male patients with Hemophilia A?
1 in 50,000 to 1 in 140,000 male patients.
115
What is the mortality rate from ICH in hemophiliacs?
Around 20%.
116
What type of bleeding is rare in Hemophilia A?
Mucosal bleeding such as epistaxis, oral bleeding, or menorrhagia unless associated with comorbid conditions.
117
What is a common initiator of bleeding in Hemophilia A?
Trauma.
118
What is involved in the comprehensive management of Hemophilia A?
A team effort including physicians, specialized nursing, physical therapy, social work, patients, and caregivers.
119
What should emergency clinicians have rapid access to for managing Hemophilia A?
Information such as primary care physician, hematologist, diagnosis, factor VIII activity level, blood type, and inhibitor status.
120
What is the typical factor VIII activity goal for minor bleeding?
40% to 50%.
121
What is the typical factor VIII activity goal for serious or life-threatening bleeding?
80% to 100%.
122
How much does 1 U/kg of factor VIII increase the circulating factor VIII level?
By 2%.
123
What should be done if there is no response to factor VIII administration?
Raise suspicion for the presence of inhibitors.
124
What is the safest immediate action in emergency care for patients with inhibitors?
Administer recombinant factor VIIa at a dose of 90 mcg/kg IV.
125
What is Desmopressin used for in Hemophilia A?
For patients with documented mild hemophilia A without inhibitors who are experiencing non-life-threatening bleeding.
126
What effect does Desmopressin have on factor VIII levels?
Raises factor VIII by three to six times baseline levels.
127
Indications for Factor Replacement in Hemophilia
128
Recommended Factor VIII Therapy and Dosing for Complications Associated
With Hemophilia
129
What is Hemophilia B?
A deficiency of factor IX activity.
130
How does the incidence of Hemophilia B compare to Hemophilia A?
Its incidence is only a fifth that of hemophilia A.
131
What type of protein is factor IX?
A vitamin K–dependent glycoprotein.
132
How is a deficiency of factor IX diagnosed?
By a factor IX assay after a normal factor VIII assay.
133
What treatment strategies for hemophilia A generally apply to hemophilia B?
Clinical presentations and treatment strategies.
134
What is the replacement factor therapy for hemophilia B?
Use of a recombinant factor IX preparation.
135
When is plasma-derived concentrate used in hemophilia B?
In an emergency situation when recombinant factor IX is unavailable.
136
Is fresh frozen plasma recommended for hemophilia B treatment?
No, it is not routinely recommended.
137
What is the maintenance factor dosing schedule for factor IX?
Every 24 hours.
138
What is the appropriate dose of factor IX for severe bleeding?
100 to 140 units/kg IV.
139
What should be administered for hemophilia B with inhibitors?
Recombinant factor VIIa at a dose of 90 mcg/kg IV.
140
What is von Willebrand disease?
What is the role of vWF?
****The most common hereditary bleeding disorder,caused by quantitative and qualitative deficits in vWF, with an estimated prevalence of 1%.
VWF does two things:
**Role:** Bridges platelets to damaged vascular endothelium;Brings factor VIII to the site of injury to generate fibrin
## Footnote
Inheritance pattern for main variants is autosomal dominant
141
What is the typical factor VIII activity level in von Willebrand disease?
In the 6% to 50% range.
142
What is the preferred treatment for mild to moderately severe von Willebrand disease?
Desmopressin, 0.3 mcg/kg IV.
143
What is the replacement therapy for severe von Willebrand disease?
Factor VIII in the form of lyophilized concentrate at a dose of 50 IU/kg.
144
What can cause an altered level or abnormal function of fibrinogen?
Deficiencies in the coagulation pathway.
145
What are the inherited forms of coagulation disorders associated with?
Rare deficiencies in components of the common pathway (factors II, V, and X).
146
What common causes are associated with acquired forms of coagulation disorders?
Vitamin K deficiency, hepatic insufficiency, or massive transfusion of stored blood.
147
Clinical Features of VWF
More common: GIB, mennorhagia, PPH, epistaxis
Less common: Joint and muscle bruising (unlike Heme A/B)
148
Types of von Willebrand disease?
**MANY polymorphisms, but 3 main types **
Type 1 – reduced amount - mostly asymptomatic, 75% of cases, autosomal dominant
Type 2 – functional issues (platelet or factor VIII)
Type 3 – rare – total deficiency, lifethreatening bleeding early in life, autosomal recessive
**Acquired:**
Malignancies (MGUS, myeloma, NHL, leukemia, Wilms tumor)
Lupus
High states of vascular flow: VSD, CHD with high flow, LVAD/ECMO
Hypothyroidism
Drugs: valproate, ciprofloxacin
149
von Willebrand Disease Management
* Desmopressin 0.3mcg/kg IV/intranasal/SC for mild to moderate disease (Induces synthesis and release of VWF from platelets/endothelial cells)
* TXA
* FFP or cyro may be used
* Replace with VWF/factor VIII product 50 U/kg.
* Recombinant VWF exists which requires giving factor VIII as well.
* Giving plasma would not require factor VIII
* Factor VIII actually accumulates and can cause thrombosis
* Can get inhibitors as well, similar treatment to heme A/B give factor VIIa
150
Review lab and coagulopathy diagnosis
151
What are the two main types of oral anticoagulants?
Vitamin K antagonists (e.g., warfarin) and direct-acting oral anticoagulants (DOACs)
## Footnote
DOACs include dabigatran, rivaroxaban, and apixaban.
152
What is the mechanism of action of dabigatran?
Dabigatran is a direct thrombin inhibitor
## Footnote
It was the first DOAC to gain FDA approval.
153
Name two common DOACs and their specific targets.
* Rivaroxaban: selective factor Xa inhibitor
* Apixaban: selective factor Xa inhibitor
154
What complications may arise from the use of DOACs in patients with impaired renal or liver function?
Excessive anticoagulation
155
What is the primary concern that brings patients to the ED regarding anticoagulants?
Supratherapeutic dosing or hemorrhage
156
How can the effects of heparin be urgently reversed?
With protamine sulfate
## Footnote
1 mg of protamine for every 100 units of heparin.
157
What is the off-label use of protamine in relation to LMWH?
To reverse effects of LMWH in life-threatening bleeding
158
What is the recommended dose of protamine for LMWH reversal depending on timing?
* 1 mg for ≤8 hours since last administration
* 0.5 mg for >8 hours since last administration
159
What should not exceed 50 mg over 10 minutes when administering protamine?
Administration of protamine
160
What is the FDA-approved reversal agent for dabigatran?
Idarucizumab, 5 g IV
161
What is the alternative to idarucizumab for dabigatran-associated bleeding?
Activated prothrombin complex concentrate (aPCC) at 50 units/kg IV
162
What factors are included in 4F-PCC?
* Factors II
* VII
* IX
* X
* Protein C
* Protein S
163
How much of dabigatran is removed with 4 hours of dialysis?
Approximately 57%
164
What is the FDA-approved reversal agent for apixaban or rivaroxaban in life-threatening bleeds?
Andexanet alfa
165
What is an alternative to andexanet alfa for apixaban or rivaroxaban?
4F-PCC at 25 to 50 units/kg IV or a fixed dose of 2000 units IV
166
What is the management approach for excessive anticoagulation from warfarin with INR below 4.5?
Withhold additional warfarin
167
What is the recommendation for INR levels between 4.5 and 10 without bleeding?
Hold additional warfarin doses for 1 to 2 doses and consider vitamin K
168
What treatment is recommended for INR levels above 10 but not bleeding?
Hold warfarin and treat with 5 mg of oral vitamin K
169
What is the treatment for patients with elevated INR and active bleeding?
Cessation of warfarin, 10 mg of vitamin K IV, plus 4F-PCC or fresh frozen plasma
170
What is the most effective route for administering vitamin K?
Orally
171
How should intravenous vitamin K be administered?
As a slow infusion over 20 to 30 minutes
172
True or False: Subcutaneous dosing of vitamin K is the preferred method of administration.
False
173
Review labs and anticoagulation
174
Adjuncts and reversal agents
175
Critical Sites for Hemorrhage
in Anticoagulated Patients
176
Treatment for
Supratherapeutic INR
177
4F-PCC dosage for Warfarin reversal in major bleeding
178
DIC Abnormal Clotting Sequence
179
What does DIC stand for?
Disseminated Intravascular Coagulation
## Footnote
DIC is an acquired coagulopathy reflecting dysregulated coagulation and fibrinolytic pathways.
180
What is the primary cause of DIC?
DIC is caused by multiple pathologic processes that disturb the balance between procoagulants and inhibitors.
181
What are the clinical consequences of DIC?
* Life-threatening bleeding from loss of platelets and clotting factors
* Fibrinolysis and fibrin degradation product interference
* Small-vessel obstruction and tissue ischemia from fibrin deposition
* RBC injury and anemia from microvascular hemolysis
182
Which patients should be considered for DIC diagnosis?
Any patient with purpura, a bleeding tendency, and signs of organ injury, especially in the central nervous system or kidney.
183
How is the clinical diagnosis of DIC confirmed?
By laboratory testing.
184
What conditions may be confused with DIC?
* Severe liver disease
* Primary fibrinolysis
185
What are the manifestations of severe liver disease?
Clinical jaundice and splenomegaly.
186
What is primary fibrinolysis?
A rare disorder affecting fibrinogen and fibrin while preserving other coagulation components.
187
What is the initial treatment focus for DIC?
Reversal of the triggering mechanism.
188
When is specific management of DIC warranted?
In cases of active bleeding, significant risk of bleeding, invasive procedures, arterial or venous thromboembolism, skin necrosis, or acral ischemia.
189
What should be included in replacement therapy for active bleeding in DIC?
* Platelets
* Fresh frozen plasma
* Cryoprecipitate
190
What is the goal of replacement therapy in DIC?
To avoid depletion of clotting factors.
191
What monitoring indicators are useful in DIC management?
* Slowing of bleeding
* Decrease in fibrin degradation products
* Rise in platelet count and fibrinogen level
192
When can heparin be selectively utilized in DIC treatment?
When fibrin deposition and thrombosis predominate the pathologic picture.
193
What are some disease states associated with fibrin deposition?
* Purpura fulminans
* Retained nonviable fetus before delivery
* Giant hemangioma
* Acute promyelocytic leukemia
194
In which conditions is heparin generally of little benefit?
* Meningococcemia
* Abruptio placentae
* Severe liver disease
* Trauma
195
What other therapeutic agents have been evaluated for DIC?
* Antithrombin III
* PCC
* Recombinant factor VIIa
* Activated protein C
196
What are the goals of emergency care for patients with DIC?
* Early recognition and close monitoring
* Focus on mitigation of the precipitating condition
* Identifying potential life-threatening complications
* Initiation of blood product or anticoagulation therapy only rarely
197
Laboratory Diagnosis of Disseminated Intravascular Coagulation
