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Presented by,
Ms. Yagnika Damor
DIC???
Disseminated
Intravascular Coagulation
INTRODUCTION
Other Name: -Consumption coagulopathy, Defibrination syndrome
 Disseminated intravascular coagulation (DIC) also known as disseminated
intravascular coagulopathy or DIC syndrome is a complex and often life-
threatening disorder in which widespread blood clotting occurs throughout
the body.
 This excessive clotting can lead to the consumption of clotting factors
and platelets, resulting in a bleeding diathesis. The hallmark of DIC is
the activation of both coagulation and fibrinolysis.
 The term disseminated intravascular coagulation can be
misleading because it suggests that blood is clotting.
 However, this condition is characterized by profuse bleeding
resulting from platelet depletion and clotting factors.
 DIC is always caused by an underlying disease or condition.
 The severity of DIC is variable, but it is potentially life-
threatening.
 The underlying problem must be treated for the DIC to
resolve.
DEFINITION
According to the International Society on Thrombosis and
Hemostasis(ISTH),
“DIC is an acquired syndrome characterized by the intravascular
activation of coagulation with loss of localization arising from
different causes.” It can originate from and cause damage to the
microvasculature, which if sufficiently severe & can produce organ
dysfunction.
EPIDEMIOLOGY OF DIC
 Prevalence of DIC patients with various medical conditions:
 1 % of hospitalized patients are estimated to develop DIC.
 10-30% of patients in the Intensive care Unit (ICU).
 20% of patients with ARDS.
 30-40% of patients with Severe head trauma.
 30-60% of patients with Severe sepsis.
ACUTE DIC SUBACUTE DIC CHRONIC DIC
• This may not be
apparent initially
but may become
fulminant as the
clinical course
progresses.
• It’s a slower-developing
and often less severe form
of DIC.
• certain cancers autoimmune
diseases, liver cirrhosis, and
chronic infections.
TYPES OF DIC
• It’s a rapidly developing
and life-threatening form
of DIC.
• Sepsis, major trauma,
burns, pancreatitis, or
certain autoimmune
diseases.
RISK FACTOR OF DIC
ACUTE DIC
 Shock:-Hemorrhagic, Cardiogenic, Anaphylactic
 Septicemia:-Bacterial, Viral, Fungal, Parasitic
 Hemolytic Processes:-Transfusion of mismatched blood, Acute hemolysis
from infection or immunologic disorders
 Obstetric conditions:-Abruptio placentae, Amniotic fluid embolism, Septic
abortion
 Malignancies:-Acute leukemia, Metastatic solid tumors
 Tissue damage:-Extensive burns and trauma, heatstroke,
Severe head injury, Transplant rejections, Post-operative
damage, Fat and pulmonary emboli, Snake bite.
SUBACUTE DIC
 Malignancy:- Metastatic cancer, Myeloproliferative malignancies.
 Obstetric:-Retained dead fetus.
CHRONIC DIC
 Liver disease
 Systemic lupus erythematosus malignancy
COAGULATION CASCADE
PATHOPHYSIOLOGY
(Extrinsic Pathway) TISSUE FACTOR
Endotoxin
Factor XII activation
(Intrinsic Pathway)
THROMBIN
GENERATION
INTRAVASCULAR
FIBRIN DEPOSITION
PLATELET
CONSUMPTION
PLASMINOGEN
ACTIVATION
THROMBOSIS
HEMOLYTIC
ANEMIA
TISSUE
ISCHEMIA
THROMBOCYTOPENIA
BLEEDING
PLASMIN
GENERATION
FIBRINOLYSIS
FIBRINOLYSIS
FIBRIN DEGRADATION
PRODUCTS
CLOTTING FACTOR
DEGRADATION
STIMULUS
TISSUE
DESTRUCTION
ENDOTHELIAL
INJURY
01
CLINICAL MANIFESTATION
 DIC has both bleeding and thrombotic manifestations.
Integumentary System:-
BLEEDING MANIFESTATION
 Pallor, petechiae,
Purpura,Oozing blood.
Venipuncture site bleeding,
hematomas & occult
hemorrhage.
THROMBOTIC MANIFESTATION
 Cyanosis, ischemic tissue
necrosis (e.g. gangrene) &
hemorrhagic necrosis.
Respiratory system:-  Tachypnea, hemoptysis, &
orthopnea.
 Tachypnea, dyspnea,
pulmonary emboli & ARDS.
01
Cardiovascular System:-
BLEEDING MANIFESTATION THROMBOTIC MANIFESTATION
Neurologic System:-
 Vision change, dizziness,
headache, change in mental
status, and irritability.
 ECG change &
venous distention
 Tachycardia &
hypotension
GI system:-
 Upper and lower GI
bleed, abdominal
distension, and bloody
stool.
 Abdominal pain
Urinary system:-  Oliguria, leading to failure.
 Hematuria
Musculoskeletal system:-  Bone & joint pain
DIAGNOSTIC
EVALUATION
 HISTORY COLLECTION:
A thorough history including recent surgeries, trauma,
infections, obstetric complications, malignancies, liver
disease, and exposure to toxins or medications that may
predispose to DIC.
 PHYSICAL EXAMINATION:
Assess for signs and symptoms suggestive of DIC, such
as bleeding from multiple sites, petechiae, ecchymosis,
organ dysfunction (e.g., renal failure, hepatic
dysfunction), and signs of underlying conditions.
LABORATORY INVESTIGATIONS
 Complete Blood Count (CBC): Evaluation of platelet count, hemoglobin,
and hematocrit. Thrombocytopenia (low platelet count) is a common finding
in DIC.
 Coagulation Profile: Assessing prothrombin time (PT), activated partial
thromboplastin time (aPTT), fibrinogen levels, and D-dimer.
 Fibrin Degradation Products (FDPs): Elevated levels of FDPs, including
D-dimer, reflect ongoing fibrinolysis and are indicative of DIC.
 Peripheral Blood Smear: Examination for schistocytes (fragmented red
blood cells) may suggest microangiopathic hemolytic anemia, a feature of
DIC.
 Liver Function Tests (LFTs)
 Renal Function Tests
LABORATORY VALUES FOUND IN DIC
Sr. No. Test Change in DIC
1. Platelet count Decreased
2. Prothrombin time (PT) Increased
3. Partial thromboplastin time activated(aPTT) Increased
4. Thrombin time Increased
5. Fibrinogen Decreased
6. D-dimer Increased
7. FDPs Increased
8. Antithrombin III Decreased (90%)
9. Protein C & Protein S Decreased
10. Factor assay II, V, VII, VIII, X, XIII Decreased
 Chest X-ray or CT scan: To assess for pulmonary embolism or other
underlying causes of DIC such as infection or malignancy.
 Ultrasound or Doppler Studies: Evaluation for deep vein thrombosis (DVT) or
thromboembolism.
IMAGING STUDIES
SCORING SYSTEMS
 Scoring systems such as the International Society on Thrombosis and
Hemostasis (ISTH) DIC score can aid in the diagnosis and severity
assessment of DIC based on various clinical and laboratory parameters.
 It provides an objective measurement of DIC.
 A score of 5 or higher suggests probable overt DIC, while a lower score
may indicate Non overt DIC or other clotting disorders.
International Society of Thrombosis and Haemostasis (ISTH)
Platelet count
< 50 × 109/L +2
≥ 50 < 100 × 109/L +1
≥ 100 × 109/L 0
Elevated fibrin-related marker
Strong increase +3
Moderate increase +2
No increase 0
Prolonged prothrombin time
≥ 6 seconds +2
≥ 3 < 6 seconds +1
< 3 seconds 0
Fibrinogen level
< 100 g/mL +1
≥ 100 g/mL 0
Diagnosis:
 if > 5, there is a positive diagnosis of overt DIC; repeat score daily
 if < 5, suggestive (not affirmative) of nonovert DIC; Repeat next 1-2 days.
MANAGEMENT OF DIC
 MEDICAL MANAGEMENT
 The management of Disseminated Intravascular Coagulation (DIC) involves addressing the
underlying cause, supportive care, and specific interventions to control the coagulopathy.
1. Treatment of Underlying Cause
 Identify and address the underlying condition precipitating DIC. This may include treating sepsis
or infections, managing trauma or surgical complications, addressing obstetric complications,
managing malignancies, or treating liver disease.
2. Supportive Care
 Fluid Resuscitation: - Maintain adequate intravascular volume with crystalloids or colloids to improve tissue
perfusion.
 Transfusion Support: Administer blood products judiciously based on clinical need and laboratory parameters.
 Red Blood Cell Transfusion: Address anemia if present or if there is active bleeding.
 Platelet Transfusion: Consider in cases of severe thrombocytopenia or ongoing bleeding.
 Fresh Frozen Plasma (FFP): This may be indicated in patients with active bleeding or prolonged clotting.
 Cryoprecipitate: Rich in fibrinogen and other coagulation factors, may be used to correct hypofibrinogenemia.
 Oxygen Therapy: Maintain adequate tissue oxygenation, especially in cases of hypoxemia or respiratory
compromise.
 Supportive Measures: Monitor and manage organ dysfunction, including renal replacement therapy for renal
failure, and respiratory support for acute respiratory distress syndrome (ARDS).
3. Anticoagulant Therapy:
 Heparin: Unfractionated heparin or low molecular weight heparin may
be considered in some cases to prevent further thrombus formation.
 If heparin induces bleeding, aminocaproic acid (Amicar) is given; cardiac,
renal, and electrolyte studies should be followed closely during its use
because amicar enhance thrombiss.
 Antithrombin III (desirudin) a natural coagulation inhibitor may also be
given and appears to shorten the course and reduce the complication of
DIC.
 Chronic DIC can be controlled by long term use of heparin.
4. Treatment of Bleeding:
 Local Measures: Direct pressure, topical hemostatic agents, or surgical intervention may be necessary to
control bleeding from specific sites.
 Pharmacological Agents: Consider specific hemostatic agents such as recombinant activated factor VII
(rFVIIa) in cases of refractory bleeding.
5. Fibrinolytic therapy:
 Fibrinolytic therapy can be used to break down blood clots. This may involve the use of alteplase,
streptokinase, or other fibrinolytic medications.
6. Monitoring and Serial Assessment:
 Regular monitoring of clinical status, vital signs, laboratory parameters (including
coagulation tests and markers of organ dysfunction), and response to treatment.
NURSING MANAGEMENT OF DIC
 Risk for Bleeding Related to Coagulopathy and Decreased Platelet Count.
 Risk for Impaired Gas Exchange Related to Pulmonary Complications.
 Risk for Infection Related to Invasive Procedures and Immunocompromised
State.
 Risk for Altered Fluid Volume Related to Blood Loss and Third Spacing.
 Impaired Skin Integrity Related to Prolonged Bed Rest and Potential Bleeding.
 NURSING DIAGNOSIS
THANK YOU!

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Disseminated Intravascular Coagulation: A Comprehensive Guide for Nursing Students"

  • 3. INTRODUCTION Other Name: -Consumption coagulopathy, Defibrination syndrome  Disseminated intravascular coagulation (DIC) also known as disseminated intravascular coagulopathy or DIC syndrome is a complex and often life- threatening disorder in which widespread blood clotting occurs throughout the body.  This excessive clotting can lead to the consumption of clotting factors and platelets, resulting in a bleeding diathesis. The hallmark of DIC is the activation of both coagulation and fibrinolysis.
  • 4.  The term disseminated intravascular coagulation can be misleading because it suggests that blood is clotting.  However, this condition is characterized by profuse bleeding resulting from platelet depletion and clotting factors.  DIC is always caused by an underlying disease or condition.  The severity of DIC is variable, but it is potentially life- threatening.  The underlying problem must be treated for the DIC to resolve.
  • 5. DEFINITION According to the International Society on Thrombosis and Hemostasis(ISTH), “DIC is an acquired syndrome characterized by the intravascular activation of coagulation with loss of localization arising from different causes.” It can originate from and cause damage to the microvasculature, which if sufficiently severe & can produce organ dysfunction.
  • 6. EPIDEMIOLOGY OF DIC  Prevalence of DIC patients with various medical conditions:  1 % of hospitalized patients are estimated to develop DIC.  10-30% of patients in the Intensive care Unit (ICU).  20% of patients with ARDS.  30-40% of patients with Severe head trauma.  30-60% of patients with Severe sepsis.
  • 7. ACUTE DIC SUBACUTE DIC CHRONIC DIC • This may not be apparent initially but may become fulminant as the clinical course progresses. • It’s a slower-developing and often less severe form of DIC. • certain cancers autoimmune diseases, liver cirrhosis, and chronic infections. TYPES OF DIC • It’s a rapidly developing and life-threatening form of DIC. • Sepsis, major trauma, burns, pancreatitis, or certain autoimmune diseases.
  • 8. RISK FACTOR OF DIC ACUTE DIC  Shock:-Hemorrhagic, Cardiogenic, Anaphylactic  Septicemia:-Bacterial, Viral, Fungal, Parasitic  Hemolytic Processes:-Transfusion of mismatched blood, Acute hemolysis from infection or immunologic disorders  Obstetric conditions:-Abruptio placentae, Amniotic fluid embolism, Septic abortion  Malignancies:-Acute leukemia, Metastatic solid tumors
  • 9.  Tissue damage:-Extensive burns and trauma, heatstroke, Severe head injury, Transplant rejections, Post-operative damage, Fat and pulmonary emboli, Snake bite. SUBACUTE DIC  Malignancy:- Metastatic cancer, Myeloproliferative malignancies.  Obstetric:-Retained dead fetus. CHRONIC DIC  Liver disease  Systemic lupus erythematosus malignancy
  • 11. PATHOPHYSIOLOGY (Extrinsic Pathway) TISSUE FACTOR Endotoxin Factor XII activation (Intrinsic Pathway) THROMBIN GENERATION INTRAVASCULAR FIBRIN DEPOSITION PLATELET CONSUMPTION PLASMINOGEN ACTIVATION THROMBOSIS HEMOLYTIC ANEMIA TISSUE ISCHEMIA THROMBOCYTOPENIA BLEEDING PLASMIN GENERATION FIBRINOLYSIS FIBRINOLYSIS FIBRIN DEGRADATION PRODUCTS CLOTTING FACTOR DEGRADATION STIMULUS TISSUE DESTRUCTION ENDOTHELIAL INJURY
  • 12. 01 CLINICAL MANIFESTATION  DIC has both bleeding and thrombotic manifestations. Integumentary System:- BLEEDING MANIFESTATION  Pallor, petechiae, Purpura,Oozing blood. Venipuncture site bleeding, hematomas & occult hemorrhage. THROMBOTIC MANIFESTATION  Cyanosis, ischemic tissue necrosis (e.g. gangrene) & hemorrhagic necrosis. Respiratory system:-  Tachypnea, hemoptysis, & orthopnea.  Tachypnea, dyspnea, pulmonary emboli & ARDS.
  • 13. 01 Cardiovascular System:- BLEEDING MANIFESTATION THROMBOTIC MANIFESTATION Neurologic System:-  Vision change, dizziness, headache, change in mental status, and irritability.  ECG change & venous distention  Tachycardia & hypotension GI system:-  Upper and lower GI bleed, abdominal distension, and bloody stool.  Abdominal pain Urinary system:-  Oliguria, leading to failure.  Hematuria Musculoskeletal system:-  Bone & joint pain
  • 15.  HISTORY COLLECTION: A thorough history including recent surgeries, trauma, infections, obstetric complications, malignancies, liver disease, and exposure to toxins or medications that may predispose to DIC.  PHYSICAL EXAMINATION: Assess for signs and symptoms suggestive of DIC, such as bleeding from multiple sites, petechiae, ecchymosis, organ dysfunction (e.g., renal failure, hepatic dysfunction), and signs of underlying conditions.
  • 16. LABORATORY INVESTIGATIONS  Complete Blood Count (CBC): Evaluation of platelet count, hemoglobin, and hematocrit. Thrombocytopenia (low platelet count) is a common finding in DIC.  Coagulation Profile: Assessing prothrombin time (PT), activated partial thromboplastin time (aPTT), fibrinogen levels, and D-dimer.  Fibrin Degradation Products (FDPs): Elevated levels of FDPs, including D-dimer, reflect ongoing fibrinolysis and are indicative of DIC.  Peripheral Blood Smear: Examination for schistocytes (fragmented red blood cells) may suggest microangiopathic hemolytic anemia, a feature of DIC.  Liver Function Tests (LFTs)  Renal Function Tests
  • 17. LABORATORY VALUES FOUND IN DIC Sr. No. Test Change in DIC 1. Platelet count Decreased 2. Prothrombin time (PT) Increased 3. Partial thromboplastin time activated(aPTT) Increased 4. Thrombin time Increased 5. Fibrinogen Decreased 6. D-dimer Increased 7. FDPs Increased 8. Antithrombin III Decreased (90%) 9. Protein C & Protein S Decreased 10. Factor assay II, V, VII, VIII, X, XIII Decreased
  • 18.  Chest X-ray or CT scan: To assess for pulmonary embolism or other underlying causes of DIC such as infection or malignancy.  Ultrasound or Doppler Studies: Evaluation for deep vein thrombosis (DVT) or thromboembolism. IMAGING STUDIES
  • 19. SCORING SYSTEMS  Scoring systems such as the International Society on Thrombosis and Hemostasis (ISTH) DIC score can aid in the diagnosis and severity assessment of DIC based on various clinical and laboratory parameters.  It provides an objective measurement of DIC.  A score of 5 or higher suggests probable overt DIC, while a lower score may indicate Non overt DIC or other clotting disorders.
  • 20. International Society of Thrombosis and Haemostasis (ISTH) Platelet count < 50 × 109/L +2 ≥ 50 < 100 × 109/L +1 ≥ 100 × 109/L 0 Elevated fibrin-related marker Strong increase +3 Moderate increase +2 No increase 0 Prolonged prothrombin time ≥ 6 seconds +2 ≥ 3 < 6 seconds +1 < 3 seconds 0 Fibrinogen level < 100 g/mL +1 ≥ 100 g/mL 0 Diagnosis:  if > 5, there is a positive diagnosis of overt DIC; repeat score daily  if < 5, suggestive (not affirmative) of nonovert DIC; Repeat next 1-2 days.
  • 21. MANAGEMENT OF DIC  MEDICAL MANAGEMENT  The management of Disseminated Intravascular Coagulation (DIC) involves addressing the underlying cause, supportive care, and specific interventions to control the coagulopathy. 1. Treatment of Underlying Cause  Identify and address the underlying condition precipitating DIC. This may include treating sepsis or infections, managing trauma or surgical complications, addressing obstetric complications, managing malignancies, or treating liver disease.
  • 22. 2. Supportive Care  Fluid Resuscitation: - Maintain adequate intravascular volume with crystalloids or colloids to improve tissue perfusion.  Transfusion Support: Administer blood products judiciously based on clinical need and laboratory parameters.  Red Blood Cell Transfusion: Address anemia if present or if there is active bleeding.  Platelet Transfusion: Consider in cases of severe thrombocytopenia or ongoing bleeding.  Fresh Frozen Plasma (FFP): This may be indicated in patients with active bleeding or prolonged clotting.  Cryoprecipitate: Rich in fibrinogen and other coagulation factors, may be used to correct hypofibrinogenemia.  Oxygen Therapy: Maintain adequate tissue oxygenation, especially in cases of hypoxemia or respiratory compromise.  Supportive Measures: Monitor and manage organ dysfunction, including renal replacement therapy for renal failure, and respiratory support for acute respiratory distress syndrome (ARDS).
  • 23. 3. Anticoagulant Therapy:  Heparin: Unfractionated heparin or low molecular weight heparin may be considered in some cases to prevent further thrombus formation.  If heparin induces bleeding, aminocaproic acid (Amicar) is given; cardiac, renal, and electrolyte studies should be followed closely during its use because amicar enhance thrombiss.  Antithrombin III (desirudin) a natural coagulation inhibitor may also be given and appears to shorten the course and reduce the complication of DIC.  Chronic DIC can be controlled by long term use of heparin.
  • 24. 4. Treatment of Bleeding:  Local Measures: Direct pressure, topical hemostatic agents, or surgical intervention may be necessary to control bleeding from specific sites.  Pharmacological Agents: Consider specific hemostatic agents such as recombinant activated factor VII (rFVIIa) in cases of refractory bleeding. 5. Fibrinolytic therapy:  Fibrinolytic therapy can be used to break down blood clots. This may involve the use of alteplase, streptokinase, or other fibrinolytic medications. 6. Monitoring and Serial Assessment:  Regular monitoring of clinical status, vital signs, laboratory parameters (including coagulation tests and markers of organ dysfunction), and response to treatment.
  • 25. NURSING MANAGEMENT OF DIC  Risk for Bleeding Related to Coagulopathy and Decreased Platelet Count.  Risk for Impaired Gas Exchange Related to Pulmonary Complications.  Risk for Infection Related to Invasive Procedures and Immunocompromised State.  Risk for Altered Fluid Volume Related to Blood Loss and Third Spacing.  Impaired Skin Integrity Related to Prolonged Bed Rest and Potential Bleeding.  NURSING DIAGNOSIS