DISSEMINATED

INTRAVASCULAR
COAGULATION

SCHWARTZ, GENNELY D.
BSN II
NU401-C
Disseminated Intravascular Coagulation
- also known consumptive coagulopathy and defibrination syndrome.
- is a pathological activation of coagulation ( blood clotting ) mechanisms
that happens in response to variety of diseases.
- DIC leads to the formation of small blood clots inside the blood vessels
throughout the body. As the small clots, consume coagulation proteins
and platelets, normal coagulation is disrupted and abnormal bleeding
occurs from the skin ( e.g. from the sites where the blood samples were
taken ), the gastrointestinal tract, the respiratory tract and surgical
wounds. The small clots also disrupt normal blood flow to organs ( such as
the kidneys ), which may malfunction as a result.
- DIC can occur acutely but also on a slower, chronic basis, depending on
the underlying problem. It is common in he critically ill, and may
participate in the development of multiple organ failure, which may lead
to death.

Acute DIC verus Chronic DIC

DIC exists in both acute and chronic forms.
DIC develops acutely when sudden exposure of blood to procoagulants occur,
including tissue factor ( tissue thromblastin) generating intravascular coagulation.
Abnormalities of blood coagulation parameters are readily identified, and organ
failure frequently occurs in Acute DIC.
Chronic DIC reflects a compensated state that develops when blood
is continuously or intermittetntly exposed to small amounts of tissue factor,
Chronic DIC is more frequently observed in solid tumors and in large aortic
aneurysms.

CAUSES:
Acute DIC
- Infections
 Bacterial ( gram-negative, sepsis, gram-positive, infections,
ricketssial)
 Viral ( HIV, cytomegalovirus (CMV), varicella, hepatitis)
 Fungal ( Histoplasma )
 Parasitic ( malaria )
- Malignancy
 Hematologic ( acute melocytic leukemias )
 Metastic ( mucin-secreting adenocarcinomas )
- Obstetrics
 Placenta Abruption
 Amniotic fluid embolism
 Acute fatty liver pregnancy
  Eclampsia
- Trauma
- Burns
- Motor vehicle accidents
- Snake bites
- Transfusion
- Hemolytic reactions
- Massive transfusion
- Liver disease – Acute hepatic failure
- Prosthetic devices
- Shunts
- Ventricular assist devices
Chronic DIC
- Malignancies
 Solid tumors
 Leukemia
- Obstetric
 Retained dead fetus syndrome
 Retained products of conception
- Hematologic
 Myeloproliferative syndromes
 Paroxysmal nocturnal hemoglobinuria
- Vascular
 Rheumatoid arthritis
 Raynaud disease
- Cardiovascular
 Myocardial infarction
- Inflammatory
 Ulcerative colitis
 Crohn’s disease
 Sarcoidosis
- Localized DIC
 Aortic aneurysms
 Giant hemangiomas ( Rasabach – Merritt syndrome )
 Acute renal allograft rejection
 Hemolytic uremic syndrome

SIGNS and SYMPTOMS

The affected person is often acutely ill and shocked with widespread
hemorrhage ( common bleeding sites are mouth, nose, and venipuncture sites ),
extensive bruising, renal failure, gangrene. Bleeding from surgical or invasive
procedure sites and bleeding gums, cutaneous oozing, petechiae, ecchymoses,
 blood vessel clotting and hematomas. May experience nausea and vomiting;
severe muscle, back and abdominal pain; chest pain; hemoptysis; epistaxis;
seizures; and oliguria. Peripheral pulses and blood pressure may decreased; may
demonstrate confusion or other changes in mental status.

Laboratory Diagnostic Procedures

 Platelet count
A stable platelet count suggests that thrombin formation has stopped
 FDPs ( Fibrin degradation products ) and D-dimers
Which may be measured as FDP by ELISA ( enzyme – linked
immunosorbent assay )
 PT and aPTT
 Fibrinogen
Acts as an acute phase reactant and despite ongoing consumption,
plasma levels can remain within the normal range for a long period of
time
Procedures
- Base procedures on the underlying pathologic processs as well as an areas
suggestive of thrombosis and hemorrhage
- Conduct invasive procedures with care because of bleeding complications.
Procedures should follow the administration of clotting factor and
platelet repletion.

NURSING MANAGEMENT
- It is important to take a thorough history, especially in relation to
previous bleeding disorders and any medications that include bleeding.
- The patient should be turned q2h to prevent pressure ulcers and to
minimize blood strasis and pooling, as this may precipitate clotting and
thrombsis formation.
- Skin should be thoroughly assessed at least two-hourly for pressure
areas and any signs of bleeding, such as petechiae.
- Prssure relieving mattresses the amount of manual handling required and
the risk of skin trauma.
- Skin should be kept clean and moisturized, as dry skin is more damaged.
Reduced the risk of skin damage, sticky tapes should be avoided, and
electric rather that blade razors should be used.
- Temperature should be monitored and recorded at least four-hourly
- Areas at risk can be washed gently with hydrogen peroxide and water to
remove the crusted blood.
- Pressure, cold compress, and topical hemostatic agents are applied to
control bleeding.
MEDICAL MANAGEMENT
1. Remove the trigger or treat the underlying cause.
2. Maintain organ perfusion.
3. Restore the balance of homeostasis.
4. Provide supportive management of complications.

MEDICATION
Therapy should be appropriate aggressive for the patient’s age,
disease, severity and location of hemorrhage/thrombosis.
Anticoagulant agents
Used in the treatment of clinically evident intravascular thrombosis
when the patient continues to bleed after initiation of primary anf
supportive therapy.
 Heparin
- used to prevent or treat clots in the veins, arteries, lungs or heart.
 Antithrombin III
- used for moderately severe –to- severe DIC or when level are
depressed markedly
Blood Components
Are used to correct hemostatic parameters
 Packed red blood cells ( PRBCs ; washed )
 Platelets
Considered safe for Acute DIC
 Fresh frozen plasma ( FFP )
- This treatment entails removing blood from body
 Cryoprecipitate or Fibrinogen concentrates
Antifibrinolytic Agents
These agents after all other therapeutic modalities have been tried
and deemed unsuccessful
 Aminocaproic Acid (Amicar)
- Inhibits fibrinolysis via inhibition of plasminogen activator
substances and, to a lesser degree, through antiplasmin activity
 Tranexamic acid cyklokapron
- Used as alternative to aminocaproic acid
- Inhibits fibrinolysis by displacing plasminogen from fibrin.
 Pre-eclampsia
- Pregnancy- induced hypertension, the phase before the pregnant woman
experiences a seizure.
- Charaterized by increasing hypertensive, proteinuria and edema
- The condition may progress rapidly from mild to severe and if untreated,
to eclampsia.
- Leading cause of fetal and maternal morbidity and death.

The cause is unknown; however the incidence is higher among adolescents, in first
pregnancies, in women who smoke, and in women who are diabetic or overweigh. The
disease mechanisms found in pre-eclampsia include generalized vasopasm, damage to
the glomerular membranes, and hypovolemia and hemoconcentration due to a fluid
shift from intravascular to interstitials compartments.

SIGN and SYMPTOMS

- sudden weight gain
- severe headaches
- visual disturbances
- complaints of epigastric or abdominal pain
- generalized, presacral, and facial edema
- oliguria
- mypereflexia

Pre-eclampsia Laboratory Tests

- 24hour urine for protein and creatine clearance
- AST
- Fibrinogen
- LDH
- BUN
- Bilirubin
- Platelet Count
- PT
- PTT
- Uric Acid
- CBC

NURSING MANAGEMENT
- Monitor vital signs and FHR
- Measure and record urine output, protein level, and specific gravity
- Assess deep tendon reflexes q4h.
- Asses for placental separation, headache and visual disturbances
epigastric pain, and altered level of consciousness
- Eclampsia treatment consists of administration of magnesium sulfate
intravenously

MEDICAL MANAGEMENT
- Provide treatment as prescribed.
- Institute seizure precaution. Seizures may occur up to 72 hours after
delivery
- Monitor for and promote the resolution of, complications

MEDICATION
- Antihypertensive therapy ( Labetolol or Nicardipine )
- Cortocosteroids
- Anticonvulsive medications