Disseminated Intravascular Coagualation

8/12/2019 Disseminated Intravascular Coagualation

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SUBMITTED TO

MRS. MEENAL SHARMA

ASSISTANT PROFESSOR

PRESENTED BY

MS.NISHA KAUSHIK

MSC NURSING Ist YEAR


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DIC is not a kind of independent disease, but a middle process or

complication of some diseases.

It is essentially an imbalance between the coagulation process and

anticoagulation process.

It is a syndrome characterized by massive activation and consumption

of coagulation proteins, fibrinolytic proteins and platelets.


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Coagulation is usually confined to a localized area by the combination

of blood flow and circulating inhibitors of coagulation ,especially

antithrombin III.

If the stimulus to coagulation is too great ,these control mechanisms

can be overwhelmed , leading to the syndrome of DIC .


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Disseminated intravascular coagulation also known as disseminated

intravascular coagulopathy or less commonly known as consumptive

coagulopathy , is a pathological activation of coagulation (blood

clotting) mechanisms that happens in response to a variety of diseases.


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ACUTE DIC

It happened rapidly .The coagulopathy is dominant

and major symptoms are bleeding and shock, mainly seen in severe

infection ,amniotic fluid embolism.

CHRONIC DIC- It happened slowly and last several weeks

,thrombosis and clotting may predominate mainly seen in cancer.


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DIC is not a primary disease, but a disorder secondary to numerous

triggering events such as serious illnesses.

Infectious disease 31%-43%

Cancer 24%-34%

Obstetric complications 4%-12%

Severe tissue injury 1%-5%

Systemic disease


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Bacterial , viral ,rickettsia ,parasitic diseases and so on).Bacterial

infection , in particular septicemia , is commonly associated with DIC.

However, systemic infectious with other microorganisms ,such as

viruses and parasites ,also may lead to DIC.


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Acute promyelocytic leukemia ,acute myelomonocytic or monocytic

leukemia, disseminated prostatic carcinoma ,lung,breast

,gastrointestinal malignancy.


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Amniotic fluid embolism, septic abortion ,retained fetus and so on.


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Burn, heart shock ,fracture and so on.

Head trauma in particular is strongly associated with DIC ;both local

and systemic activation of coagulation may be detected after such an

event.

The increased risk of DIC ,after head trauma is understandable in

view of the relatively large amount of tissue factor in the cerebral.


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Malignant hypertension, acute respiratory distress

syndrome(ARDS),hemolytic transfusion reaction.


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DIC occurs when monocytes and endothelial cells are activated or

injured by toxic substances elaborated in the course of certain diseases.

The response of monocytes and endothelial cells to injury is to

generate tissue factor on coagulation cascade.


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AN EXPLOSIVE GENERATION OF THROMBIN DEPLETESCLOTTING FACTORS AND PLATELETS

ACTIVATES FIBRINOLYTIC SYSTEM

BLEEDING INTO THE SUBCUTANEOUS TISSUES SKIN ANDMUCOUS MEMBRANES OCCURS ALONG WITH OCCLUSION OF

BLOOD VESSELS CAUSED BY FIBRIN IN THE MICROCIRCULATION


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LESS EXPLOSIVE GENERATION OF THROMBIN DEPLETES

CLOTTING FACTOR

TIME FOR COMPENSATORY RESPONSES &DIMINISH

BLEEDING

HYPERCOAGULABLE STATE


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INTRAVASCULAR

THROMBOSIS

HYPOPERFUSION TO

TISSUE S AND

ORGANS

ISCHEMIC

DAMAGEBLEEDING

INABILITY TO FORM A

STABLE CLOT

CONSUMPTIOTN OF

COAGULATION FACORS

SECONDARY

ACTIVATION OF

THROMBOLYSIS

RELEASE OF

ANTICOAGULANTS

BLEEDING

STIMULATION OF COAGULATION


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Bleeding

Thrombosis

Hypotension or shock

Organ dysfunction


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It may occur at any site , but spontaneous bleeding and oozing at

venipuncture sites or wounds are important clues to the diagnosis.


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It is commonly manifested by digital ischemia and gangrene , renal cortical

necrosis and hemorrhagic adrenal infarction may occur.


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CLINICAL FINDINGS

Multiple bleeding sites

Ecchymoses of skin , mucous membranes

Visceral hemorrhage

Ischemic tissue


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CLINICAL FINDINGS

Signs of deep venous or arterial thrombosis or embolism

Superficial venous thrombosis, especially without varicose veins

Multiple thrombotic sites at the same time

Serial thrombotic episodes


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Platelet count

Prothrombin time(PT)

Activated partial thromboplastin

time (APTT)

Fibrin degradation products (FDP)

Fibrinogen

Antithrombin III(AT III)Protein C

Markedly decreased

Increased

Increased

Markedly increased

Normal or decreasedMarkedly decreased

Markedly decreased


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Liver diseases

Vitamin K deficiency

Sepsis

TTP(Thrombotic thrombocytopenic purpura)


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Liver disease may prolong both the PT and PTT, but fibrinogen levels

are usually normal, and the platelet count is usually normal or only

slightly reduced.

Severe liver disease may be difficult to distinguish from DIC.


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Vitamin K deficiency will not affect the fibrinogen level or platelet

count and will be completely corrected by vitamin K replacement.


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Sepsis may produce thrombocytopenia and coagulopathy may be

present because of vitamin K deficiency .However in these cases , the

fibrinogen level should be normal.


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TTP may produce fever and MAHA(Microangiopathic hemolytic

anemia).However , fibrinogen levels and other coagulation studies should

be normal.


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Treatment of the underlying disorder

Replacement therapy

Heparin therapy

Other treatment


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The primary focus should be the diagnosis and treatment of the

underlying disorder that has given rise to DIC.


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Coagulation factor deficiency require replacement with FFP(fresh

frozen plasma).

Platelet transfusion should be used to maintain a platelet count greater

than 30000/ul, and 50000/ul.


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Fibrinogen is replaced with cryoprecipitate.

One unit of cryoprecipitate usually raises the fibrinogen level by 6-8mg/dl

, so that 15 units of cryoprecipitate will raise the level from 50 to 150mg/dl.


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In some cases heparin therapy is contraindicated , but when DIC is

producing serious clinical consequences and the underlying cause is

not rapidly reversible, heparin may be necessary.

Dose : 500-750 u/h is necessary.


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Aminocaproic acid ,1 g/h iv

Tranexamic acid ,10 mg/kg, iv ,q8h,


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Those two drugs should be added to decrease the rate of fibrinolysis , raise the fibrinogen

level and control bleeding.

ATTENTION :Aminocaproic acid can never be used without heparin in DIC because of

the risk of thrombosis.


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Without bleeding or evidence of ischemia No treatment

With bleeding

Blood component as needed

Fresh frozen plasma

Cryoprecipitate

Platelet transfusions

With ischemia

Anticoagulants after bleeding risk is corrected with blood products.


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Without thromboembolism No specific therapy needed but prophylactic drugs (eg low dose heparin

, low molecular weight heparin) may be used for patients at high risk of

thrombosis.

With thromboembolism

Heparin or low-molecular weight heparin ,trial of warfarin sodium

(Coumadin).

If warfarin is unsuccessful, long term use of low molecular weight

heparin may be helpful.


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Severe bleeding

Stroke

Ischemia of extremities or organs


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ASSESSMENT

Decrease urine output

Increase bleeding

Oozing from wound Hematuria

Hematemesis

NURSING DIAGNOSIS

Risk for deficient fluid volume related to bleeding.

GOAL-Hemodynamic status maintained ;urine output >30ml/h

NURSING INTERVENTIONS


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Avoid procedures that can increases intracranial pressure(eg-coughing, straining

to have a bowel movement)

Monitor vital signs closely ,including neurologic checks;

a) Monitor hemodynamics

b) Monitor abdominal girth

c) Monitor urine output

Avoid rectal probes ,rectal medications.

Avoid IM injections.

Monitor amount of external bleeding carefully:

a) Assess suction output.

b) Monitor pad counts in women with vaginal bleeding.

c) Females may receive progesterone to prevent menses.

Use low pressure with any suctioning needed.

ASSESSMENT


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Decrease sensation

Cyanosis in extremities , nose ,earlobes ;focal ischemia ,superficial gangrene.

NURSING DIAGNOSIS

Risk for impaired skin integrity related to ischemia or bleeding.

GOALS-Skin integrity remains intact ;oral mucosa remains intact.


Assess skin with particular attention to bony prominences ,skin folds.

Reposition carefully ;use pressure reducing mattress.

Perform careful skin care every 2 hours ,emphasizing dependent areas ,all bony

prominences, perineum.

Use prolonged pressure after injection or procedure when such measures must be


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performed

(at least 5 minutes).

Perform oral hygiene carefully.

ASSESSMENT

Distended abdomen

Increased abdominal girth

NURSING DIAGNOSIS

Risk for imbalanced fluid volume related to excessive blood or factor componentreplacement.

GOALS-Absence of edema ;absence of rales ;intake not greater than output.


Auscultate breath sounds every 2-4 hour. Monitor extent of edema.

Monitor volume of IVs, blood products ;decreased volume of IV medications if

indicated.

ASSESSMENT


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Hypoxia

Decrease breath sounds

NURSING DIAGNOSIS

Ineffective tissue perfusion related to micro thrombi.

GOALS-Neurologic status remains intact ;absence of hypoxemia ;peripheral

pulses remain intact ;skin integrity remains intact ;urine output >30 ml/h


Assess neurologic ,pulmonary ,integumentary systems.

Monitor response to heparin therapy.

Assess extent of bleeding. Monitor fibrinogen levels.

ASSESSMENT


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Restlessness

Anxiety

NURSING DIAGNOSIS

Anxiety related to uncertainty or possible death.

GOALS-Fears verbalized ;realistic hope maintained.

NURSING INTERVENTION

Identify previous coping mechanism, if possible ;encourage patient to use them

as appropriate.

Explain all procedures and rationale for these in terms patient and family can

understand.

Assist family in supporting patient.

Use services from behavioral medicine ,chaplain as needed.


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Disseminated Intravascular Coagualation

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