Mrs. Mahdia Samaha Alkony

The bleeding vessel constricts Platelets aggregate at the site, forming an

unstable hemostatic plug. Coagulation factors are activated on the

surface of these aggregated platelets, forming fibrin, which anchors the platelet plug to the site of injury.

The failure of normal hemostatic mechanisms can result in bleeding.

Causes of bleeding : Trauma It can occur spontaneously. Vascular abnormalities Some patients have defects in more than one

hemostatic mechanism.

The site of spontaneous bleeding can be anywhere in the body.

The bone marrow may be stimulated to increase platelet production (thrombopoiesis).

Sometimes,the increase in platelets does not result from increased production but from a loss in platelet pooling within the spleen.

The spleen holds about one third of the circulating platelets at any time. If the spleen is lost (eg, splenectomy), the platelet reservoir is also lost, and an abnormally high amount of platelets enter the

circulation.

Local bleeding, usually into the skin. If platelet defects develop:o Petechiae, often in clusters on the skin and

mucous membranes. o Bleeding can be severe. If bleeding is not severe it can be

stopped when local pressure is applied

Coagulation factor defects bleeding occurs deeper within the body:

1. subcutaneous or intramuscular hematomas

2. hemorrhage into joint spaces).

If bleeding is significant; transfusions of blood products.

If fibrinolysis is excessive; hemostatic agents such as aminocaproic acid (Amicar) can be used.

Observe the pt. carefully for bleeding. The pt. needs to understand the importanceof avoiding activities that increase the risk of

bleeding. The skin is observed for petechiae and ecchymoses(bruises) and the nose and gums for bleeding

Hospitalized patients may be monitored for bleeding by testing (feces, urine, emesis, and gastric drainage) for occult as well as obvious blood.

Thrombocytopenia (low platelet level) can result from various factors:

1. decreased production of platelets within the bone marrow

2. increased destruction of platelets3. increased consumption of platelets.

Hematologic malignancy, especially acute leukemias Myelodysplastic syndromes (MDS): metastatic

involvement of bone marrow from solid tumors Aplastic anemia Megaloblastic anemia Toxins Medications Infection (esp. septicemia, viral infection, tuberculosis) Alcohol Chemotherapy

Treat leukemia; platelet transfusion Treat MDS; platelet transfusion Treat solid tumor Treat underlying condition Treat underlying anemia Remove toxin Stop medication Treat infection Refrain from alcohol consumption

Due to Antibodies Idiopathic thrombocytopenic purpura Lupus erythematosus Malignant lymphoma Chronic lymphocytic leukemia (CLL) Medications Due to Infection; Bacteremia, Postviral infection Sequestration of platelets in an enlarged spleen

Disseminated intravascular coagulation (DIC

Bleeding and petechiae with platelet counts less than 50,000/mm3

When the platelet count drops below20,000/mm3:1. petechiae 2. nose and gingival bleeding3. excessive menstrual bleeding4. excessive bleeding after surgery or dental extractions. When the platelet count is less than 5000/mm3, spontaneous,

potentially fatal central nervous system or gastrointestinal hemorrhage can occur.

Bone marrow aspiration and biopsy Enlarged spleen results in increased

sequestration of platelets.

Treatment of the underlying disease. If platelet production is impaired, platelet

transfusions Splenectomy

ITP affects people of all ages more common among children and young women.

There are two forms of ITP: 1. The acute form occurs in children, often appears 1

to 6 weeks after a viral illness.This form is self-limited; remission often occurs spontaneously within 6 months. Occasionally, corticosteroids are needed for a brief time.

2. Chronic ITP is often diagnosed by exclusion of other

causes of thrombocytopenia.

Unknown cause, viral infections precede ITP in children. medications such as sulfa drugs can induce ITP. Systemic lupus erythematosus (SLE) Pregnancy. Anti-platelet autoantibodies that bind to the

patient’s platelets are found in the blood of patients with ITP.

When the platelets are bound by the antibodies, the RES or tissue macrophage system ingests the platelets, destroying them.

The body attempts to compensate for this destruction by increasing platelet production

within the marrow.

Many patients have no symptoms low platelet count (often less than 20,000/mm3. easy bruising, heavy menses, and petechiae on

the extremities or trunk. Dry purpura:simple bruising or petechiae Wet purpura: gastrointestinal tract bleeding

(including the mouth) and pulmonary system (eg, hemoptysis), which is termed .

Patients with wet purpura have a greater risk for intracranial bleeding than do those with dry purpura.

Patients whose counts exceed 30,000 to 50,000/mm3 may be carefully observed without additional intervention.

If the count is lower than 20,000/mm3, or if bleeding occurs, the goal is to improve the patient’s platelet count, rather than to cure the disease.

If the patient is taking a medication that is known to cause ITP, medication must be stopped immediately.

immunosuppressive agents block the binding receptors on macrophages so that the platelets are not destroyed.

Corticosteroid therapy Intravenous gamma globulin (IVIG) is also

commonly used to treat ITP Splenectomy is an alternative treatment Chemotherapy agent anti-D in patients who are Rh(D)-positive. platelet transfusions are usually avoided

Determine the risk of bleeding from activity. Detailed history Avoid intramuscular injections or rectal

medications and rectal temperature measurements

Observe the pt. for S.E. of corticosteroid including osteoporosis, proximal muscle wasting, cataract formation, and dental caries

should avoid constipation avoid Valsalva maneuver avoid flossing of the teeth. Electric razors should be used for shaving soft-bristled toothbrushes should replace stiff-

bristled ones. Patients should also be counseled to refrain from

vigorous sexual intercourse when the platelet count is less than 10,000/mm3

Most blood coagulation factors are synthesized in the liver. Therefore, hepatic dysfunction can result in diminished amounts of the factors needed to maintain coagulation and hemostasis.

Prolongation of the PT Minor bleeding is common (eg, ecchymoses), Risk for significant bleeding, related especially to

trauma or surgery.

Transfusion of fresh frozen plasma may be required

Patients may also have life-threatening hemorrhage from peptic ulcers or esophageal varices.

In these cases, replacement with fresh frozen plasma, PRBCs, and platelets is usually required.

The synthesis of many coagulation factors depends on vitamin K.

Causes: malnourishement some antibiotics decrease the intestinal flora that

produce vitamin KTreatment: Administration of vitamin K either orally or as a

subcutaneous injection) adequate synthesis of coagulation factors is reflected

by normalization of the PT.-

These agents, particularly warfarin or heparin, can result in bleeding.

If the PT or PTT is longer than desired and bleeding has not occurred, the medication can be stopped or the dose decreased.

Vitamin K is administered for warfarin toxicity. Protamine sulfate is rarely needed for heparin

toxicity, because the half-life of heparin is very short. With significant bleeding, fresh frozen plasma replaces the vitamin K–dependent coagulation factors.

DIC is not a disease but a sign of an underlying condition.

DIC may be triggered by sepsis, trauma, cancer, shock, abruptio placentae, toxins, or allergic reactions

It is potentially life-threatening.

In DIC, the normal hemostatic mechanisms are altered so that a massive amount of tiny clots forms in the microcirculation.

Initially, the coagulation time is normal. as the platelets and clotting factors are consumed to form

the microthrombi, coagulation fails. the result of excessive clotting is bleeding. The clinical manifestations of DIC are reflected in the

organs, which are affected either by excessive clot formation (with

resultant ischemia to all or part of the organ) or by bleeding. The bleeding is characterized by low platelet and fibrinogen levels; prolonged PT, PTT, and thrombin time; and elevated fibrin degradation products (D-dimers)

The mortality rate can exceed 80% Identification of patients who are at risk for DIC and recognition of the early clinical manifestations of this syndrome can

result in earlier medical intervention, which may improve the prognosis.

Treating the underlying cause of the DIC. Correct the secondary effects of tissue

ischemia by:1. improving oxygenation2. replacing fluids3. Correcting electrolyte imbalances4. Administering vasopressor medications.

Transfusion of blood and blood products: 1. Cryoprecipitate is given to replace

fibrinogen and factors V and VII2. fresh frozen plasma is administered to

replace other coagulation factors

Heparin may inhibit the formation of microthrombi and thus permit perfusion of the organs (skin, kidneys, or brain) to resume.

Heparin is typically reserved for the patient in whom thrombotic manifestations predominate or in whom extensive blood component replacement fails to halt the hemorrhage or increase fibrinogen and other clotting levels.

When heparin is administered, bleeding may actually worsen initially until the thrombotic process is interrupted.

The effectiveness of heparin can best be determined by observing for normalization of the plasma fibrinogen concentration and diminishing signs of bleeding.