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Plenary 3 - Gangguan Hemostasis dan Trombosis

Plenary 3 - Gangguan Hemostasis dan Trombosis

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Published by Nadiah Ismail
Gangguan hemostasis dan trombosis
Gangguan hemostasis dan trombosis

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Published by: Nadiah Ismail on Feb 27, 2013
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Esha Almara Rurin Ardiyanti Nadiah Ismail Anelia Tiara Suci Cindy Aulia Dani Putra Amerta Esha Almara Putri Maghfirah Bahri Rizky Dwi Utami Satrya Aji Pamungkas

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Mufi, boy aged 10 years, was brought to the clinic because of his bleeding not being stopped after circumcision done by the head nurse in the village. From anamnesis Mufi often have swelling in the knee since childhood. On examination, seen blood seeps in kassa that covering the wound Circumcision. The results of laboratory tests of blood routine normal, checking filter hemostasis obtained 270.000/mm3 platelet count, bleeding time 1'30'', clotting time 15 '. Mufi immediately referred to hospital with suspected hemorhagik diathesis. In M.Djamil Mufi undergo further examination and obtained hematologic within normal limits, PT 11’’ and APTT 60’’. Mufi then planned for factor assay examination, while for initial management done cryoprecipitat transfusion. In the hospital, Mufi met a mother 60-year-old with right leg swelling and pain. according to the mother, she had blockage of blood vessels in the legs.

How do you explain what happened to Mufi and mother as well as the

The function of this inspection was to assess the clotting factor 4. Clothing time Time used the blood to clot. Cryopresipitat Deposition of substances in solution after cooling as factors in blood plasma hemofilik 1. . Bleeding time Tests to measure the time required for the cessation of blood flow. The purpose of this inspection is to evaluate the function of blood vessels and hemostasis systems 3.hemorrhagic diathesis Bleeding tendency in the hemostasis system 2. dimuali of blood discharge from the network.

APTT (activated partial thromboplastin time) Examination of coagulation factors to assess the intrinsic coagulation time on track 7. and performed an elongated PT or APTT . PT (protombin time) Protombin conversion speed to thrombin in a given area and additional calcium citrate. factor assay Examination to test the activity of clotting factors.5. Its function is to assess the extrinsic coagulation pathway and common pathway 6.

2.Why mufi’s bleeding didn’t stop? Why mufi often swollen knees as a child? How did the clinical interpretation of laboratory tests? 4. What is the interpretation of further investigation? 7. What is the basis of a doctor's diagnosis of hemorrhagic diathesis disease? 6. Why do cryoprecipitate administration before making any factor screening assay? 1. Is there any effect of age and sex mufi against illness? 5. 3. Why mufi are advised to check the assay factor? 8. .

11. 12. 15. except cryopresipitat? Why swelling only occurs on the right leg? . 16. 10. 14.9. How is the relationship with a swollen knee mufi bleeding after circumcision? What causes blood vessel blockage mother? Is there a connection between swelling and pain experienced by the mother? Is the same mufi experienced swelling with mothers who met? Is the age of the mother is a trigger swelling and pain they experienced? What should be given to treatment of the mother and mufi? Is there a procedure of beginning. 13.

Analysis problem 1. .CT 15 minutes  when using the tube is still considered normal (9-15 minutes).Damage caused by bleeding synovial joints each friction .clotting factor disease hemophilia .Platelets  unable to aggregate . The cause of the bleeding does not stop: There might be abnormalities in hemostasis system .000mm3) . but an object is said elongated glass 2. so it is not resistant to a twisting motion  absolute blood vessel damage Interpretation of clinical laboratory tests: .Blood vessels  brittle Mufi frequent cause of knee swelling: .Platelets 270.5 minutes (1-6 minutes) . 3.The knee is a hinge joint.400.000 .BT 1.000/mm3  normal (150.

.The blood that do not stop after circumcision .. Primary diagnosis of hemorrhagic diathesis: . Interpretation of further investigation: There may be a disorder intrinsic pathway .APTT 60 seconds elongated (20-40 seconds) 6.Analysis problem 4. Effect of age of 10 years old: If mufi mufi including hemophilia  mild hemophilia.PT 11 seconds  normal (11-15 seconds) .. because the onset> 2 years Influence of sex: If mufi hemophilia  men more often show clinical manifestations 5.Based on laboratory tests with CT elongated .

APTT increased..the cause is unknown..circumcisionBoth of these symptoms are signs of hemostasis disorders . Basic checks assay factors: .That do not stop bleeding .To determine what factors deficiency . Causes of cryoprecipitate given first: 9. hipofibrinogenemia. and other coagulation factor deficiencies.Cryoprecipitate an initial relief in patients hemorrhagic diathesis 8.If mufi hemophilia. So.. to determine the type of hemophilia . cryoprecipitate also treat diseases hemoagik diathesis such as von Willebrand disease. .There are factor VIII.Analysis problem 7. Relationships with bleeding knee swelling post: . when mufi disease hemophilia A .

Hypertension  turbulence  platelet vascular endothelial contact with ill . Meanwhile prostalgladin able to stimulate nerve pain 12. because: .Hiperfungsi platelets . Swollen and painful relationship: Vascular endothelium is able to issue protalgladin capable of destroying thrombus..Old age is susceptible to autoimmune arthritis can cause reumathoid . mufi and mother equally impaired hemostasis system 13. Yes.Old age are particularly vulnerable occurrence of thrombosis .Immobilization  static blood flow  blockages 11. the incidence of thrombosis by 62% .High cholesterol  thrombosis  allow clog blood vascular . Yes. Causes of deep vein thrombosis: ...At the age of 46-72 years old.Analysis problem 10.

. Causes swelling of the legs just right: Effect of activity  right leg more often a pedestal ..Analysis problem 14. Then do the proper management of .Give anticoagulation 15. Treatment of disease mufi: ..Causal therapy .Advise malakukan routine examination of clotting factors .Provide education about trauma . Another early Procedures: Give oral desmopressin  factor VII 16.Determine a definite diagnosis first.Conducting joint care .Do not give aspirin Management of maternal disease: .


Diathesis Hemorragic 2. Trombosis .Students are able to explain:             Definition Etiology Classification Risk factors Epidemiology Pathogenesis Clinical symptoms Laboratory abnormalities Basic diagnostics Therapy Complication Referral cases Of: 1.


Coagulation.Fibrinolisis If this system:  Balanced  Lacking  Overload Normal hemostasis Bleeding (dithesis hemorragic) thrombosis .  Maintain the blood solution & cover endotel from damage.Trombosit. Consist of : Vaskular.



 Vascular disorders  Acquired : Purpura  Herediter : Talangiectasia herediter hemorragic  Trombosit disorders  Trombopati  Trombositopenia : PTI  Coagulation factor disorders  Acquired : Vit. vWD .K deficiency. DIC  Herediter : Hemofilia.

vWD .K deficiency. DIC  Herediter : Hemofilia. Vascular disorders  Acquired : Purpura  Herediter : Talangiectasia herediter hemorragic  Trombosit disorders  Trombopati  Trombositopenia : PTI  Coagulation factor disorders  Acquired : Vit.


recurrent.autoimun Often in women 15-50 years old. after an thrombocytopeni acute viral infection / vaccine.Definition : Klasifikasi : Abnormalities  PIT acute due to Often in children. hematologi-onkologi anak . Chronic. 5-10% become chronic Etiology :  PIT kronic idiophatic .hematologi klinik ringkas. Rarely cured spotan. Sumber:ipd. a Most of the recovered spontaneously.

epistaxis.CNS bleeding rarely. echymosis. easy bruising.Onset slowly by bleeding through the skin / mucosal form: petechie. if occurred fatal . mwnorrhagia. . or bleeding gums.Patogenesis : Trombosit-Ab (IgG) antibody coated platelets difagosit makrofag dlm RES trtma lien trombositopenia kompensasi SST megakariosit utk mmbntk trombosit. Clinical Manifestation: .Splenomegaly <10% .

thrombocytopenia 3. Diagnose: ITP enforced if 1. Immunology: The anti-platelet IgG on the surface of platelets / within serum (gpIIb / IIIA or GPIB).Lab abnormalities: 1. skin or mucosal bleeding 2. Antiplatelet antibodies (IgG) positive 5. peripheral blood: Trombosit 10-50rb/mm³ 2. SST : megakariosit 3. No cause of secondary thrombocytopenia . SST: normal or increased megakaryocytes 4.

. High dose Ig to suppress the function of macrophages c. Within 3 months not responding: .Splenoktomi-most brespon good .Suppression of macrophage activity that decreases platelet destruction . Androgens (danazol) b. Corticosteroids (prednisone 60-80 mg / day and lower dose slowly about 15 mg / hr) .Therapy to reduce the immune a. azathioprim) 2.Other immunosuppressant drugs (vincristine. Supportive therapy to reduce the influence of thrombocytopenia a.<< Binding of IgG and suppress antibody synthesis b. Platelet concentrates transfusion if the patient is at risk of bleeding 1.

In children sometimes happen complete remission without treatment.  .  Worse prognosis in pregnant women and if there are complications.Complication  Hemorrhages  Impairment of consciousness  Splenomegaly Referral : (2) Prognosis:  In generally good. ± 90% of patients with ITP in remission after receiving treatment for 3 weeks. 3 months and no more symptoms arise.  10% become chronic ITP and <1% died.  In adults often relapse within 4-15 years. especially bleeding of the brain that can lead to death.

vWD .K deficiency. DIC  Herediter : Hemofilia. Vascular disorders  Acquired : Purpura  Herediter : Talangiectasia herediter hemorragic  Trombosit disorders  Trombopati  Trombositopenia : PTI  Coagulation factor disorders  Acquired : Vit.


Etiology : A . Mild hemophilia: 5-30% clotting factor Sumber:ipd.Deficiency of factor IX • Hereditary or spontaneous mutations in> 30% of cases. Classification: 1. blood coagulation function difficult to clot.factor VIII deficiency B . Severe hemophilia: clotting factor <1% 2.HEMOFILIA A & B Definition : Hereditary disorders. hematologi-onkologi anak .hematologi klinik ringkas. Moderate hemophilia: 1-5% clotting factor 3.

000 population / year Hemophilia A 85% Hemophilia B is 15% Manifest in men.Epidemiology: • • • • • • The most frequently encountered The incidence of 1-2 per 10. in women carrier Hereditary (X-linked recessive / Xh) or spontaneous mutation> 30% of cases .

oral mucosal bleeding. intracranial (peny.IX Clinical Manifestation: . Bleeding muscles (especially the flexor muscles such as the calf muscles. hematoma.VIII Jal. • Hemofilia B – def. F.kematian).VIII clotting activity krn penurunan sintesis atau pembentukan F. epistaxis and hematuria. tooth extraction. especially bleeding joints (haemarthros) at the hinge joint. or injury posttrauma .Frequent spontaneous bleeding. . Intrinsik terganggu pmbentukan fibrin berkurang.Patogenesis : • Hemofilia A – def F.Bleeding from childhood: when circum.VIIIC dg struktur abnormal Def F. hip and forearm). Haemarthros repetitive joint damage (anklylose) and impaired walking.

IX . TT normal 2. Confirmatory tests .If F. Hemostasis Filter test -Elongated APTT (normal in mild hemofili) -BT. PT.VIII & F.VIII << proceed with the examination of vWF 3. Examination of karrier women .VIIIC also decreased (50%) .F.Lab abnormalities: 1.Quantitative measurements F.

sendi.IX Tes Ristosetin Sex linked Otot.DD/: Hemofilia A Inhiritance Tempat perdarahan BT PT APTT F. posttrauma/operasi Memanjang N Memanjang N Rendah N (-) . posttrauma N N Memanjang N N Rendah N vWD Autosomal dominan Mukosa. posttrauma N N Memanjang Rendah N N N Hemofilia B Sex linked Otot.VIIIR:AG (vWF) F. luka kulit.VIIIC F. sendi.

Curative therapy:
1. Providing F.VIII – Hemofilia A & F.IX – hemofilia B lifetime -Cryoprecipitate (F.VIII, vWF, fibrinogen, F.XIII) -Lyophilized F.VIII - Lyophilized F.IX-prothrombin complex concentrate (vit.K – dependant factor) Gen therapy(?) Mild hemophilia : DDAVP. Overcome acute hemorrhage with Rest,Ice,Compressio,Elevation

3. 4. 5.

Preventive therapy:
Health education to prevent disability -Keep your ideal body weight. Obesity is a higher risk of joint bleeding -Avoid injuries and impact -Maintenance teeth and gums - Vitamin K -Avoid giving aspirin, salicylic acids, AINS, heparin

Rehabilitative therapy:

Artritis hemophilia – exercise passive / active, hot and cold therapy, the use of orthosis, psychosocial therapy, recreational therapy and education

Complication :
-Progressive arthropathy -Hepatitis (transfusion) -Allergic reactions – due to transfusion of blood products -Antibody formed as an antagonist to f.VIII & IX -Hemolytic anemia -AIDS (HIV) due to exposure to contaminated blood products..

Referral: (2)

Prognosis: Indeed, there is no word 'cured' for hemophilia. Without treatment most children died of severe hemophilia, but with the right treatment to ensure children grow up normal and productive adulthood. Availability of fresh blood facilities, kropresipitat and F VIII causes hemophilia a good prognosis.

DIC  Herediter : Hemofilia. vWD .K deficiency. Vascular disorders  Acquired : Purpura  Herediter : Talangiectasia herediter hemorragic  Trombosit disorders  Trombopati  Trombositopenia : PTI  Coagulation factor disorders  Acquired : Vit.


• Tipe 3 – vWF synthesis nonexistent .Decrease in activity within the plasma F.Impaired platelet adhesion .VON WILLEBRAND DISEASE Definition : Reduced synthesis of vWF resulting in: .VIIIC Classification : • Tipe 1 – decreased synthesis of vWF • Tipe 2 A .Impaired synthesis of large & moderate vWF multimers B – formation of large vWF multimers abnormal so quickly removed from the blood.

in the INDO not many. there are subtypes 2A. the most severe / serious clinical manifestations. and 2M) • Type 3.Epidemiology : • Type 1. the most common of about 70-80%. 2B. • Inherited autosomal dominant . • Are common in the West. 2N. • Type 2.

<< vwF vWF reduced activity of factor VIII vWF carrying factor VIII.Patogenesys : << vWF vWF can not act as adhesive to hold the platelets in the blood vessels around the area were damaged. Factor VIII is needed to form a strong network. tooth extraction or postoperative. Clinical Manifestation: • Abnormal bleeding (epistaxis. menorrhagia. major bleeding. hematoma. bleeding rarely joints • Easy bruising . Platelets can not coated blood vessel walls. bleeding from cuts. In the absence of factor VIII in the normal amount of the blood clotting process will take longer.

Imunoelektroforesis : big multimers (-) in tipe IIa big multimers (-) moderatemultimers in type IIb DD/ : Should be distinguished from hemophilia. BT ectends 2.Lab abnormalities: 1. except type IIb 4. APT slightly 3. Ristocetin induced platelet aggregation test (-). in vWD: • BT extends • Ristocetin test (-) • VWF levels decreased . Elektroforesis : vWF decrease in type I or 0 in type III 5.

Cryoprecipitate 3.Therapy : 1. • Antibodies to vWF and F. Epsilon aminocaproic acid / asam traneksamat (inhibitor fibrinolitik) Komplikasi : • Anemia. • Deaths due to bleeding.VIII in type III patients Referral: 1 . Infus Desmopressin (DDAVP) 2.

DIC  Herediter : Hemofilia.K deficiency. vWD . Vascular disorders  Acquired : Purpura  Herediter : Talangiectasia herediter hemorragic  Trombosit disorders  Trombopati  Trombositopenia : PTI  Coagulation factor disorders  Acquired : Vit.


Long term Antibiotik Sumber:ipd. Less input 1. hematologi-onkologi anak . Disrupted absorption 2. Late VKDB Etiology : 1.hematologi klinik ringkas.K by antikoagulan. Classical VKDB 3. Inhibitory function of Vit. anti TBC 3.Vitamin K Deficiency Bleeding (VKDB) Definition : Tendency to bleed due to coagulation disorders because lacking of vitamin K Classification : 1. Early VKDB 2. antikonvulsan.

Epidemiology: • The incidence ranged from 1:200 to VKDB 1:400 births who did not receive of vitamin K prophylaxis. Through 2004 found 21 cases in RSCM Jakarta. especially in preterm infants) • impaired function of the liver (cholestasis) • lack of of vitamin K intake can occur in infants who are breastfed exclusively morbidly • Malabsorption syndrome and chronic diarrhea. 6 cases at the hospital Dr. Risk factors: • mother during pregnancy taking medications that interfere with of vitamin K metabolism • synthesis of of vitamin K by intestinal bacteria less (use of antibiotics. In Indonesia. Sardjito Yogyakarta and 8 cases in RSU Dr. . data on national VKDB yet available. Soetomo.

Patogenesys : • Vitamin K is necessary for the synthesis of procoagulant factors II. prothrombin complex is stored in an inactive form. IX and X (prothrombin complex) as well as the anticoagulant proteins C and S • In the liver. Vitamin K is required to activate it . VII.

• pale • mild hepatomegaly . Can be a hematoma at the site of trauma. Result is the emergence of further intracranial hemorrhage is a cause of mortality or morbidity were settled. ecchymoses or bleeding through needle puncture marks.Clinical Manifestation : • Bleeding. such as hematoma sefal. especially in the umbilicus. gastrointestinal tract. mucous membranes. circumcision and venous puncture. Bleeding is often a skin purpura.

TT normal Diagnose : Established if there is clinical suspicion. PPT elongated 2.Lab abnormalities: 1. perform laboratory tests. Prophylaxis: VitK 5mg/day peroral . APTT normal 3. Therapy: If there is major bleeding give 25mg subcutaneous VitK1. Also give transfusion of fresh plasma or fresh frozen plasma.

Complication : Intracranial hemorrhage in newborns Prognosa: If treated the prognosis is very good. Symptoms usually disappear after giving vit. Referral case: thoroughly handled(4) .K or later than 24 hours thereafter.

K deficiency. DIC  Herediter : Hemofilia. vWD . Vascular disorders  Acquired : Purpura  Herediter : Talangiectasia herediter hemorragic  Trombosit disorders  Trombopati  Trombositopenia : PTI  Coagulation factor disorders  Acquired : Vit.


hematologi klinik ringkas.KOAGULASI INTRVASKULAR DISEMINATA(DIC) Definisi : Clinical syndrome because deposition (deposition) systemic fibrin and in the same time there bleeding tendency. In the United States approximately 18. chronic and subacute • Epidemiology : DIC can occur in 30% 50% of patients with sepsis.000 cases occur DIC in 1994. In addition it is estimated DIC occurs 1% of all patients admitted to the hospital. Sumber:ipd. Can occur in acute. Characteristics: Uncontrolled activation of coagulation and fibrinolysis. hematologi-onkologi anak .

shock anafilatik.Etiology: • Infection (dengue hemorrhagic fever. lobectomy. acute leukemia). amniotic fluid embolism). severe liver damage / gigita . • Transfusion reactions. by pass cardiopulmonal. meningitis. sepsis. infection by some types of rickets). splenectomy). intrauterine fetal death. lung carcinoma. malaria. pneumonia. • After surgery (lung surgery. tropical. • Complications of pregnancy (solutio placenta. • Malignancies (prostate carcinoma. extensive tissue damage (burns / trauma). gastrectomy.

Patogenesis .

Decreased consciousness . hematemesis.Clinical symptoms: • Bleeding: skin(petechie and echymosis). renal failure b. mucosal (epistaxis. etc. Gangrene in peripheral c. Jaundice .the brain • Basic disease symptoms . easy bruising and bleeding organs • Hemorrhagic tissue necrosis and occlusion of multiple small blood vessels leading to multiorgan failure: a.).liver d. bleeding gums.

5. 3. 4. 8. 7. PT & TT elongated Fibrinogen plasma decrease FDP (fibrinogen degradation product) increase F. 6. Minimal criteria for DIC diagnosis are manifestations of bleeding. 2. thromboembolism or both accompanied tromboitopenia and burr cell picture in RBC or DD-dimer (+) .Lab Abnormalitis: 1.VIII & F.V decrease Pheripheral blood: anemia mikroangiopatik DD-dimer (+) Tes parakoagulasi (+) Diagnose: Diagnosis is based on clinical symptoms and laboratory results. Pheripheral blood & trombosit count : Trombositopenia APTT.

Giving heparin 200 U / kg iv every 4-6 hours.Therapy : 1. fresh frozen plasma. Supportive therapy with fresh blood. or platelet concentrate fibrinoge (When the fresh blood platelet counts remained low up to a week) 3. Basic disease therapy 2. after 24-48 hours after reaching normal values​. The increase in plasma fibrinogen levels evident in 6-8 hours. ​ .

Adrenal Insufficiency .More than 50% death Prognosis: Depending in etiology and treatment of the primary disease and coagulopathy. Rujukan : (2) for the treatment refer to a specialist . arrhythmias .Complication : (because multiorgan failure) .Impaired liver .Acute respiratory distress syndrome (ARDS) .Gastrointestinal mucosal ulceration: bleeding .Purpura fulminant .Decreased kidney function .CNS Disorders .Increased cardiac enzymes: ischemia.

 Vascular disorders  Acquired : Purpura  Herediter : Talangiectasia herediter hemorragic   Trombosit disorders  Trombopati  Trombositopenia : PTI Coagulation factor disorders  Acquired : Vit.K deficiency. vWD . DIC  Herediter : Hemofilia.


Hereditary disorders .disorder platelet adhesion .TROMBOPATI Classification : 1.Platelet Aggregation disorder .platelet secretion disorder 2. Acquired disorders .Storage Disease .Anti-platelet drugs: inhibitors of the enzyme cyclooxygenase .Heart Disorders: less all coagulation factors and impaired adhesion therapy: DDAVP / cryoprecipitate / platelet transfusions .Hiperglobulinemia: disruption of adhesion and the enzyme cyclooxygenase .Abnormalities mieloproliperatif & mielodisplastik .Disease Glanzmann .Bernard-Soulier syndrome .Uremia .

skin bruising. mucosal bleeding nose. APTT . Lab Examination: • Platelet count .elongated • Test PT.normal . bruising until bleeding • Often found in the form of petechie.normal • Test fibrinolysis .Clinical Symptomp: • Variable. vagina and bleeding that elongated to the wound.normal / slightly decrease • BT .

Syndrom Bernard-Soulier • • • • Autosomal resesif GPIb not found in the membranes of platelets GK: bruising / bleeding P.clot retraction N -SADT: giant platelet • Terapi: Transfusi eritrosit dan trombosit .Lab:-Trombosit N/slightly << -BT elongated .

epistaksis.Clot retraction did not occur • Terapi: Transfusi trombosit . perd GI) • P. menorrhagi.jumlah & morf trombosit N .Glanzmann Disease • • • • Autosomal resesif Rare << GPIIb/IIIa GK: The bleeding is not too severe (ptekie. perdarahan mukosa.Lab :.BT elongated .

Storage Pool Disease • • • • Dense granul <</(-) BT elongated Pheripheral trombosit morfology normal Clinical manifestation: Mild – severe bleeding .


 Definition: Obstruction of bloodflow formed of trombosit & fibrin.  Classification :  Arteri Trombosis  Vein Trombosis  Etiology :  Blood flow deceleration  Blood  Sign & Symptom :  Pain  swollen hypercoagulability  Endotel damage   Numb Complication : Emboli .

   White trombus (>> trombosit & fibrin) Inflamation sign more severe than vein trombosis Risk factor :       Man Hyperlipidemia DM Smoke F.VII & Fibrinogen increase Hypertensi .

   Red trombosis Usually beian from calf vein and extends to vena proksimal Risk Factor:  Statis/Immobilization  Idiopathic  Herediter (mutasi F. antifosfolipid syndrom) . Mutasi G20210A. Protein C deficiency. malignancy. Antitrombin deficiency. Defek fibrinogen)  Acquired (post-operation.V Leiden.

 Diagnose :  Venografi (gold standar)  USG doppler  MRI  D-dimer .

APTT TT Fibrinogen examination protein C resistance test DNA test – F.V Antitrombin Protein C & Protein S .         Blood count & LED Peripheral blood smear PT.

Tiklopidin.PHARMACOLOGY  NON-PHARMACOLOGY Anti Coagulan  Heparin  Anticoagulan oral  Anti platelet aggregtion  Aspirin. elevate the extremities position  warm compresses  the scope of the joint exercise  elastic stockings  rTPA . klopidrogel. Urokinase. Dipisidamol  Trombolitik / Fibrinolitik  Streptokinase.

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