Anemia Aplastik SGD I Presentation

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Information about Anemia Aplastik SGD I Presentation
Education

Published on March 16, 2014

Author: SkmarinaLarose

Source: slideshare.net

Skmarina Hanna Larose S. P. Vesper J. N. Zamili Adolf Finsensius Sarumaha Agnes Meinulo Duha Alhoi Lesley Davidson Annisa Maichie Kurniasih Evie Clarensia Lase Louis Mapolo Sutian Maruli Freddy Simamora Nikko Fernando Venesia Nita Fatmasari Bangun Rosnilam Moho Siti Ramadhani Sri Wahyu Ratnasari Nasution Tiorasi Pakpahan

Adi, a six-year-old-boy, can’t take school activities in his school for six days because of having severe fever, myalgia and anorexia, but lately, Adi’s face comes paler, his heart beats faster, malaise, lose appetite, bleeding around his gums and petechiae, ecchymosis in superficial. Adi has history of eating Chlorampenicol often and antipiretic which are bought by his mother. Hence Adi’s condition is worse, Adi is taken to pediatrician. Doctor suggests to do a complete blood examination and Bone Marrow Punction. What has happened to Adi and how is the management?

• Myalgia : pain on muscle • Ecchymosis : patch of bleeding under skin with diameter > 2 mm • Petechiae : patch of bleeding under skin with diameter < 2 mm • Anorexia : appetite disruption • Bone Marrow Punction : an examination by doing aspiration of bone marrow liquid

1. Adi, a six-year-old-boy, can’t take school activities in his school for six days because of having severe fever, myalgia and anorexia, but lately, Adi’s face comes paler, his heart beats faster, malaise, lose appetite, bleeding around his gums and petechiae, ecchymosis in superficial. 2. Adi has history of eating Chlorampenicol often and antipiretic which are bought by his mother. 3. Doctor suggests to do a complete blood examination and Bone Marrow Punction.

1. - Probably caused by infection - Probably caused by aplastic anemia - Patient has hemostatic disfunction - Probably having thrombosis disfunction - Probably having pancytopenia 2. - Probably caused by toxin of medicines - Lack of knowledge of patient’s mom 3. To uphold the final diagnose

Adi, a-six-year-old-boy, probably is having anemia aplastic

1. Classification of anemia 2. Definition of aplastic anemia 3. Etiology of aplastic anemia 4. Epidemiology of aplastic anemia 5. Classification of aplastic anemia 6. Pathophysiology of aplastic anemia 7. Clinical symptoms of aplastic anemia 8. Anamnesis of aplastic anemia 9. Physical examination of aplastic anemia 10. Supporting examination of aplastic anemia 11. Management of aplastic anemia 12. Prevention of aplastic anemia 13. Complication of aplastic anemia 14. Prognosis of aplastic anemia

A. Based on etiopathogenesis I. Disturbance in erythrocytes formation and marrow bone a. Deficiency of essential a. Iron Deficiency b. Folic acid deficiency c. Vitamin B12 deficiency b. Disturbance in Iron utilization a. Chronic disease b. Sideroblastic anemia

c. Marrow bone destruction a. Aplastic anemia b. Mieloptisica anemia c. Hematologic anemia d. Dyserythropoiesis anemia e. Myelodisplastic syndrome d. Deficiency of erithropoiesis II. Hemorrhagic cause III. Hemolitic cause IV. Unknown and complex pathogenesis

B. Based on morphology I. Hypochromic microcytic II. Normochromic normocytic III. Macrocytic a. Megaloblastic b. Non-megaloblastic

Aplastic anemia is a condition caused by decreasing of peripheral blood hematopoietic cells such as erythrocytes, leukocytes and platelets as a result of the cessation of cell production in bone marrow hemopoetic.

a. Congenital Factor : Fanconi syndrome b. Acquired factors : • Chemicals : Benzene, insecticides, compound As, Au, Pb. • Drugs : Chloramphenicol, mesantoin (anticonvulsants), piribenzamin (antihistamines ), santonin - calomel, a drug sitostatica (myleran, methrotrexate, TEM, vincristine, rubidomycine etc. ), anti- tumor drugs (nitrogen mustard), anti- microbial. • Radiation : Roentgen rays, radioactive. • Infection : Miliary tuberculosis, hepatitis and others - others. • Malignancy : Kidney disease, endocrine disorders, and idiopathic.

The incidence of acquired aplastic anemia varies around the world and range from 2 to 6 cases per 1 million population per year with geographic variation. Acquired aplastic anemia generally appears at the age of 15 to 25 years; peak incidence appears after the age of 60 years.

I. Primary 1 . Congenital abnormalities 2 . Idiopathic II . Secondary : 1 . Due to radiation, chemicals, or drugs 2 . Due to other causes : a. Virus Infection : Hepatitis Viruses / other viruses b . Due to pregnancy c . Radiation

1. Tachycardia 2. Increasing of breathing frequency 3. Pale 4. Weakness 5. Dizzy 6. Nausea 7. Decreasing quality of skin and hair

a. Complaints eritroblastopenia b. Complaints thrombocytopenia c. Complaints eukopenia d. History of treatment : • Consume drugs in a long period of time • Chemotherapy • Often exposed to radiation like x-rays and radioactive rontgen e. previous Illness History d. Family history of sitopenia

a. Inspection : 1. Pale 2. There are bruises, petechiae, or ecchymosis 3. bleeding gums b. Palpation : 1. body temperature increase 2. cold extremities 3. tachicardy 4. Hepatomegaly (found in a several patients) c. Percussion : Hepatomegaly (found in a fraction of patients) d. Auscultation : gallop rhytm and wheezing

1. Laboratory Examination a. Peripheral Blood According to The International Agranulocytosis and Aplastic Anaemia Study (IAAS) is called anemia aplastik when: i. the levels of hemoglobin ≤ 10 g/dl or Hematokrit ≤ 30% ii. Count of platelets ≤ 50,000/mm3 iii. Leukocyte Count ≤ 3500/mm3 or Granulocytes ≤ 1.5 × 109/l

2. bone marrow Biopsy 3. Radiological Examination 1. Nuclear Magnetic Resonance Imaging 2. Radionuclide Bone Marrow Imaging (Scanning Bone Marrow)

Diagnosis differential 1. Idiopathic Thrombocytopenic Purpura (ITP) and Thrombocytopenic Purpura Amegakaryocytic (ATP) 2. Type of aleukemik acute Leukemia, especially ALL (Acute Lymphocytic Leukemia) 3. Preleukemik Stage of acute leukemia

Management 1. Supportive therapy 1. Leukocyte-poor red cells Transfusion (overcome anemia) 2. Platelet suspension transfusion (Overcome bleeding) 3. Antibiotics ( for infections, recommended antibiotics are b-lactam and aminoglycosides) 4. Blood, urine, faeces, sputum, CSF culture 5. Avoiding the chemical and physical toxic and drugs.

2. Medication Therapy 1. Androgen Oksimetolon is better instead of testosteron, with dose 1-2 mg/kg/day 2. Imunosuppressive a. Methylprednisolon ( 5 mg/kg IV 8 days then tappering) b. Antilymphocyte-Globulin (40mg/kg IV for 12hours +methylprednisolon 1mg/kg/hours IV for 4 days) c. Antithymocyte-Globulin (100-2000mg/kg IV) d. Cyclosporin A (8mg/kg/day PO for 14 day continue with 15mg/kg/day) e. Cyclophosphamide (50mg/kg/day for 4 days, still controversy) 3. Growth factor ( G-CSF with dose 5 ig/kg/day)

4. Combination therapy combination of ALG/ATG, methylprednisolon and CsA. 3. Blood Transfusion 4. Chelation Therapy given when there is accumulation of iron due to blood transfusion 5. bone marrow transplant 6. Food 7. Rest Relaps in case of relaps then can be given CsA and if unsuccessful then can be given repeat ATG

Prevention 1. Avoiding toxic materials 2. Avoiding drugs consumption which can trigger aplastic anemia 3. Avoiding radiation 4. Good hygiene 5. Management of bleeding and infection

1. Infection 2. Bleeding 3. GVHD after transplantation 4. Death

Based on : 1. Bone Marrow representation 2. HbF > 200 mg% give a better prognosis 3. Granulocyte > 2000/mm3 give better prognosis 4. Secondary infection prevention

Diagnose : Adi, 6-year-old-boy, suffers Aplastic anemia Supporting examination : • Peripheral blood count to see pancytopenia, morfology of erythrocyte, leucocyte and thrombocyte and count the sums. • Bone Marrow Punction to see bone marrow representation. Management : • Stop using Chlorampenicol • Give supporting therapy, such as : • Make sure the etiology of Adi’s fever, if it is caused by bactery infection, give antibiotic, such as B-Lactam and Aminoglicoside • Take care of self-hygiene

• Result of supporting examination : • If Hb , 7 gr% then do transfusion of red-packed cell • If thrombocyte < 20.000/uL then do thrombocyte transfusion • Observation patient, wether Adi’s condition comes better. If not do combination therapy, consist of : • Methylprednisolon 5 mg/KgBW IV for 8 days, then tappering until 1 mg/KgBB/day for 9-14 days. • ALG is given 40 mg/KgBW for 12 hours, continued with infuse that combinated with Methylprednisolon. • Siklosporin A is given 8 mg/KgBB • Last option is Transplation of Bone Marrow

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