Clinical approach for diagnosis

and management of anemia

Kurniyanto

Moderator by
Dr. dr. Aru W. Sudoyo, SpPD-KHOM
Outline
• Background
• Physiology of hematopoiesis
• Patophysiology
• Classification of anemia
• Approach to diagnosis
• Treatment
• Conclusion
Outline
• Background
• Physiology of hematopoiesis
• Patophysiology
• Classification of anemia
• Approach to diagnosis
• Treatment
• Conclusion
Prevalence
• > 2 billion or one third of world population suffered from anemia1
• Majority in developing country, half to one third population of anemia is
women and children
• In developed country, 9% of population suffered from anemia, In contrary
to developing country, 43% of population is anemic1,2
• In Indonesia3 :
• Pregnant women 50-70%
• Non-pregnant women 30-40%
• Men 20-30%
• School age children 25-35%
• In 2002, WHO report the most cases of anemia is iron deficiency anemia1
1. WHO. Worldwide prevalence of anemia 1993-2005, WHO global data base on anemia.2008:1-2
2. Balarajan Y, Ramakrishnan U, Ozaltin E, Shankar AH, Subramanian SV. Anemia in low-income and middle income countries. Thelancet.2011;378:2123-35
3. Bakta IM. Pendekatan klinis anemia. Buku ajar Ilmu Penyakit Dalam jilid II. Jakarta : Penerbit interna.2009:1109-15
Prevalence

USAID. Anemia prevention and control.2003:15-23

 Impact of anemia
• It is more difficult for men and women to earn incomes, carry out daily tasks,and
care for their families.
• It makes women weaker during pregnancy and delivery, reducingtheir chances of
having healthy babies and surviving blood loss during and after childbirth.
• Anemic infants and children grow more slowly than non-anemic infants and
children. They are apathetic and anorexic, do not have enough energy to play,
and have trouble learning.1
A 2002 World Health Organization report lists iron deficiency, a major cause of anemia,
as one of the top 10 risk factors in developing countries for “lost years of healthy life.”2

1. USAID. Anemia prevention and control.2003:15-23

2. WHO. Worldwide prevalence of anemia 1993-2005, WHO global data base on anemia.2008:1-2.
 Definition

Anemia is defined as a low level of hemoglobin in the

blood, as evidenced by a reduced quality or quantity of
red blood cells

WHO. Worldwide prevalence of anemia 1993-2005, WHO global data base on anemia.2008:1-2
• Normal Hb value is different
among population
• Diagnosis should be made based
on age and sex
Outline
• Background
• Prevalence
• Individual and social impact
• Definition
• Physiology of hematopoiesis
• Patophysiology
• Classification of anemia
• Approach to diagnosis
• Treatment
• Conclusion
Regulation of erythropoiesis
• Erythropoiesis is influenced by a number of hormones/cytokines,
receptors, and transcription factors1
• The lineage-specific transcription factor GATA-1
• EPO
• HIF
• RAAS
• MicroRNAs
• Insulin-like growth factor
• antiapoptotic protein Bcl-xL39
• FOG-140 and PU.1
• Growth arrest-specific 6 (Gas6) protein

1. Lichtman M. Clinical manifestation and classification of erythrocyte disorders. William’s Hematology 8th ed. China: McGraw-Hill.2010:350-70.
Interaction of EPO and EPO-R1
• Stimulation of erythroid cell division
• Erythroid differentiation by induction of erythroid-specific protein
expression, and
• Prevention of erythroid progenitor apoptosis

1. Jelkmann W. Regulation of erythropoietin production. J Physiol 589.6 (2011) pp 1251–1258

 Role of erythropoietin

Jelkmann W. Regulation of erythropoietin production. J Physiol;589.6 (2011) pp 1251–1258

Role of Hipoxia Inducible Factor (HIF)
• Adaptive physiologic responses to hypoxia serve to1
• Increase O2 delivery to cells
• Allow cells to survive under reduced O2 by activating glycolysis, and
• Reduce the formation of reactive oxygen species

1. Lichtman M. Clinical manifestation and classification of erythrocyte disorders. William’s Hematology 8th ed. China: McGraw-Hill.2010:350-70.
Outline
• Background
• Prevalence
• Individual and social impact
• Definition
• Physiology of hematopoiesis
• Patophysiology
• Classification of anemia
• Approach to diagnosis
• Treatment
• Conclusion
When anemia occurred, following features are responding1 :
• Effects on oxygen transport
• Decreased Oxygen Affinity
• Increased Tissue Perfusion
• Increased Cardiac Output
• Increased Pulmonary Function
• Increased Red Cell Production
• Uncorrected Tissue Hypoxia

1. Lichtman M. Clinical manifestation and classification of erythrocyte disorders. William’s Hematology 8th ed. China: McGraw-Hill.2010:350-70.
• Effects on oxygen transport
• Appoximately 1000 ml/min of oxygen are available in tissue level
• Extraction of one-fourth of this amount reduces the oxygen tension of 100 torr in the arterial
end of the capillary to 40 torr in the venous end.
• This partial extraction ensures the presence of sufficient diffusion pressure
• In anemia, extraction of the same amount of oxygen leads to greater hemoglobin
desaturation and lower oxygen tension at the venous end of the capillary.
• This will lead the compensatory mechanism
• Decreased Oxygen Affinity
• Efficient increase of tissue oxygen delivery is accomplished by decreasing the
affinity of hemoglobin for oxygen
• In chronic anemia, increased oxygen tissue delivery is accomplished by
increased amounts of 2,3-bisphosphoglycerate.
• 2,3-bisphosphoglycerate increase in anemia  increasing the intracellular pH
of red cells by respiratory alkalosis resulting from increased respiration.

Bunn HF, Aster JA. Pathophysiology of blood disorders. New York: McGraw-Hill.2010:1031-38.
• Increased Tissue Perfusion
• Changing vasomotor activity and angiogenesis provide tissue perfusion.
• Shunting the blood from nonvital donor areas to oxygen-sensitive essential
recipient organs.
• In acute anemia, the major donor areas for redistribution of blood are the
mesenteric and iliac beds.
• In chronic anemia in humans, the donor areas are the cutaneous tissue and
the kidneys.
• Increased Cardiac Output
• Increased cardiac output is an excellent but metabolically expensive
compensatory device.
• It decreases the fraction of oxygen that must be extracted during each
circulation, thereby maintaining higher oxygen pressure.
• Long standing anemia will lead to heart failure
 • Increased Pulmonary Function
• Compensatory increase in respiratory rate
• Exertional dyspnea and orthopnea are characteristic clinical manifestations of
moderate to severe anemia
• Increased Red Cell Production
• The most appropriate response to anemia  2-3x acutely 4-6x chronically
• Erythropoietin play important role
• Increase stress reticulocyte

Lichtman M. Clinical manifestation and classification of erythrocyte disorders. William’s Hematology 8th ed. China:
McGraw-Hill.2010:350-70.
• Uncorrected Tissue Hypoxia
• A certain residual degree of tissue hypoxia remains despite
mobilization of compensatory mechanisms.
• severe tissue hypoxia can cause the following symptoms:
• dyspnea on exertion or even at rest;
• angina;
• intermittent claudication;
• muscle cramps,
• headache;
• fatigue.
Outline
• Background
• Prevalence
• Individual and social impact
• Definition
• Physiology of hematopoiesis
• Patophysiology
• Classification of anemia
• Approach to diagnosis
• Treatment
• Conclusion
Classification of anemia
• Morphologic classification
• Microcytic hypochromic anemia
• Normocytic normochromic anemia
• Macrocytic anemia

• Etiologic classification
• Hypoplastic disorders
• Maturation disorders
• Blood loss or hemolytic disorders

Hillman RS, Ault KA, Rinder HM. Approach to anemia. Hematology in Clinical Practice. Philadelphia: McGraw-Hill.2005:235-42.
 Morphologic classification

Bakta IM. Pendekatan klinis anemia. Buku ajar Ilmu Penyakit Dalam jilid II. Jakarta : Penerbit interna.2009:1109-15
Etiologic classification

Adamson JW, Longo DL. Anemia and polycitemia. Harrison’s Principles of Internal Medicine vol 1. Philadelphia: McGraw-Hill.2005:329-36
Outline
• Background
• Prevalence
• Individual and social impact
• Definition
• Physiology of hematopoiesis
• Patophysiology
• Classification of anemia
• Approach to diagnosis
• Treatment
• Conclusion
Approach to diagnosis
• Mostly anemia is not a single disease, it came with concomitan
disease
• The clinical features of anaemia are largely caused by compensatory
measures mobilised to counteract hypoxia.
• The signs and symptoms of an anemia are a function of :
• its severity,
• its rapidity of onset,
• and the age of the patient
• Carefull history taking, physical examination and directed laboratory
evaluation is the key of anemia work up
• History
The patient should be questioned extensively regarding :
• Timing of the onset of symptoms
• Transfusion history
• Past blood count measurements
• Nutritional habits, alcohol intake
• Any associated symptoms of acute or chronic illness such as weight loss, fever,
or night sweats
• Alcohol consumption
• Menstrual condition in women
• Defecation such chronic GI blood loss
Family history
Is essential to work up of anemia, several disorders are inherited :
• Hereditary telangiectasia
• β-thalassemia
• Fanconi’s anemia
• Pyruvate kinase deficiency
• Hemostasis disorders
• History of gallstones
• ect
Signs and Symtoms anemia
• Cardiovascular and pulmonary : dyspnea, palpitation, fatigue, angina
pectoris, intermitten claudication
• Neuromuscular features : vertigo, dizziness, faintness, lack of mental
concentration, muscular weakness, paresthesia
• Gastrointestinal : dysphagia, nausea
• Pallor in conjungtiva, pharynx, nail bed
 glossitis

Spoon nail
Pale conjungtiva

Thalassemia face
• Physical examination
• Skin and mucose pallor
• Ocular examination : pale retinae
• Vitiligo suggest an autoimmune and cobalamin deficiency
• Koilonychia in iron deficiency anemia
• Angular stomatitis
• Jaundice in hemolytic disorders
• Cardiomegaly, systolic murmurs
• Splenomegaly in hemolytic anemia
• Hepatomegaly : acute hepatitis, cirrhosis, metastasis of cancer
• Rectal examination : GI bleeding
• Neurologic abnormalities : paresthesia in pernicious anemia
Laboratory work up
Others laboratory work up for specific diagnosis

• GFR, erythropoietin level, ureum and cretinin

• LDH
• Vitamin B12 and folate serum
• LFT, e.g : ALT, AST, bilirubin, albumin, globulin
• Urinalisis
• Haptoglobulin
• Fecal test for blood
• hemoglobin Electrophoresis
• Coombs test
• Red blood cell indices
• microcytic hypochromic : MCV < 80fl and MCH < 27 pg
• normocytic normochromic : MCV 80-95 fl and MCH 27-34 pg
• macrocytic MCV > 95 fl
• Peripheral blood smear
• anisocytosis  increases in the RDW or the range of cell sizes.
• Poikilocytosis  defect in the maturation of red cell precursors in the bone
marrow or fragmentation of circulating red cells.
• polychromasia—red cells  premature reticulocytes or stress reticulocyte
• Reticulocyte count
• Essential to evaluate marrow responds
• Need to be corrected in 2 steps
1. Absolute reticulocyte count
2. Reticulocyte production index
• Step 1 : absolute reticulocyte count

• Step 2 : reticulocyte production index

RPI interpretation :
1-2%  normal
<1%  hypoproliferative
>2%  blood loss/hemolytic
• Test of iron supply
• SI (serum iron) : 50-150 µg/dl
• TIBC (total iron binding capacity): TIBC 300-360 µg/dl
• Feritin (iron storage): male 100 µg/L, female 30 µg/L
• Transferin saturation (iron transporter) : transferrin 25-50%.
• Bone marrow examination
• Assesed when hypoproliferative anemia and normal iron status
• M:E ratio
• Hypoproliferative and RPI < 2%, M/E ratio 2 or 3 : 1
• Hemolytic and RPI > 2%, M/E ratio 1 : 1
• Iron store in form of ferritin or hemosiderin
Algorithm of diagnosis

Adamson JW, Longo DL. Anemia and polycitemia. Harrison’s Principles of Internal Medicine vol 1. Philadelphia: McGraw-Hill.2005:329-36.
Approach to microcytic anemia
• Most of the case is due to deficient of Hb synthesis
• Associated with low iron or impaired used
• Most cases that clinically should be distinguished are :
• Iron deficiency anemia, predominates in children and young women
• Anemia of chronic disease, predominates in elderly
• Thalassemia trait
Parameters Iron deficiency anemia Chronic disease anemia
SI low Low
TIBC low Low
Ferritin low Normal or high
Bone marrow iron store low Increase
Morphologic microcytic Mostly macrocytic but can
be microcytic
Glader B. Anemia : general considerations. Wintrobe’s Clinical Hematology 13th edition. Philadelphia: Lippincott William and wilkins.2005:948-75
• Anemia of chronic disease mechanisms are due to :
• Tumor necrosif factor-α (TNF- α), IL-1 and interferons  suppressive effect on
erythroid colony formation
• Shortened erythrocytes life span
• Inadequate Erythropoietin Secretion and Resistance to Erythropoietin
• Hepcidin inhibit release of iron from macrophage and intestinal iron uptake

Common Conditions Associated with anemia of chronic disease

Category Conditions Associated with AI

Infection AIDS/HIV, tuberculosis, malaria (contributory), osteomyelitis, chronic abscesses, sepsis
Inflammation Rheumatoid arthritis, other rheumatologic disorders, inflammatory bowel diseases,
systemic inflammatory response syndrome
Malignancy Carcinomas, myeloma, lymphomas
Cytokine dysregulation Anemia of aging

Lichtman M. Clinical manifestation and classification of erythrocyte disorders. William’s Hematology 8th ed. China: McGraw-Hill.2010:350-70
Modification of Glader B. Anemia : general considerations. Wintrobe’s Clinical Hematology 13th edition. Philadelphia: Lippincott William and wilkins
Anemia in elderly
• A multipathology condition
• Symptoms are clinically non specific
• Related to QoL

Guralnik JM, Eisenstaedt RS, Ferrucci L, Klein HG, Woodman RC. Prevalence of anemia in persons 65 years and older in the United States: evidence for a high rate of
unexplained anemia. Blood. 2004;104:2263-2268
Approach to macrocytic anemia
• Morphological and biochemical classification :
• Megaloblastic
• retarded DNA synthesis
• Neutrophil hypersegmentation and oval macrocytes
• Non-megaloblastic
• DNA synthesis is unimpaired
• Macrocytes without features of nuclear and cytoplasmic finding of megaloblastic
• Macrocytes tend to be mild 100-110 fl MCV
Macrocytic anemia
Megaloblastic Non-megaloblastic
Vit B12 deficiency Alcoholism
Folate deficiency Liver disease
Inherited disorders of DNA synthesis Myelodisplastic syndrome
Drug and toxin induced disorders of DNA synthesis Associated with accelerated erythropoiesis
e.g methotrexate, AZT, arsenic, trimethoprim • Hemolytic anemia
• Post hemorrhagic anemia
Hypothyroidsm
Aplastic anemia
Glader B. Anemia : general considerations. Wintrobe’s Clinical Hematology 13th edition. Philadelphia: Lippincott William and wilkins.2005:948-75.
• Myelodysplastic syndrome
• “a group of clonal marrow failure syndromes originating in a hematopoietic
progenitor or stem cell “
• Increase incidence with age, mostly over 60 years
• Characterized by progressive peripheral cytopenias, however the marrow is
hypercellular with at least dysplastic in one lineage
• Most of cases peripheral morphology is macrocytic or rarely
microcytic/normocytic and blast > 5%

Surveilance, epidemiology and end result (SEER), national institute of cancer, 2011
Modification of Glader B. Anemia : general considerations. Wintrobe’s Clinical Hematology 13th edition. Philadelphia: Lippincott William and wilkins.2005:948-75
Approach to normocytic anemia
• When reticulocytosis and polychromasia macrocyte prominent, most
case are due to hemolytic anemia or post hemorrhagic anemia
• Therefore, marrow examination is not necessary
• Hemolytic anemia clasification based on site of hemolysis
• Intravascular : within circulation
• Extravascular : within tissue macrophage

Hemolysis test Extravascular hemolysis Intravascular hemolysis

Bilirubin Increased Increased
Haptoglobulin Normal to absent Absent
Hemoglobinuria Absent Present
Free Hb in plasma Absent Present
Urine hemosiderin Absent Present

Sudoyo AW. Anemia dalam praktek sehari-hari: tidak hanya terapi besi. Downloaded March, 4th 2014, 12:00 www.papdi.org/papdi.php
 Cause of intravascular hemolysis Cause of extravascular hemolysis
Blood transfusion Bacterial and viral infections
ABO mismatched transfusion Malaria
Infected blood Mycoplasma pneumoniae
Thermal burns
Infectious mononucleosis
Snake bites
Bacterial/parasitic infections Drug-induced hemolysis
Clostridial sepsis G6PD/GSH deficiency
Malaria Autoimmune drug reactions
Bartonellosis Strong oxidant drugs/chemicals
Mycoplasma pneumoniae Autoimmune hemolysis
Mechanical heart valves
Warm-reacting (IgG) AIHA
Paroxysmal hemoglobinuria
PNH Cold-reacting (IgM) AIHA
PCH Hemoglobinopathies
Membrane structural defect
Hereditary spherocytosis
Hereditary elliptocytosis
Acanthocytosis
Environmental disorders
Malignancy/DIC
TTP/HUS
Hillman RS, Ault KA, Rinder HM. Approach to anemia. Hematology in Clinical
Practice. Philadelphia: McGraw-Hill.2005:235-42.
Eclampsia or preeclampsia
Modifcation of Glader B. Anemia : general considerations. Wintrobe’s Clinical Hematology 13th edition. Philadelphia: Lippincott William and wilkins.2005:948-75
Treatment
• The management of any anemia must be based on the diagnosis
• The sooner the workup is complete and the diagnosis confirmed, the
better
• Shotgun therapy can make accurate diagnosis nearly impossible
• If the patient is physiologically unstable, therapy should not be delayed
• This condition needs to be treated immediately with transfusion of packed
red blood cells to stabilize the patient while the anemia workup proceeds
• Modalities to correct Hb level
• Hematinics (sulfas ferosus, Vit B12, folate)
• Erythropoietin
• PRC tranfusions
• Splenectomy
Conclusions
• Anemia is not a single disease, mostly with concomitant disorders
• Clinical features are due to degree of anemia
• Compensation is activated to hypoxic state of anemia
• Definite cause of anemia is essential for management
• Etiologic and morphologic classification help to trace the primary
cause
• Therapy should be directed to it’s underlying pathogenesis, not just
giving hematinics or transfusion
• If unstable, immediate transfusion is indicated
Conclusions
• Anemia is not a single disease, mostly with concomitant disorders
• Clinical features are due to degree of anemia
• Compensation is activated to hypoxic state of anemia
• Definite cause of anemia is essential for management
• Etiologic and morphologic classification help to trace the primary
cause
• Therapy should be directed to it’s underlying pathogenesis, not just
giving hematinics or transfusion
• If unstable, immediate transfusion is indicated
Conclusions
• Anemia is not a single disease, mostly with concomitant disorders
• Clinical features are due to degree of anemia
• Compensation is activated to hypoxic state of anemia
• Definite cause of anemia is essential for management
• Etiologic and morphologic classification help to trace the primary
cause
• Therapy should be directed to it’s underlying pathogenesis, not just
giving hematinics or transfusion
• If unstable, immediate transfusion is indicated
Conclusions
• Anemia is not a single disease, mostly with concomitant disorders
• Clinical features are due to degree of anemia
• Compensation is activated to hypoxic state of anemia
• Definite cause of anemia is essential for management
• Etiologic and morphologic classification help to trace the primary
cause
• Therapy should be directed to it’s underlying pathogenesis, not just
giving hematinics or transfusion
• If unstable, immediate transfusion is indicated
Conclusions
• Anemia is not a single disease, mostly with concomitant disorders
• Clinical features are due to degree of anemia
• Compensation is activated to hypoxic state of anemia
• Definite cause of anemia is essential for management
• Etiologic and morphologic classification help to trace the primary
cause
• Therapy should be directed to it’s underlying pathogenesis, not just
giving hematinics or transfusion
• If unstable, immediate transfusion is indicated
Conclusions
• Anemia is not a single disease, mostly with concomitant disorders
• Clinical features are due to degree of anemia
• Compensation is activated to hypoxic state of anemia
• Definite cause of anemia is essential for management
• Etiologic and morphologic classification help to trace the primary
cause
• Therapy should be directed to it’s underlying pathogenesis, not just
giving hematinics or transfusion
• If unstable, immediate transfusion is indicated
Conclusions
• Anemia is not a single disease, mostly with concomitant disorders
• Clinical features are due to degree of anemia
• Compensation is activated to hypoxic state of anemia
• Definite cause of anemia is essential for management
• Etiologic and morphologic classification help to trace the primary
cause
• Therapy should be directed to it’s underlying pathogenesis, not just
giving hematinics or transfusion
• If unstable, immediate transfusion is indicated
Laporan kasus
• Nama : Ny. N
• Usia : 55 tahun
• Pekerjaan : ibu rumah tangga

• Keluhan utama
Nyeri kepala memberat sejak 18 hari SMRS
• Riwayat penyakit sekarang
Pasien mengeluh nyeri kepala sejak 18 hari SMRS, tidak ada kejang dan
penurunan kesadaran. Pandangan kabur sedikit, kelemahan salah anggota
gerak disangkal, lemas (+). Pasien juga mengeluh memar-memar sejak 1
bulan SMRS, diikuti dengan muntah darah beberapa kali, terakhir 1 hari
SMRS. BAK berdarah, ada pendarahan gusi terus menerus tiap kali
meludah. Demam hilang timbul, nyeri tulang ada, keluhan benjolan
disangkal. Keluhan ini baru berlangsung 1 bulan SMRS. Sesak nafas (-),
batuk (-), perut buncit disangkal, pasien sempat dirawat di RSUD Bekasi,
dilakukan tranfusi darah PRC dan TC, tapi trombosit turun lagi sehingga
dirawat di RSCM.
• Riwayat alergi : alergi obat (-)
• Riwayat penyakit dahulu : DM (-), HT (-)
• Riwayat penyakit keluarga : DM (-), HT (-), keganasan (-)
• Riwayat pekerjaan, social, ekonomi, kejiwaan dan kebiasaan : IRT,
menikah, 9 anak.
• Pemeriksaan umum
Kesadaran/mental : CM
Tekanan darah : 100/60
Nadi : 85x/menit
Pernafasan : 18x/menit
Suhu : 36,2°C
 Mata : konjungtiva pucat, sclera tidak ikterik
Leher : JVP 5-2 cmH2O, KGB tak teraba
Jantung : S1, S2 normal, murmur dan gallop (-)
Pulmo : vesikuler, rhonki dan wheezing tidak ada
Abdomen : datar, lemas, bising usus normal, nyeri
tekan epigastrium tidak ada, spleen tak
teraba, hepar teraba 3 jari BAC
Ekstremitas : akral hangat, tidak ada oedem
• Pemeriksaan penunjang
USG abdomen : organ intraabdomen dalam batas normal
EKG : SR, NA, QRS rate 70x/menit, P wave N, PR int 0,16,
QRS complex 0,08, ST changing (-), T inv v1,v2, LVH (-), RVH (-).
CT scan : tidak tampak perdarahan intra kranial
Laboratorium
• Hemoglobin : 8.3 gr/dl • Laju endap darah : 54 mm/jam
• Hematokrit : 24.0 % • Gambaran darah tepi
• Eritrosit : 2.98 x 106 /µl Eritrosit : normositik
• MCV : 80.5 fl Leukosit : kesan jumlah kurang,
morfologi normal
• MCH : 27.9 pg
Trombosit : kesan jumlah kurang,
• MCHC : 34.6 gr/dl morfologi normal
• Trombosit : 107x 103 / µl Kesan : pansitopenia
• Leukosit : 2.28 x 103 / µl • Retikulosit
• Hitung jenis Absolut : 2100 / µl
Basophil : 0.0 % Relative : 0.07 %
Eosinophil : 0.4 % • Protein total : 7.1 mg/dl
Neutrophil : 36.5 % Albumin : 3.33 mg/dl
Limfosit : 36.5 % Globulin : 3.77 mg/dl
Monosit : 4.8 % Albumin – globulin ratio: 0.9
• Serum iron (SI) : 112 µl/dl
TIBC : 165 µl/dl
Sat transferrin : 68 %
Ferritin : 1067 ng/ml
• Serologi HIV : negative
• HBsAg : non-reaktif
• Anti HCV : non reaktif
• Ureum : 36 mg/dl
• Kreatinin : 0.86 mg/dl
• GDS : 140 mg/dl
• SGOT : 15 mg/dl
• SGPT : 13 mg/dl
• Diagnosis kerja
Pansitopenia e.c dd/MDS
anemia aplastik
Trombositopenia dengan manifestasi perdarahan (gum bleeding,
hematuria, hematemesis)
Cephalgia e.c susp perdarahan intracranial
Iskemia septal
• Penatalaksanaan
NaCl 500 cc/12 jam
Transamin 3 x 500 mg, iv
Ultracet 3 x 1
Omeperazole 2 x 40 mg
Pro BMP