PENDEKATAN TERHADAP

PASIEN ANEMIA
ANEMIA
 Definisi fungsional: penurunan jumlah massa eritrosit
(redcell mass)  tidak dapat memenuhi fungsi membawa
O2 yg cukup ke jaringan perifer (penurunan O2 carrying
capacity).

 Anemia bukan kesatuan penyakit tersendiri, tp merupakan

gejala gejala berbagai peny dasar.

 Parameter : kadar Hemoglobin, Hematokrit, & hitung

eritrosit.
  WHO (2001), anemia:
 Laki-laki dewasa: Hb<13g/dl
 Wanita dewasa tidak hamil : Hb<12g/dl
 Wanita hamil: <11g/dl
• Di Indonesia, Hb < 10g/dl  awal work up anemia

• Prevalensi di Indonesia, Husaini dkk (1989):

 Anak prasekolah: 30-40%
 Anak usia sekolah: 25-35%
 Perempuan dewasa tidak hamil: 30-40%
 Perempuan hamil: 50-70%
 Laki-laki dewasa: 20-30%
 Pekerja berpenghasilan rendah: 30-40%

 Peningkatan kadar Hb palsu :
 -Berkurangnya plasma
 -Luka bakar
 -Diuresis berkurang
 -Dehidrasi

 Penurunan kadar Hb palsu

 -Hamil
 -Dekompensasi jantung.
ETIOLOGI
Dasar penyebab anemia:
 Gangguan pembentukan eritrosit oleh ss tulang.
 Kehilangan darah keluar tubuh (perdarahan)
 Proses penghancuran eritrosit oleh tubuh sebelum
waktunya.
Classification
Berdasarkan morfologi (indeks eritrosit & hapusan
darah tepi:
 Anemia hipokromik mikrositer, bila MCV <80 fl dan
MCH <27 pg
 Anemia normokromik normositer, bila MCV 80-95 fl
dan MCH 27-34 pg
 Anemia makrositer, bila MCV >95 fl
Classification
• Based on determination of the red cell mass, anemia
and polycythemia can be classified as (1) relative
(2) absolute.
• Relative anemia is characterized by a normal total red
cell mass. The conditions usually are not thought of as
hematologic disorders but rather as disturbances in
plasma volume regulation
• Classification of the absolute anemias with
decreased red cell mass is difficult because the
classification has to consider kinetic,
morphologic, and pathophysiologic interacting
criteria.

• Initially, all anemias should be divided into

anemias caused by
- decreased production and
- anemias caused by increased destruction of
red cells.
The differentiation is based largely on the
reticulocyte count.
 Morphologic classification subdivides anemia into
(1) macrocytic anemia
(2) normocytic anemia, and
(3) microcytic hypochromic anemia
based on readily available red cell indices (MCV and
MCHC)
FLOW CHART ANEMIA MIKROSITIK HIPOKROM
Anemia
MCV<80fl & MCHC<30g/dL or MCH ≤ 27 pg/dL

Indeks retikulosit <10‰ Indeks retikulosit 10-15‰ Indeks retikulosit >15‰

SI/IBC, Transferin, Feritin Elektroforesis hemoglobin

Normal Abnormal
Normal/Tinggi Defisiensi Fe

Dalam terapi Fe ? Hemoglobinopati

BMP Pasokan, Absorpsi ?

Hemolitik ? Thalasemia
Gangguan metabolisme Fe

Mielodisplasia (MDS)

Anemia of Chronic Diseases (ACD)

FLOW CHART ANEMIA NORMOSITIK NORMOKROM
Anemia
MCV 80-100 fL and MCHC  30 g/dL or MCH > 27 pg/dL

Indeks retikulosit <10‰ Indeks retikulosit 10-15‰ Indeks retikulosit >15‰

Abnormal Kehilangan/Penghancuran Berlebihan

Periksa: Bilirubin indirek, LDH
Hambatan BMP
Produksi/Pematangan
Normal Tinggi

Normal Perdarahan ? Anemia Hemolitik

Anemia hemolitik/def.Fe
dalam terapi ? Tidak Ya
Periksa ACTH
Periksa urin

Infiltrasi Keganasan
Negatif Positif Hb/
Hipoplasia SSTL hemosiderin
Tes coombs, C3/C4
Cincin sideroblastik ? Anti dsDNA
Hemolisis Hemolisis
Positif Ekstravaskular Intravaskular
AIHA Primer or Secunder
Defect Extra corpuscular
Negatif Mekanik, Toksin, Infeksi
Defect Intra corpuscular
Pathophysiology and
Manifestations
 Effect on Oxygen Transport
 The red cells also carry carbon dioxide from the tissues
to the lungs and help distribute nitric oxide
throughout the body, but transport of these gases does
not appear to be dependent on the number of red cells
available and remains normal in anemic patients
 Tissue hypoxia occurs when the pressure of oxygen
in the capillaries is too low to provide cells with
enough oxygen for the cells' metabolic needs.

 In an average person, the red cell mass must

provide the total body tissues with about 250
ml/min of oxygen to support life.

 Because the oxygen-carrying capacity of normal

blood is 1.34 ml per gram of hemoglobin
(approximately 200 ml per liter of normal blood)
and cardiac output is approximately 5000 ml/min,
1000 ml/min of oxygen is available at the tissue
level.
Hypoxia-Inducible Transcription Factor 1
 Hypoxia-inducible transcription factor 1 (HIF-1)
plays a central role in the body's response to
hypoxia.

 HIF-1 was first identified as a factor regulating the

transcriptional activity of erythropoietin gene.

 Its actions include respiratory control,

transcriptional regulation of glycolytic enzyme
genes, angiogenesis, and energy metabolism.
Increased Tissue Perfusion
 The effect of decreased oxygen-carrying capacity on
the tissue tension of oxygen can be compensated by
increasing tissue perfusion by changing vasomotor
activity and angiogenesis

 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 tissue13 and the kidneys.
Vasoconstriction and oxygen deprivation in the skin
causes characteristic pallor of anemia
Increased Cardiac Output
 Because the viscosity of blood in anemia is decreased
and selective vascular dilatation decreases peripheral
resistance, high cardiac output can be maintained
without any increase in blood pressure
 Signs of cardiac hyperactivity include tachycardia,
increased arterial and capillary pulsation, and
hemodynamic "flow" murmurs.
 The murmurs usually are heard during systole at the
apex, over the pulmonary valve area, or at the
pulmonary valve area. Murmurs and bruits have been
described in many regions, such as over the jugular
vein, the closed eye, and the parietal region of the
skull, and may be sensed by the patient as roaring in
the ears (tinnitus), especially at night
Increased Pulmonary Function
 Significant anemia leads to compensatory increase
in respiratory rate that decreases the oxygen
gradient from ambient air to alveolar air and
increases the amount of oxygen available to
oxygenate a greater than normal cardiac output

 Consequently, exertional dyspnea and orthopnea

are characteristic clinical manifestations of severe
anemia
Increased Red Cell Production
• The most appropriate response to anemia is a
compensatory increase of red cell production, which
may increase about twofold to threefold acutely and
fourfold to sixfold chronically, and occasionally as
much as 10-fold in the latter case.

• The increase is mediated by increased production of

erythropoietin

• Erythropoietin concentration can increase from

approximately 10 mU/ml at normal hemoglobin
concentrations to 10,000 mU/ml in severe anemia
 Uncorrected Tissue Hypoxia
 severe tissue hypoxia can cause the following
symptoms: dyspnea on exertion or even at rest,
angina, intermittent claudication, muscle cramps
typically at night, headache, light-headedness, and
fatigue.

 A number of diffuse gastrointestinal and

genitourinary symptoms are associated with
anemia (e.g., abdominal cramps, nausea), but
whether the symptoms should be attributed to
tissue hypoxia, compensatory redistribution of
blood, or the underlying cause of anemia is
uncertain
 Gejala Khas :
 Anemia def besi: disfagia, atrofi papil lidah,
stomatitis angularis, dan kuku sendok
(koilonychia)
 Anemia megaloblastik: glositis, gangguan
neurologik.
 Anemia hemolitik: ikterus, splenomegali, dan
hepatomegali
 Anemia aplastik: perdarahan & tanda-tanda
infeksi
PEMERIKSAAN UNTUK DIAGNOSIS ANEMIA
 Pemeriksaan Laboratorium:
 Hb, indeks eritrosit, hapusan darah tepi, lekosit,
trombosit, hitung retikulosit, LED,
 Pemeriksaan sumsum tulang:
 Mengetahui keadaan hemopoesis
 Mutlak utk Dx anemia aplastik, megaloblastik, dan
kelainan hematologik yg dapt mensupresi sistem
eritroid.
 Pemeriksaan khusus:
 Anemia def besi: kadar besi serum, TIBC, saturasi
transferin, protoporfirin eritrosit, feritin serum, reseptor
tranferin, dan pengecatan besi pada ss tulang (perl’s
stain). Pemeriksaan telur cacing, darah samar
(benzidin test)

 Anemia megaloblastik: folat serum, vit B12 serum, tes

supresi deoksiuridin, dan tes schiling.

 Anemia hemolitik: bilirubin serum, tes coomb,

elektroforesis Hb, dll.

 Anemia aplastik: BMP

RETIKULOSIT
 Dipengaruhi oleh kadar eritrosit dalam darah  dapat
menyesatkan  perlu dikoreksi

 Koreksi untuk anemia

Pada pasien yg hitung retikulositnya 9%, Hb 7,5, Ht 23%,
hitung retikulosit absolut : 9x(7,5/15) atau 9x(23/45) =
4,5%
TES SUPLAI DAN CADANGAN BESI
 Kadar besi serum, N: 50-150 ug/dl
 TIBC, N: 300-360 ug/dl
 Saturasi transferin, didapat dari besi serum dibagi TIBC x
100%. N: 25-50%
 Kadar Ferritin, melihat cadangan besi total tubuh. N pada
laki2: 100 ug/dl
PENDEKATAN DIAGNOSIS
 Tahap-tahap dlm diagnosis anemia:
 Menentukan adanya anemia

 Menentukan jenis anemia

 Menentukan etiologi dan penyakit dasar

anemia
 Menentukan ada tidaknya peny penyerta yg
akan mempengaruhi hasil pengobatan.
Pendekatan tradisional :
Diagnosis berdasarkan anamnesis, pemeriksaan fisik,
hasil lab,
Pendekatan fungsional anemia:
Penurunan angka retikulosit  anemia akibat
penurunan produksi ss tlg atau perdarahan/hemolisis.
Pendekatan morfologi:
Indeks eritrosit/hapusan darah tepi  Anemia
hipokromik mikrositer, normokromik normositer,
makrositer.
Pendekatan probabilistik:
 Di dunia & di daerah tropis tersering dijumpai
anemia def besi, disusul anemia akibat penyakit
kronik, dan thalasemia.
 Wanita hamil terbanyak karena def folat
 Anak-anak tersering karena thalasemia.
 Didaerah tertentu tersering karena malaria.
PENDEKATAN KLINIS
BERDASARKAN :
 Kecepatan timbulnya penyakit (awitan anemia)
 Berat ringannya derajat anemia
 Gejala yang menonjol
Kecepatan timbulnya penyakit (awitan anemia)

 Anemia yang timbul cepat ( hari sampai minggu)

1. Perdarahan akut
2. Anemia hemolitik yang didapat : AIHA
Anemia hemolitik intravaskular : salah tranfusi, An.
def G6PD
3. Anemia yang timbul ok leukemia Akut
4. krisis aplastik pd An. Hemolitik kronik
 Anemia yang timbul pelan-pelan :
1. Anemia def. Besi
2. Anemia def. Folat atau B12
3. Anemia akibat penyakit kronik
4. Anemia hemolitik kronik yg kongenital
Berdasarkan Berat ringannya derajat anemia
Anemi berat biasanya :
1. An. Def Besi
2. An. Aplastik
3. Anemia pd Leukemia Akut
4. Anemia hemolitik kongenital / didapat : Thalassemia
mayor
5. Anemia pasca perdarahan akut
6. Anemia pd GGK stadium terminal
Berdasarkan Berat ringannya derajat anemia
Anemi ringan sampai sedang biasanya :
1. An. Akibat penyakit kronik
2. An. Pd penyakit sistemik
3. Thalasemia trait
Berdasarkan sifat dan gejala anemia
Anemi lebih menonjol dibanding gejala penyakit dasar
biasanya :
1. An. Def Besi
2. An. Aplastik
3. An. Hemolitik
Gejala penyakit dasar lebih menonjol :
1. An. Akibat penyakit kronik
2. An. Sekunder Pd penyakit sistemik, peny Hati, atau
ginjal
PENDEKATAN TERAPI
 Pengobatan berdasarkan diagnosis definitif
 Pemberian hematinik tanpa indikasi yang jelas tidak
dianjurkan
 Pengobatan anemia dapat berupa:
 Darurat, misal pd perdarahan akut akibat anemia
aplastik yg mengancam jiwa, atau pd anemia
perdarahan dg gangguan hemodinamik.
 Terapi suportif
 Terapi khas untuk masing2 anemia.
 Terapi kausal penyebab anemia.
 Transfusi dilakukan pd anemia pasca perdarahan dg
tanda2 gangguan hemodinamik.
PENDEKATAN TERAPI
 Transfusi dilakukan pd anemia pasca perdarahan dg
tanda2 gangguan hemodinamik.

 Pada anemia kronik tranfusi hanya diberikan jika

anemia bersifat simtomatik atau adanya ancaman
payah jantung

 Pada anemia kronik sering dgn peningkatan volume

darah tranfusi diberikan dgn tetesan pelan dan
dapat juga diberikan diuretik kerja cepat.
TERIMA KASIH
TES SUPLAI DAN CADANGAN BESI
 Kadar besi serum, N: 50-150 ug/dl
 TIBC, N: 300-360 ug/dl
 Saturasi transferin, didapat dari besi serum dibagi
TIBC x 100%. N: 25-50%
 Kadar Ferritin, melihat cadangan besi total tubuh.
N pada laki2: 100 ug/dl
 RETIKULOSIT
Dipengaruhi oleh kadar eritrosit dalam darah  dapat
menyesatkan  perlu dikoreksi
Koreksi #1 untuk anemia
Pada pasien yg hitung retikulositnya 9%, Hb 7,5, Ht 23%, hitung
retikulosit absolut : 9x(7,5/15) atau 9x(23/45)
= 4,5%
Koreksi #2 untuk masa hidup prematur reikulosit yg dilepaskan,
indeks produksi retikulosit:
9x (7,5/15)(koreksi hemoglobin)
2 (koreksi waktu maturasi)
= 2,25
 Anemia?

Production? Survival/Destruction?

The key test is the …..

The reticulocyte count
(kinetic approach)
 Increased reticulocytes (greater than 2-3% or
100,000/mm3 total) are seen in blood loss and hemolytic
processes, although up to 25% of hemolytic anemias will
present with a normal reticulocyte count due to immune
destruction of red cell precursors.
 Retic counts are most helpful if extremely low (<0.1%) or
greater than 3% (100,000/mm3 total).
The reticulocyte count
 To be useful the reticulocyte count must be adjusted for
the patient's hematocrit. Also when the hematocrit is
lower reticulocytes are released earlier from the marrow
so one can adjust for this phenomenon. Thus:
 Corrected retic. = Patients retic. x (Patients Hct/45)
 Reticulocyte index (RPI) = corrected retic.
count/Maturation time
(Maturation time = 1 for Hct=45%, 1.5 for 35%, 2 for
25%, and 2.5 for 15%.)
 Absolute reticulocyte count = retic x RBC number.