Aspek Klinis Anemia

8/10/2019 Aspek Klinis Anemia

1/93

ASPEK KLINIS ANEMIA

DAN HEMOLISIS

dr Erlina Marfianti, MSc, SpPD

Dept Ilmu Penyakit Dalam FK UII


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DEFINITION

Normally defined as haemoglobin concent less than :

13. g/dl in adult male

12. g/dl in adult female

11. g/dl in pregnance women

Children : Newborn Hb 15-21 g/dl

3 month Hb 9.5-12.5 g/dl

1 year-puberty Hb 11.0-13.5 g/dl


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Subtances needed for

erythropoiesis Metal: Fe, Mg, Co

Vitamins: B1, B6, B12,riboflavin, panthothenic

acid, Folate, Vit C, Vit E

Amino acids Hormones: erythropoietin,

androgens, thyroxine


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Main function Hb :

Carry oxygenthe

tissue

Return carbon dioxide(CO2) from the tissue

to the lung.


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A. Classification of anemia based on

functional defect/ Pathofisiologic :

I. Hemorrhage (Blood loss):

a. acutepost acute

hemorrhagehipovolemia

b. chronicIronDeficiencyAnemia


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II. Increase destruction RBC

a. Herediter:

Defect of red cell cytosceleton

membranhereditary spherocytosis

,eliptocytosis

metabolicdefect/enzyme deficiency

G6PD, Piruvat Kinase deficiencyDefect of globin synthesis/globin

struc.abnormality:thalassemia,

hemoglobinopathi: sickle cell

anemia,HbC, HbE,

1. Hemolytic Intrinsic Anemia /Intracorpuscular


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2. Ekstracorpuscular/Hemolytic Extrinsic

Anemia.

a. Immun Hemolytic AnemiaIso/Allo Immun Hemolytic:

- HDN (Hemolytic Disease of The Newborn),

- hemolytic transfusion reaction

Auto immun Hemolytic Anemia (AIHA)

Drug Induced Immun Hemolytic Anemia

viral infection : mycoplasma, mononucl inf

b. Non Immun Hemolytic Anemia

mechanical: artificial valve dysfunction,MAHA (Microangiopathic Hemolytic Anemia)

chemical, burn

parasitic infection : malaria


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III. Failure in RBC production /

hipoproliferatif:

1.EPO production / response to EPO

chronic inflamation and renal disease,

endocrin disease.

2. Marrow damage

Stem cell proliferation & differentiation

failure hipoplastic, aplastic

3. Bone marrow replacement:

* fibrosis,

* infiltration (lekemia, limfoma),

* metastatic neoplasm


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IV. Maturation defect/maturation

disorder

1. Cytoplasmic maturation defect

Abnormal globin development

thalassemia

Abnormal iron metabolism: Iron def An,ACD

Abn porphyrin synthesisAn.

sideroblastik

2. Abnormal nuclear development :

Vit B12 deficiency

folic acid deficiency


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Anemia

Klasifikasi morfologi

Defek fungsional

A. mikrositik hipokromik

A. normositik normokromik

A. Makrositik

Destruksi

Blood Loss:

Kronik

Akut

Hemolitik

Defek maturasi Hipoproliferatif

Inti : A. Megaloblastik

Sitoplasma :

- Fe : A..Def Besi

- Heme:A.Sideroblastik

- Globin:

* Thalassemia

* Hb Pati

- Peny. Ss tulang

Intrinsik : aplastik

Infiltasi: lekemia

-Peny. Kronis

-Peny. Endokrin

-Peny. GinjalExtrapusculer

Intracorpusculer

Imun Non Imun

HDN

Reaksi

transfusi

AIHA

Drug induce

Infeksi virus

H.mekanis:

disfungsi

katub, MAHA

Bahan kimia,

luka bakar

Inf.parasit:

malaria

Herediter

Defek struktur globin:

-Kuantitas: thalassemia

-Kualitas:

sickle cell,

Hb-pati

Defek membran:

sferositosis hered,

elliptositosis hered.

Defek enzim: def.G6PD,piruvat kinase

Didapat

Defek

membran

erits: PNH


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Classification of anaemia


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Measurement of :

Hb, RBC count, Hct , MCV,MCH,MCHC

Manual /

Automatic Cell

Counter

Direct examination of redcell morphology in a

stained blood film

Morphologic classification of anemia according to RBCcount, size & Hb content.

MORPHOLOGY

The components of the CBC

also help in the classification

of anemia. Microcyt icisreflected by a lower than

normal MCV (100) reflect

macrocyt ic. The MCH and

MCHC reflect defects in

hemoglobin synthesis(hypochromia).


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MCV: Mean Corpuscular Volume: Is the average

volume of the RBC, ex pressed in FL (10-15/L) &

calculated as follows

Hct (%)

MCV= x 10 (Normal 81-100 fL/m3)

RBC count (x 106/L)

MCH: Mean Corpuscular Haemoglobin: is the average

weight of Hb in an each RBC, expressed in

picogram/10-12g

Hb (gm/dl)

MCH= x 10 (Normal 26-34 pg)

RBC count (x 106

/L)


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MCHC: Mean Corpusc Haemoglobin Conctr

is the average concentration of Hb

Hb (gm/dl)

MCHC= x 100% (Normal 31- 36%)Hmt (%)


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MACROCYTIC NORMOCHROMIC ANEMIA

RBC size > 8 m

normal Hb content

RBC count relatively low compared to Hb

MCV MCH, normal MCHC.

* Macrocytosis associated with a megaloblasticmarrow

(marrow erythroid precursor with morphologicabnormality, increase in size )

vit B12, folic acid deficiensy* Macrocytosis associated with anormoblasticmarrow:

* hemorrhagic & hemolysis

*def. folic acid/vit B12

reticulocytosis+


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- Low Hb- Normal MCV / MCH/ MCHC- Acute hemorrhage-Hemolytic anemia

- Disturbed iron utilizationAnemia of chronic disorders (ADC)

-B.Marrow disease:Intrinsic or infiltration

Aplastic An., metastatic,

lekemia, lymphoma, myeloma-Decreased erythropoietin drive-chronic renal failure-endocrin disorders

Anemia with appropriate

marrow response

Anemia with

inadequate

marrow

response

ANEMIA NORMOCYTIC NORMOCHROMIC


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Inadequat Hb formationRBC count relatively high compare with [Hb]

low MCV & MCH, MCHC

Blood film : Impaired Hb contentRBC size


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Normal Blood


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Normocytic - normochromic


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CLINICAL PRESENTATION OF

ANEMIA

1 Mild

2 Moderate

3 Several


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Table 61-1. Laboratory Tests in Anemia

Diagnosis

I. Complete blood count (CBC)A. Red blood cell count

1. Hemoglobin

2. Hematocrit

B. Red blood cell indices

1. Mean cell volume (MCV)

2. Mean cell hemoglobin (MCH)

3. Mean cell hemoglobin concentration

(MCHC)

4. Red cell distribution width (RDW)C. White blood cell count

1. Cell differential

2. Nuclear segmentation of neutrophils

D. Platelet count


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E. Cell morphology

1. Cell size

2. Hemoglobin content

3. Anisocytosis

4. Poikilocytosis

5. Polychromasia

II. Reticulocyte count

III. Iron supply studies

1. Serum iron

2. Total iron-binding capacity

3. Serum ferritin, marrow iron stain

IV. Marrow examination

A. Aspirate1. E/G ratioa2. Cell morphology3. Iron stain

B. Biopsy

1. Cellularity2. Morphology


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Approach to the Pat ient

Sign and Simptoms

Such as bleedingFatique

Malaiese

Fever

Weight loss

Sistemic symptoms

blood in the stool,

lymphadenopathy,

splenomegaly

petechiae.


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Iron Deficiency Anaemia

microcytic hypochromic anaemia

Ferrum = a constituent of hemoglobin

The aims in treating iron deficiencyanaemia :

* To remove the cause

* To increase red cell mass bygiving iron


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Causes of Iron Deficiency Anaemia

1. Chronic blood loss

* Gastrointestinal

- Disease of the GI tract (i.e. peptic ulcer,carcinoma of the large bowel, intestinal

parasites)- Drug induced ( i.e. aspirin , other NSAID)

- Menstrual (over 80 ml/cycle = 45 mg iron)

- Recurrent haemoptysis ( i.e. vascular

abnormalities, pulmonary haemosiderosis)


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2. Increased requirements

PregnancyTreatment of

megaloblastic anaemia

3. Malabsorption

Malabsorption syndromes

Post gastrectomy

4. Dietary deficiency


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Table 105-1. Body Iron Distribution

Iron Content, mg

Adult Male (80kg)

Adult Female (60kg)

Hemoglobin 2500 1700

Myoglobin/enzy

mes

500 300

Transferrin iron 3 3

Iron stores 600-1000 0-300


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Table 105-4. Diagnosis of Microcytic Anemia

Tests Iron

Deficiency

Inflammatio

n

Thalassemia Sideroblastic

Anemia

Smear Micro/hyp

o

Normal

micro/hypo

Micro/hypo

with

targeting

Variable

SI


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TREATMENT:

1. Suplement Fe oral

2. Fe Parenteral

M l bl ti A i


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Megaloblastic Anemia

The cell proliferation are needed an adequate folate and vitamin B12.

Folate = efficient thymidilate synthesis and production of DNA.

B12 = incorporate circulating folic acid into developing RBCs and retaining thefolate in the RBC.

Lack of folate or B12

decreased dTTP synthesis

a slowing of DNAsynthesis.

A i


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Anemia :

history and symptoms Tired

pallor

infections slow growth

pica (eating stones, mud, paper)

ask for:

diet (enough and good food?)

family history (hereditary disease?)


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Etiology Megaloblastic anemia

Malabsorbsi

Gastrointestinal disease

Malnutrition Inadekuat intake


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What about the food?

Does it contain meat, fish, egg,

vegetables? Contain iron

Does it contain fruit/juice? Vit C doubles iron absorption

Does child drink tea often? Tea halves iron absorption

Does child drink cows milk? Can induce allergy and less resorption

Special attention points for


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Special attention points for

doctors :

General well being nutritional status

sick or not? tachycardia?

pallor, icterus icterus may point to hemolysis

spleen, liver enlargement spleen: hemolysis?

enlargement spleen+liver: malignant?

lymph nodes general enlargement: leukemia?


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Nutritional anemia

Iron deficiency

microcytic

iron is needed for Hb production, so absence

causes low Hb and therefore small cells

Vit B12 or Folic acid

megaloblastic B12 and F are needed for cell division, so

absence causes low Ery count and large cells


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Screening tests

1. CBC :

MCV 100-150 fL range (>120 fL)

RDW

Morphologic: oval macrocytes andhypersegmented neutrophils (the cause isnot understood)


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The peripheral blood reveals a pancytopenia

(decreased RBCs, white cells, and platelets),

hypersegmented neutrophils (> five lobes), and

oval macrocytes.


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AplasticAnemia

bone marrow produces too few of all three types

of blood cells: red blood cells, white blood cells,

and platelets.

A reduced number of red blood cells causes

hemoglobin to drop. A reduced number of white

blood cells makes the patient susceptible to

infection. And, a reduced number of plateletscauses the blood not to clot as easily.


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Clinicallyand Diagnostic

pancytopenia- decreased numbers oferythrocytes, leukocytes, and platelets in theperipheral blood. anemia syndrome, infection,hemorhage.

Aplasia must be confirmed by bone marrowbiopsy.

Other hematopoietic disorders can present with

pancytopenia and must be distinguished fromaplastic anemia. These include paroxysmalnocturnal hemoglobinuria, myelodysplasia, andacute leukemia.


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Manajemen


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Anemia in Systemic Diseases

1. Anemia of Chronic Disease

2. Anemia with Chronic Endocrine Disease

3. Anemia with Chronic Renal Disease4. Anemia associated with Liver Disease

Anemia of Chronic


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Anemia of Chronic

DiseaseACD is associated with an underlying disease(usually inflammation, infection, or malignancy), but iswithout apparent cause (not due to a lack of thenutrients iron, vitamin B 12, or folic acid). ACDresolves when the underlying disease resolves.

Anemia of chronic disease (ACD) is difficult to defineas its eitology and pathogenesis is not clear.

ACD is the most common anemia in hospitalizedpatients.

Ca ses of Chronic inflammatory diseases


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Causes of

Anemia of

ChronicDisease

Chronic inflammatory diseases

Infectious

Tuberculosis

Pulmonary infections,pneumonia

Pelvic inflammatory diseaseChronic fungal disease

Subacute bacterial endocarditis

Osteomyelitis

Meningitis

Non Infectious

Rheumatic arthritis

Thermal injury

Systemic lupus erythematosus

Malignant Disease

Carcinoma

Hodgkin Disease

Non-Hodgkin lymphoma

Leukemia

Multiple Myeloma

P th h i l


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Pathophysiology

1. Failure of erythropoiesis

2. Lack of iron forhemoglobin synthesis

3. Decreased RBC survival


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Anemia in Endocrine Disease

Anemia in DM patients:

ACD

Enteropathy poor absorption of iron,

vit B12, and folate.Suffer from chronic blood loss andchronic renal insufficiency


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Anemia with chronic Renal Disease

Pathophysiology:

1. Decreased erythropoiesisEPOor

nonfunctional

2. Azotemiasuppressed the bone marrow and

RBC survival

3. Chronic blood lossdefects of plt and vessel

4. Folate and iron deffChronic hemodialysis


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Anemia in Liver Disease

The most common liver disease linked to anemia inalcoholism

Anemia generall mild to moderate, but can periodically

become more severe

Pathophysiology:

1.Direct toxic effects of alcohol2.Various nutritional deficiencies

3.RBC survival defects

4.Abnormal iron metabolism

H l ti A i


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ClassificationExtracorpucular Hemolytic Anemiaa. Immune Hemolytic Anemia

1. Alloimmune Hemolytic Anemia

2. Autoimmune Hemolytic Anemia (AIHA)

3. Drug induce immune Hemolytic Anemia

b. Non-immune Hemolytic Anemia

1. Mechannical: arterial valve dysfunction- MAHA: TTP, HUS

2. Chemical, burn

3. Parasitic infection: malaria

Hemolytic Anemia


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Immune Hemolytic anemia

Alloimmune hemolytic anemia

Transfusion : ABO incompatibility

Hemolytic disease of the newborn (HDN)

ABO incompatibility

Rhesus incompatibility

Autoimmune hemolytic anemia

Warm-reactive antibodies Cold-reactive antibodies

Drug induce


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Gene Glycosyltransferase

(enzyme)

Immunodominant

Sugar

Antigen

H -2-L-fucosyltransferase L-fucose H

A

-3-N-

acetylgalactosaminyl

transferase

N-acetyl-D-

galactosamin A

B

-3-D-

galactocylltransferase D-galactose B

Donor nucleotides and immunodominant sugars responsible

for H, A and B antigen


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ANTIGLOBULIN TEST ( COOMBS TEST )

The antiglobulin test is based on the

principle that antihuman globulin(AHGs)obtained from immunized nonhuman speciesbind to human globulinsuch as

IgG or complement, either free in serum or

attached to antigens on RBCs


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Serum COOMBS (ANTIHUMAN GLOBULIN)


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Direct Antiglobulin Test /DAT

(Direct Coombs Test)

The DAT detects in vivo sensitization of RBCs with

IgG and/or complement components

Detects of incomplete antibody that has alreadyattached on RBCs

Clinical condition that can result in in vivo coating of

red cells with antibody an/or complement are:

Hemolytic disease of the newborn (HDN) Hemolytic transfusion reaction

Autoimmune and drug induce hemolytic anemia (AIHA)

Normal catabolism


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Normal catabolism

of aged RBCs

Intravascular


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hemolytic

anemia

Removal of hemoglobin from blood plasma after intravascular hemolysis


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Lysed RBC

In blood vessel

/dimers

Kidney

Hemoglobinuria

Hemosiderinuria

Urobilinogenuria


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Extravascular

hemolytic

anemia


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Clinically Findings

Symptomp of Anemia

Icteric

Organomegali (splenomegali)

Hematopoesis ekstra meduller

Change in colour of urin

Laboratory findings indicating accelerated RBCs


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destruction

Test sample Result of testing

Serum

Anticoagulated

blood

Urine

increased unconjugated bilirubin

increased LDH activity

absence of haptoglobin

decreased glycosylated hb

increased free hbincreased methemalbumin

decreased hemopexin

decreased hematocrit

decreased hb

decreased RBCs

increased urobilinogen

positive free hb

positive methemoglobin


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production

Test sample Result of testing

Anticoagulated

blood

Bone marrow

special studies

increased reticulocyte count

increased MCV

increase leukocytes

increased thrombocytes

presence of morphology specific to

hemolytic disorder (polychromasia, NRBCs)

presence of erythroid hyperplasia

increased plasma iron turnover

increased erythrocyte iron turnover

increased activity of certain erythrocyte

enzymes

Intravascular hemolytic anemia


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Intravascular hemolytic anemia

Serum:

increased unconjugated &bilirubin increased urobilinogen

increased LDH activity

absence of haptoglobin

decreased glycosylated hb

increased free hb

increased methemalbumin decreased hemopexin

Urine

increased urobilinogen (urobilinogenuria)

positive free hb (hemoglobinuria)

positive methemoglobin

hemosiderinuria

Stools

Fecal urobilinogen

Coombs test : + (positive)

Extravascular hemolytic anemia


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Extravascular hemolytic anemia

Serum: increased unconjugated bilirubin

increased conjugated bilirubin


Urine increased urobilinogen

Stools


Coombs test : + (positive)


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ALLOIMMUNE HEMOLYTICANEMIA

Hemolytic Transfusion Reactions


H l ti T f i R ti


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Hemolytic transfusion reactions result from intravascularbreakdown, which is commonly due to an incompatibilty in the

ABOsystem or to destruction occuring in the macrophage

system

Two types reactions: immediate & delayed

Immediate symptoms begin within minuteshours (chills, fever, urticaria,

tachycardia, nausea, vomiting, chest & back pain, shock,

anaphylaxis, pulmonary edema & congestive heart failure

The laboratory diagnosis:

Based on the evidence of hemolysis & a blood group incompatibility

Hemoglobinemia, hemoglobinuria

Bilirubin level is increased

The entire typing & crossmatch procedures should be repeated



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Delayed may occur days or weeks after transfusion

may result in jaundice and anemia due to hemolysis

development of undetected antibodies occurs 4-14 after

transfusion of apparently compatible blood

Patient has been alloimmunized by previous pregnancy or

transfusion

Antibody concentration at the time of transfusion was

below the level of serologic detection

DAT +


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Laboratory findings in HDN caused by ABOincompatibility: Anemia (anemia is milder than in HDN Rh

incompatibility) Increased reticulocyte count mikrospherocytosis Direct Coombs test +

Slightly increased of unconjugated bilirubin

Laboratory findings in HDN caused by Rhincompatibility: Mild severe anemia

Reticulocyte count > 10% NRBCs ++, polichromasia, leukocytosis,

thrombocytopenia Unconjugated bilirubin is markedly increase

Direct Coombs test ++


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HDN caused by destruction of the RBCs of the fetus

by antibodies produced by the mother

Only antibodies of the IgG class are actively

transported across the placenta

The antibodies are directed against those antigens

on the fetal RBCs that were inherited from the father

HDN

ABO incompatibility

Rh incompatibility

HEMOLYTIC DISEASES OF NEWBORN / HDN


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ABO INCOMPATIBILITY

HEMOLYTIC DISEASES OF NEWBORN / HDN

Mother: group O, fetus: group A/BMothers antibodies (IgG) enter across the placentaPromotes interaction of Ag-Ab

hemolysis

Ag-Ab

Mother, group O

lyse

Fetal circulation

B

Anti B

Anti A

B


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Hemolytic Disease of

Newborn (HDN)

Mother Rh -

Fetus Rh +


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AUTOIMMUNE HEMOLYTIC

ANEMIA(AIHA)

Autoimmune Hemolytic Anemia (AIHA)


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y ( )

16% cases

< 20C

Ig M

>> infectious diseases: MYCOPLASMA

PNEUMONIAE

Infectiousmononucleosis (EBV)

Cytomegalovirus HIV etc.

Intravascular hemolysis

70-75% cases

37C

Ig G

>> autoimmune disease: Lymphoproliferative ds

Systemic Lupus Erythematosus(SLE)

Infections diseases

Non-lymphoid neoplasm

Colitis ulcerative

drugs

Extravascular hemolysis

COLDWARM


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Laboratory findingsAnemia Increased reticulocyte count

Direct Coombs test +Mikrospherocytosis (warm ab), clumping (cldab)

increased of unconjugated bilirubin

Accelerated of RBCs productionAccelerated of RBCs destruction

Bl dAIHA


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Blood smear

Polychromasianucleated RBCs

Clumping (Cold-antibody)

Micro-spherocytes (warm-antibody) clumping


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Microangiopathic hemolytic anemia

Macrovascular hemolytic anemia

Hemolytic anemia caused by infection withmicroorganism

Hemolytic anemia caused by chemicals,

drugs and venoms

Hemolytic anemia caused by thermal injury

Non-immunohemolytic anemia

RBC b liti th t t


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RBC abnormalities that repressent

diagnostic characteristic (sickle cell,

spherocytes, target, fragmentocytes)


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Drugs and Chemicals


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g

Drugs and Chemicals that Have Been Reported to Cause

Clinically Significant Hemolytic Anemia.

CHEMICALS

Aniline

ApiolDichlorprop (herbicide)

Formaldehyde

Hydroxylamines

LysolMineral spirit

Nitrobenzene

Resorcin

DRUG:


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DRUG:

Amyl nitrite

MephenesinMethylene bule

Omeprazole

Phenazopyridine (Pyridium)Salicylazosulfapydine

Salicylazosulfapyridine (Azulfidine)

O gen


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Oxygen:

Hemolytic anemia has developed inpatientsreceiving hyperbaric oxygenation and in astronautsexposed to 100% oxygen.

Insect and Arachined venoms

Severe hemolysis may occur in some patients

following bites by bees wasps, spiders, or scorpionsSnake bites are only rarely a caused of hemolysis

Heat

Patient with extensive burns may develop severehemolytic anemia apparently as a result of directdamage to the red cells by heat

Hemolytic Anemia Resulting from Infectious


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y g

Agent

Mechanisms:

Hemolysis may be caused by:

Direct invasion by infecting organisms

(malaria)Elaboraion of hemolytis toxins (Clostridium

perfringens)

Development of autoantibodies againt red

blood cell antigens (Mycoplasma pneumoniae)


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Alhamdulillah

Aspek Klinis Anemia

Text of Aspek Klinis Anemia

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Aspek Klinis Anemia

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