hemolytic anemia

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What is Anemia ?: 

What is Anemia ? Important to remember Anemia is a clinical sign of disease It is not a single disease by itself Need to look for the underlying cause ! Will we ignore a fever with out investigation ? Its diagnosis is not that simple !! We’ll make it Its very common and imp. in our practice Drug Rx. depends on the cause

Definition of Anemia : 

Definition of Anemia Decrease in the quantum of circulating red blood cell mass and there by ↓ O 2 carrying capacity Most common hematological disorder by far Almost always a secondary disorder As such, critical for all practitioners to know how to evaluate / determine its cause / treat

Normal Red Cells: 

www.drsarma.in Normal Red Cells No nucleus, enzyme packets Biconcave discs – Haem + Gl Center 1/3 pallor Pink cytoplasm ( Hb filled) Cell size 7- 8 µ - capill . 2 µ EM pathway, HMP Negative charge – no phago Na less, K more inside 100-120 days life span

The Factory – Bone Marrow: 

www.drsarma.in The Factory – Bone Marrow Sternum, pelvis, vertebrae, long bones, skull bones, Tibia (paed) From stem cells (pleuripotent) 75% of marrow for WBC 25% of BM for Red cells Erythrod / Granulocyte Ratio 1:3 E:G ratio increases in Anemia Large white areas are marrow fat

Hemoglobin (Hb): 

www.drsarma.in Hemoglobin (Hb)

HEMOLYTIC ANEMIA Hemolytic anemia = reduced red-cell life span : 

HEMOLYTIC ANEMIA Hemolytic anemia = reduced red-cell life span


HAEMOLYTIC ANAEMIAS The normal red cell life is 110-120 days after which the senile cells are removed by bone marrow and splenic macrophages. Reduced red cell survival leads to increased red cell production due to erythropoietin drive that can compensate for the reduced red cell life and maintain a normal Hb level. The mean red cell life is affected by molecular changes in either the red cell membrane or haemoglobin.

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A haemolytic state exists when the in vivo survival of the RBC is shortened. Anaemia occurs if the onset of haemolysis is sudden with no time for marrow compensation or in severe chronic haemolysis when the mean red cell life is very short.

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CLINICAL FEATURES Jaundice : generally mild and often not noticed by the patient. Anaemia : recent onset = acquired long-standing = possibly congenital. Haemoglobinuria : intravascular haemolysis. Urobilinogenuria : increased Hb catabolism. Splenic pain : spenomegaly or splenic infarction. Leg ulcers : intrinsic red cell disorders, e.g. sickle cell disease. Skeletal hypertrophy : severe congenital haemolytic anaemias and thalassaemias.


CLASSIFICATION OF HAEMOLYTIC ANAEMIAS GENETIC EXAMPLES Membrane: Hereditary spherocytosis elliptocytosis, pyropoikilocytosis Haemoglobin: Haemoglobinopathies Unstable haemoglobins Thalassaemias Enzymes: G6PD or PK deficiency Other: Abeta-lipoproteinaemia

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ACQUIRED EXAMPLES Immune: Isoimmune, autoimmune or drug Mechanical: March haemoglobinuria, burns or microangiopathy Infections: Malaria, Clostridium welchi. Bartonellosis (Oroya fever) Toxins: Arsenic, copper, lead, venoms Dyserythropoietic: PNH Other: Osmotic effects, liver disease, hypophosphataemia

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50% of patients infected with Mycoplasma pneumoniae show a rise in the titre of anti-I, an IgM cold antibody normally present in low titre. This antibody reacts optimally with adult red cells in the cold. Neonatal red cells only express i antigen and are therefore not agglutinated. Following infectious mononucleosis (IM) a similar cold-reacting antibody, anti-i, is frequently produced which in rare cases can affect adult red cells. Cold antibodies produced secondary to these infections are polyclonal (contain both lambda and kappa light-chains).


PATHOGENESIS AND CLASSIFICATION OF HEMOLYTIC ANEMIAS The course of the disease acute chronic The place of RBC distraction intravascular extravascular The whence acquired inherited

Etiologic and Pathogenetic Classification of the Hemolytic Disorders: 

Etiologic and Pathogenetic Classification of the Hemolytic Disorders I. Inherited Hemolytic Disorders A. Defects in the erythrocyte membrane 1. Hereditary spherocytosis D. Deficiencies of enzymes involved in the pentose phosphate pathway and in glutathione metabolism 1. Glucose-6-phosphate dehydrogenase (G6PD ) E. Defects in globin structure and synthesis 1. Unstable hemoglobin disease 2. Sickle cell anemia 3. Other homozygous hemoglobinopathies (CC, DD, EE; Chapter 52) 4. Thalassemia major 5. Hemoglobin H disease 6. Doubly heterozygous disorders (such as hemoglobin SC disease and sickle thalassemia)

Etiologic and Pathogenetic Classification of the Hemolytic Disorders: 

Etiologic and Pathogenetic Classification of the Hemolytic Disorders II. Acquired Hemoltyic Anemias A. Nonimmune: due to 1. Traumatic and microangiographic hemolytic anemias 2. Infectious agents 3.Chemicals, drugs, and venoms 4. Physical agents 5. Hypophosphatemia 6. Spur-cell anemia in liver disease 7. Vitamin E deficiency in newborns

Etiologic and Pathogenetic Classification of the Hemolytic Disorders: 

Etiologic and Pathogenetic Classification of the Hemolytic Disorders II. Acquired Hemoltyic Anemias B. Immunohemolytic anemias Iso (allo) immune: transfusion of incompatible blood Hemolytic disease of the newborn 2. Heteroimmune: Virus, bacterial infections, chemical, Drug-induced 3. Autoimmune hemolytic anemia Idiopathic (the essential cause is unknown) Secondary or symptomatic (in case of lymphoma, chronic lymphocytic leukemia, Other malignant disease, Immune-deficiency states, Systemic lupus erythematosus and other autoimmune disorders, Virus and mycoplasma infections) Autoimmune hemolytic anemia caused by warm-reactive antibodies (Coomb’s positive). Autoimmune hemolytic anemia caused by cold-reactive antibodies Cold hemagglutinin disease Paroxysmal cold hemoglobinuria

Etiologic and Pathogenetic Classification of the Hemolytic Disorders: 

Etiologic and Pathogenetic Classification of the Hemolytic Disorders II. Acquired Hemoltyic Anemias C. Paroxysmal nocturnal hemoglobinuria


CLINICAL MANIFESTATIONS Chronic Congenital Hemolytic Anemia: anemia, jaundice, the occurrence of crises, splenomegaly, and the development of cholelithiasis. Less common manifestations include chronic leg ulcers and bony abnormalities.
















ACQUIRED HAEMOLYTIC ANAEMIAS Immune mediated haemolysis is caused by the attachment of antibody to the red cell membrane. The rate and site of haemolysis depends on the type of antibody (IgG or IgM) and its ability to fix complement.

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The optimal temperature for binding of antibody is important. Usually, IgG antibodies are warm (37 0 C) and IgM are cold reacting. Cells coated with IgG are removed directly by splenic macrophages that bear Fc receptors. Both IgG and IgM can fix complement but usually only part of the sequence is fixed, thus avoiding intravascular haemolysis. Cells coated with C3 are removed by macrophages of the RE system but this component has a short half-life and gives rise to C3d to which macrophage receptors are insensitive.

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Part of the red cell membrane is lost during immune adherence and gives rise to spherocytes that are a feature of warm autoimmune haemolytic anaemia (AIHA). Cold-reacting IgM antibodies are more likely to trigger the entire complement cascade and give rise to intravascular haemolysis.

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Classification Of Immune Haemolytic Anaemias 1. Alloimmune : Transfusion reactions, Haemolytic Disease of the Newborn (HDN) 2. Autoimmune : Warm AIHA, Cold AIHA, Paroxysmal Cold Haemoglobinuria (PCH) 3. Drug-induced : Immune complex, drug adsorption (hapten), methyldopa-induced


ANTIGLOBULIN TESTS The direct antiglobulin test (DAT) is designed to react with cells bearing IgG and/or complement. IgM always binds complement so the reagent does not contain anti-IgM. Washed red cells are mixed directly with the antiglobulin reagent and agglutination recorded. The DAT is positive in most cases of AIHA. Monospecific reagents demonstrate IgG alone or together with C3 components. In immune haemolysis associated with SLE, IgG is detected together with C3. Only C3 is present in cold AIHA.

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The indirect antiglobulin test (IAT) is used to detect free antibody in the patient's serum using cells with known antigenic characteristics. It is often positive in severe AIHA. An eluate of antibody from the patient's cells can be used to determine antigenic specificity.

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Cold haemagglutinin disorders are characterised by in vivo agglutination of red cells at temperatures below 37 0 C . Cold autoantibodies are responsible for: secondary cold AIHA cold haemagglutinin disease (CHAD) paroxysmal cold haemoglobinuria (PCH)

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50% of patients infected with Mycoplasma pneumoniae show a rise in the titre of anti-I, an IgM cold antibody normally present in low titre. This antibody reacts optimally with adult red cells in the cold. Neonatal red cells only express i antigen and are therefore not agglutinated. Following infectious mononucleosis (IM) a similar cold-reacting antibody, anti-i, is frequently produced which in rare cases can affect adult red cells. Cold antibodies produced secondary to these infections are polyclonal (contain both lambda and kappa light-chains).

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The anti-I found in cold haemagglutinin disease (CHAD) and cold haemagglutination secondary to lymphomas is a monoclonal (IgM with kappa light-chain specificity). The low thermal amplitude of these antibodies results in red cell agglutination in the cooler peripheral circulation of the hands, feet, nose and ears. Intravascular haemolysis occurs if sufficient complement is bound.

Paroxysmal Cold Haemoglobinuria: 

Paroxysmal Cold Haemoglobinuria PCH is characterised by haemoglobinuria following cold exposure. It occurs in children in association with viral disorders and is caused by the Donath-Landsteiner antibody, an IgG biphasic haemolysin with anti-P specificity. Diagnosis rests on the demonstration of in vitro haemolysis when red cells and serum are first chilled (0 0 C) and then rewarmed (37 0 C). PCH is an acute haemolytic anaemia occurring almost exclusively in children and young adults.

Non-Immune Hemolytic Anemias: 

Non-Immune Hemolytic Anemias Hemolytic anaemias due to mechanisms or agents other than antibodies +/or complement e.g.: Mechanical (traumatic) (fragmentation) Toxins Infections Splenomegaly (hypersplenism) Burn (physical) Renal failure and liver failure Chemical

Non-Immune Acquired Hemolytic Anemia: 

Non-Immune Acquired Hemolytic Anemia Cause Infections Examples Malaria Babesiosis Bartonella Meningococcal sepsis Pneumococcal sepsis Gram-negative sepsis Clostridium perfringens Mechanisms Intracellular organisms Microangiopathic hemolysis Enzymatic toxins Cont…

Non-Immune Acquired Hemolytic Anemia: 

Non-Immune Acquired Hemolytic Anemia Cause Chemical & physical agents Mechanical lysis Acquired membrane disorder Examples Drugs Industrial/domestic substance Burns Drowning Diffuse intravascular coagulation Vasculitis Cardiac prostheses Liver disease Paroxysmal nocturnal hemoglobinuria Mechanisms Oxidative hemolysis Membrane damage Osmotic lysis Microangiopathic hemolytic anemia “ Foreign surface ” hemolysis Lipid abnormalities Somatic mutation

Mechanical (Traumatic) (Fragmentation): 

Mechanical (Traumatic) (Fragmentation) This is due to direct trauma (stress) to the RBCs causing fragmentation of the RBCs & intra-vascular hemolysis. The fragmented cells can be seen on peripheral blood smears & are called (schistocytes). Types: Cardiac – most common Due to: Prosthetic valves Patches Valvular diseasse e.g., stenosis Cont…

Mechanical (Traumatic) (Fragmentation) (cont…): 

Mechanical (Traumatic) (Fragmentation) (cont … ) Microangiopathic: mechanical hemolysis due to contact between the RBCs & the abnormal intema of thrombosed, narrowed, necrotic small vessels or fibrin strand formation. Caused by many diseases e.g., DIC (disseminated intravascular coagulation), malignant hypertension, disseminated malignancies especially mucin secreting adenocarcinomas, TTP (thrombocytopenic purpura), hemolytic uremic syndrome (HUS).

Causes of Microangiopathic Hemolytic Anemia: 

Causes of Microangiopathic Hemolytic Anemia Disease Hemolytic uraemic syndrome of childhood Hemolytic uraemic syndrome with bacterial infection (especially Esch . coli 0157) Thrombotic thrombocytopenic purpura Renal cortical necrosis Acute glomerular nephritis Pre- eclampsia Microangiopathy Endothelial cell swelling, microthrombi in renal vessels Endotoxaemia , microthrombi in renal arteries Platelet plugs, microaneurysms , arteriolitis . Necrotizing arteritis. Fibrinoid necrosis Cont…

Causes of Microangiopathic Hemolytic Anemia (cont…): 

Causes of Microangiopathic Hemolytic Anemia (cont … ) Disease Vasculitis Polyarteritis nodosa Wegener ’ s granulomatosis Systemic lupus Homograft rejection Meningococcal sepsis Carcinomatosis Primary pulmonary hypertension Cavernous haemangioma ( Kasabach - Merritt Syndrome) Microangiopathy Arteritis Microthrombi in transplanted organ Endotoxaemia , diffuse intravascular coagulation Abnormal tumour vessels, intravascular coagulation – local or diffuse Abnormal vasculature Local vascular changes and thrombosis

Mechanical (Traumatic) (Fragmentation) (cont…): 

Mechanical (Traumatic) (Fragmentation) (cont … ) Causes intravascular hemolysis Hemoglobinurea Hemoglobinemia Low haptoglobin Fragmented RBCs (schistocytes) on peripheral blood film Hemosidrinurea

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Clostidium Perfringens: Due to action of lipase and proteinase enzymes produced by the organism. Meningococcal: Due to DIC

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Malaria due to: Direct invasion causing intravascular lysis &/or extravascular lysis. Immune complex formation. Splenomegaly. Black water fever: Is an example of severe intravascular hemolysis due to falciparum sp.

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Chemical: e.g., some toxins e.g., spider venom, snake venom, bacterial toxins, arsenic (As), (Cu). Physical: Burn: characterized by the presence of many spherocytes in the peripheral blood. Splenomegaly Renal failure and liver failure Due to change in the metabolic structure of the RBCs,


DRUG INDUCED HAEMOLYTIC ANAEMIAS Immune Complex Mechanism Drug Adsorption Mechanism Methyldopa-induced Mechanism

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Immune Complex Mechanism (acute intravascular haemolysis) The drug, e.g. quinidine, provokes antibody formation and the resulting immune complex is loosely adsorbed onto the red cell where it can fix complement, detectable by the DAT. The red cells become " innocent bystanders ".

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Drug Adsorption Mechanism (slow reacting). The drug, e.g. penicillin, binds to the red cell and IgG against the drug then attaches leading to extravascular destruction of coated cells. The drug may act as a hapten and only provoke antibody formation after attachment to the red cell or after reacting with certain serum proteins. The DAT is positive due to IgG sensitisation. Intravascular haemolysis can occur if complement is fixed.

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Methyldopa-induced Mechanism . This was first reported in association with methyldopa. L-dopa and aldomet can cause haemolysis by a similar mechanism . After at least four months of treatment, 15-20% of patients develop a positive DAT due to IgG coating but less than 1% show evidence of haemolysis. The antibody often shows Rh specificity (anti-e). Haemolysis is extravascular.


NON-IMMUNE HAEMOLYTIC ANAEMIA Haemolysis Caused Directly by Infection Mechanical Causes of Haemolysis Chemical and Physical Causes of Haemolysis Acquired Membrane Disorders

Haemolysis Caused Directly by Infection: 

Intracellular infection : Malaria and Babesiosis (parasites physically disrupt the red cell membrane). Extracellular Infection : Bartonella and Clostridia welchi attack the red cell membrane with enzymes. Bacterial sepsis produces haemolysis secondary to DIC. Red cells are also vulnerable to certain viruses. Haemolysis Caused Directly by Infection


MECHANICAL CAUSES OF HAEMOLYSIS Red cells are flexible and must deform many times during their lifespan to pass through small capillaries. Fragmentation occurs when excessive shear stresses are applied resulting in intravascular haemolysis and/or the formation of red cell fragments (schistocytes).

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Cardiac Prosthesis Shear stresses are caused by turbulent blood flow in a high pressure system. This arises around prosthetic heart valves, particularly if the valve malfunctions.

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Micro-Angiopathic Haemolytic Anaemia (MAHA) results from small blood vessel abnormalities that impede blood flow, e.g. fibrin deposition, microthrombi and disseminated intravascular coagulation (DIC). The coagulation screen may be abnormal with associated thrombocytopenia due to chronic DIC.

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Thrombotic Thrombocytopenic Purpura (TTP) is related to aggregation of platelets in small capillaries with consequent occlusion of the vessel by platelet plugs and fibrin. Haemolytic Uraemic Syndrome (HUS); there is endothelial damage with fibrin deposition in small vessels. HUS is characterised by intravascular haemolysis, renal failure and thrombocytopenia.

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March Haemoglobinuria First described in a German soldier after marching exercise. The anaemia has been described in joggers and marathon runners. Red cells are disrupted as they pass through capillaries subjected to pounding. Haemoglobinuria is only present following exercise.

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A careful history and examination will often reveal the cause of mechanical haemolysis as indicated by the presence of red cell fragments in the peripheral blood. Perls's stain of urinary sediment can show the presence of iron; a useful test for any chronic low grade intravascular haemolysis when there is little evidence on blood film inspection.


CHEMICAL AND PHYSICAL CAUSES OF HAEMOLYSIS Oxidative Haemolysis Nonoxidative Haemolysis Osmotic Effects Burns

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Oxidative Haemolysis : Oxidative stress on the red cell may affect the haemoglobin molecule with either the globin chains or the haem group being affected. Most oxidizing agents will produce either Heinz body formation by denaturing globin chains or by oxidizing the haem group to produce methaemoglobinaemia .

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Nonoxidative Haemolysis : Arsenic, lead and copper are all toxic agents and can produce haemolytic anaemias . Venoms, e.g. from spiders, bees and snakes, contain potent enzymes causing haemolysis.

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Osmotic Effects : Survivors of near drowning in fresh water may show evidence of intravascular haemolysis. The peripheral blood generally shows many spherocytes . Burns : Patients who have suffered severe burns to greater than 15% of their body will generally show evidence of intravascular haemolysis due to the formation of heat induced spherocytes .


ACQUIRED MEMBRANE DISORDERS Some mechanisms can produce changes to the red cell membranes that can result in the shortened lifespan of the cell. Any change that compromises the cell's deformability or its resistance to oxidative stress can contribute to a haemolytic process. Lipids in the red cell membrane are in equilibrium with those of the surrounding plasma. The lipid content of the plasma therefore affects that of the red cell and may lead to changes in the shape and osmotic fragility of the cell.

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Liver disease : Hepatocellular disease or biliary obstruction usually lead to the presence of target cells but not to haemolysis. In severe hepatocellular disease and alcoholic cirrhosis, however, spur cells and acanthocytes may be seen with evidence of reduced red cell survival. Abeta-lipoproteinaemia : This is a rare, recessively inherited deficiency of beta lipoprotein that leads to an imbalanced distribution of membrane phospholipids. Most of the circulating red cells are acanthocytes with reduced life span.

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Vitamin E Deficiency : Alpha tocopherol protects polyunsaturated fatty acids in the red cell membrane against oxidative stress. Deficiency has been implicated as the cause of a haemolytic anaemia with acanthocytosis seen in infants. Hypophosphataemia : Starvation or misuse of antacids can lead to depression of the serum phosphate with consequent depletion of intracellular phosphate that is necessary for ATP production. This leads to an acquired spherocytic haemolysis that is readily reversed by phosphate administration.

Paroxysmal Nocturnal Haemoglobinuria (PNH): 

Paroxysmal Nocturnal Haemoglobinuria (PNH) PNH is an acquired intracorpuscular defect due to an abnormality in haemopoietic cell membranes. This abnormality causes cells, especially erythrocytes, to be more sensitive to the lytic action of complement. The abnormal clone, usually co-existing with normal haemopoietic cells, results in cells that are deficient in a membrane regulatory protein of complement known as decay-accelerating factor (DAF).

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DAF regulates C3 activation by accelerating the spontaneous decay of C3 convertase for both complement activation pathways. Patient's red cells may be graded as Type I to Type III according to complement sensitivity or DAF content. Their proportions will vary with time, with Type III cells often disappearing after an episode of haemolysis. PNH is associated with other disorders of the bone marrow such as hypoplasia and myeloproliferative disorders.

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Diagnosis is made by demonstrating a positive acidified serum lysis test (Ham's test). The sucrose lysis test (also positive) is useful for initial screening of suspected cases of PNH. Red Cells + Fresh Serum + Acid = Haemolysis (Complement) Red Cells + Fresh Serum = No Haemolysis Red Cells + Acid = No Haemolysis

The Three Primary Measures: 

www.drsarma.in The Three Primary Measures Measurement Normal Range RBC count (RCC) 5 million 4 to 5.7 Hemoglobin 15 g% 12 to 17 Hematocrit (PCV) 45 38 to 50 A x 3 = B x 3 = C - This is the rule of thumb Check whether this holds good in a given result If not -indicates micro or macrocytosis or hypochro.

The Three Derived Indicies: 

www.drsarma.in The Three Derived Indicies Measurement Normal Range RCC 5 million 4 to 5.7 Hemoglobin 15 g% 12 to 17 Hematocrit 45 % 38 to 50 MCV C ÷ A x 10 = 90 fl MCH B ÷ A x 10 = 30 pg MCHC (%) B ÷ C x 100 = 33%

Types of Anemia: 

www.drsarma.in Types of Anemia

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www.drsarma.in Anemia Suspected Thorough Clin, Bleed Hb%, RCC, Hct Decreased RPI, Retic count <2 RPI, Retic count >2 Hemolytic Anemia Coombs DAT, IDAT Hb electrophoresis Osmotic fragility MCV, MCH, MCHC, PSE Microcytic hypochromic Macrocytic hypo/normo Megaloblastic Normoblastic Iron Def. Anemia Ferritin, TIBC, BM Fe Thalassemia, Hb pathy Sederoblastic Anaem. Chr. Infection, Lead Folate defici. B12 def., PA Ca, Leukemia, Ulcer Identify the cause ALD, CLD, Drug Chr. Renal dis. Hypothyroid BM infiltration Acid hemolysis Cold agglutinins Coagulopathy, DIC Algorithm for Diagnosis of Anemia

Hemolytic Anemia: 

www.drsarma.in Hemolytic Anemia Anemia of increased RBC destruction – Normochromic, normocytic anemia – Shortened RBC survival – Reticulocytosis – due to ↑ RBC destruction Will not be symptomatic until the RBC life span is reduced to 20 days – BM compensates 6 times

Tests Used to Diagnose Hemolysis : 

www.drsarma.in Tests Used to Diagnose Hemolysis Reticulocyte count Combined with serial Hb Hemoglobin electrophotesis Serum LDH Serum bilirubin Haptoglobin Urine hemosiderin Hemoglobinuria

Findings in Hemolytic Anemia: 

www.drsarma.in Findings in Hemolytic Anemia Reticulocyte count and RPI Increased Serum Unconjugated Bilirubin Increased Serum LDH 1: LDH 2 Increased Serum Haptoglobin Decreased Urine Hemoglobin Present Urine Hemosiderin Present Urine Urobilinogen Increased Cr 51 labeled RBC life span Decreased

Tests to define the cause of hemolysis : 

www.drsarma.in Tests to define the cause of hemolysis Hemoglobin electrophoresis Hemoglobin A 2 ( β eta-Thalassemia trait) RBC enzymes (G6PD, PK, etc) Direct & indirect antiglobulin tests (immune) Cold agglutinins Osmotic fragility (spherocytosis) Acid hemolysis test (PNH) Clotting profile (DIC)


www.drsarma.in MAHA Micro Angiopathic Hemolytic Anemia


www.drsarma.in MAHA Micro Angiopathic Hemolytic Anemia

Hyperactive BM – Skull Hemolytic Anemia : 

www.drsarma.in Hyperactive BM – Skull Hemolytic Anemia

Hemolytic Uremic Syndrome: 

Hemolytic Uremic Syndrome Acquired-disorder affecting mainly infants and children. Characterized by: Intravascular hemolysis Renal failure Thrombocytopenia

Classification : 

Classification Sporadic: Occuring denovo with no preceeding disease. Believed to be due to an inherited defect in vascular hemostasis. Epidemic, typical form: Following a systemic illness of fever, diarrhea and vomiting. In many cases, no organisms are identified. However, in some cultures are positive e.g., for E. coli. Mechanisms: Endothelial swelling & disruption resulting in platelet deposition on the vessel wall.

Clinical Features: 

Clinical Features Jaundice, hemoglobinuria, proteinuria. Hypertension, uremia, oliguria. Anemia, thrombocytopenia purpura. CNS – unusual: convulsion, coma

Laboratory Findings (Cont…): 

Laboratory Findings (Cont … ) Chemistry: Elevated urea Elevated creatinine Elevated bilirubin Proteinuria + hemoglobinuria Coagulation: Prolonged PT, PTT but not always

Laboratory Findings: 

Laboratory Findings Blood film: Fragmentation of RBCs Thrombocytopenia Polychromasia CBC: Anemia Thrombocytopenia: usually <50,000 Bone marrow: Hypercellular with increased erythropoiesis + increased megakaryopoiesis

Stomatocytes Slit like central pallor in RBC : 

www.drsarma.in Stomatocytes S lit like central pallor in RBC Liver Disease Acute Alcoholism H Stomatocyosis Malignancies

Echinocytes Evenly distributed spicules > 10: 

www.drsarma.in Echinocytes Evenly distributed spicules > 10 Uremia Peptic ulcer Gastric Ca PK-D Called Burr Cells

Acanthocytes 5-8 spikes of varying length, irregular intervals: 

www.drsarma.in Acanthocytes 5-8 spikes of varying length, irregular intervals Called Spur Cells, Occur in A H A


www.drsarma.in Shistocytes MAHA Prosthetic valves Uremia Malignant HT Fragmented, Helmet or triangle shaped RBC

Leukoplakia - Aplastic Anemia: 

www.drsarma.in Leukoplakia - Aplastic Anemia Chloramphenicol Neomercazole Sulfonamides Analgin Phenytoin Butazolidin group Anti Ca drugs

Normal BM High Power: 

www.drsarma.in Normal BM High Power E : G = 1 : 3