Anemia in Pregnancy Trans

7/28/2019 Anemia in Pregnancy Trans

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ANEMIA IN PREGNANCY

OBSTETRICS II 6th LONG EXAM

Dr. Ganzon


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HEMATOLOGIC CHANGES IN

PREGNANCY

Hypervolemic state

40-45% above non-pregnant blood volume

Occurs after 32-34 weeks AOG Also seen in hydatidiform moles (form of

pregnancy without fetus)


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HYPERVOLEMIA IN PREGNANCY

1. Meet metabolic demands of enlarged uterus

(hypertrophied blood vessels)

2. Provide abundant nutrients to rapidly

growing placenta and fetus

3. Protect mother and fetus from impaired

venous return in the supine and erect

positions

4. Protect mother from adverse effects of blood

loss during delivery


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BLOOD VOLUME INCREASE

12 weeks

- 15% increase

Much of the increase occurs in 2nd trimester

Slower rate in 3rd trimester then plateaus

Plasma & erythrocytes increase cause increased

volume

-Erythroid hyperplasia in bone marrow

-Elevated reticulocyte count

-Increased maternal erythropoeitin levels (peak during

early 3rd

trimester)


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HEMOGLOBIN & HEMATOCRIT

Hemoglobin & hematocrit decrease slightly

due to relative increase in plasma


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IRON METABOLISM

Total iron content = 2.0-2.5 g for normal adult women

Total iron stores = 300 mg

1000 mg of iron required for normal pregnancy

-300 mg actively transferred to fetus and placenta-200 mg lost, excreted via GIT

-500 mg stored in erythrocytes / red blood cells

Iron requirements 6-7 mg/day esp during midpregnancy

-iron supplements necessary during this time

-iron in diet & iron stores insufficient for metabolic needs

Around 5 months of gestation we give iron supplementation


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ANEMIAS IN PREGNANCY

Mostly occur or diagnosed during mid-

pregnancy

Most are relative decrease in hemoglobin and

hematocrit due to increased plasma volume

Influenced by economic status & dietary

customs


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CAUSES OF ANEMIA IN

PREGNANCYACQUIRED HEREDITARY

Iron deficiency anemia Thalassemias

Acute blood loss Sickle cell hemoglobinopathies

Due to inflammation or malignancy

sepsis, UTI

Other hemoglobinopathies

Megaloblastic anemia Hereditary hemolytic anemias

Acquired hemolytic anemia

Aplastic or hypoplastic anemia


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CONSEQUENCES OF ANEMIA IN

PREGNANCY

Increase risk of preterm birth

Low birthweight

Small for gestational age infants-related to degree of anemia

-influence on placental vascularization

-alteration in angiogenesis during earlypregnancy


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PARADOX OF INCREASED HEMOGLOBIN

CONCENTRATION IN PREGNANCY

Also increased risk for adverse perinatal

outcomes

Low plasma volume with increased red cell

mass

Also with increased preterm or growth

restricted infants (due to blood thickness)


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IRON DEFICIENCY ANEMIA

Seen as drop in hemoglobin concentration

3rd trimester; need for additional iron

-transport to fetus and augment maternal Hgb

-newborn of severely iron deficient mother does not

suffer iron deficiency anemia

-neonatal iron stores are related to maternal iron status

and timing of cord clampingMost common cause of anemia

During the 3rd trimester or 28th week of gestation there

is a need for more iron


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IRON DEFICIENCY ANEMIA

Hypochromic RBCs

Microcytosis

Serum ferritin lower than normal Due to expansion of plasma volume without

normal expansion of maternal Hgb mass


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DIAGNOSTICS

Hemoglobin/hematocrit

Red cell indices

Peripheral blood smear Sickle cell preparation (if African in origin)

very prone to sickle cell anemia

Serum iron / ferritin levels On CBC, if very low Hgb/Hct you may have IDA


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TREATMENT

Ferrous sulfate (oral)

Ferrous fumarate (oral) will not cause

vomiting compared to ferrous sulfate

Ferrous gluconate (oral)

-provide 200 mg of elemental iron per day

Ferrous sucrose safer than iron dextran(parenteral)

-continue treatment 3 months after anemia has

been resolved


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ACUTE BLOOD LOSS

Abortion, ectopic pregnancy, H.mole are

pregnancies that may also cause anemia due

to acute blood loss

Most common = obstetrical hemorrhage


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ASSOCIATED WITH CHRONIC

DISEASE Weakness

Weight loss

Pallor

Chronic renal failure (kidneys do not produce

erythropoeitin)

Cancer & chemotherapy

Human immunodeficiency virus infection Chronic inflammation (e.g. SLE)

-hypochromic & microcytic RBCs


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A. CHRONIC RENAL DISEASE

Erythropoeitin deficiency

Intensified during pregnancy

Ex: Acute pyelonephritis with sepsis -> anemia-acute red cell destruction from endotoxin

mediated sepsis. Treat with recombinant

erythropoeitin when hematocrit is 20% & lower


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MEGALOBLASTIC ANEMIA

Blood and bone marrow abnormalities

DNA synthesis is impaired

1. Folic acid deficiency2. Vitamin B12 deficiency


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FOLIC ACID DEFICIENCY

Pernicious anemia of pregnancydo not eat 3x a day

especially on charity patients

Neurologic abnormalities

Dietary insufficiency

-inadequate consumption of fresh green leafy vegetables,

legumes or animal protein

Consequently cause anorexia

Ethanol ingestion -> folic acid deficiency 400 ug/day is required

Hypersegmented neutrophilsmicroscopic examination

Newly formed erythrocytes


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Hypersegmented neutrophils

Newly-formed erythrocytes

Macrocytic RBCs Peripheral nucleated RBCs are also seen if folic

acid deficiency is severe


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Fetus & placenta extract folate from maternal

circulation

Folic acid, nutritious diet, & iron

1 mg folic acid per day for pregnant women

with folic acid deficiency

-4 mg if with previous baby with neural tube

defect

Prevents neural tube defects in fetus


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INCREASED FOLATE DEMANDS

DURING

Multifetal pregnancy

Hemolytic anemia

Crohns disease Alcoholism

Inflammatory skin disorders/problems


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VITAMIN B12 DEFICIENCY

Vitamin B12 = cyanocobalamin

megaloblastic anemia

Rare Addisonian pernicious anemia (lack of intrinsic

factor for absorption of vitamin B12)

May be due to partial or total gastric resection Associated with Crohn disease, ileal resection

& bacterial overgrowth in small bowel


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VITAMIN B12 DEFICIENCY

During pregnancy, cobalamin levels are low

-decreased binding proteins, haptocorrin &

transcobalamin II

Treatment would be 1000 ug vitamin B12 IM

monthly


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HEMOLYTIC ANEMIAS

Primary hemolytic anemias are of unknown causes

Most common are secondary types

1. Lymphomas

2. Leukemias

3. SLE

4. Connective tissue diseases

5. Infections

6. Drug induce antibodies (ketoconazole, cefuroxime)

7. Epstein barr virus


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AUTOIMMUNE HEMOLYTIC

ANEMIA COLD AGGLUTININ DISEASE

-Hemolysis

-Induced by infections (i.e. Mycoplasma pneumoniae or Epstein

Barr virus mononucleosis

Characteristics

-hemolysis

-positive antiglobulin test

-spherocytosis-reticulocytosis

Fetal red cells are not affected IgM does not cross placenta


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ANEMIA

Uncommon

Production of aberrant antibody

Positive Direct & Indirect Coombs test 80-90% caused by warm active autoantibodies

Primary AIHA have unknown causes

Secondary AIHA are due to:

-Lymphomas, leukemia, connective tissue

diseases, infections, chronic inflammatory

diseases & drug induced antibodies


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ANEMIA

Treatment:

Prednisone 1mg/kg per orem per daily

Blood transfusions should be at bodytemperature to prevent destruction by cold

agglutinins


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DRUG INDUCED HEMOLYTIC

ANEMIA

Mild resolves with withdrawal of the drug,

drug acts as hapten & it attaches to your RBC

& antibodies recognizes & destroys your RBC

Drug mediated immunological injury to red

cells

Probenecid, quinidine, rifampin, thiopental,

antibiotics and anti-fungals


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DRUG INDUCED HEMOLYTIC

ANEMIA

Mild to moderate chronic hemolysis

Also related to a congenital erythrocyte

enzymatic defect G6PD

G6PD deficiency undergoes hemolytic

anemia


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PREGNANCY INDUCED HEMOLYTIC

ANEMIA

Unexplained rare condition

Occurs during pregnancy

Immune mediated Intraerythrocytic or extraerythrocytic defects

Possibly an autoimmune disease


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PAROXYSMAL NOCTURNAL

HEMOGLOBINURIA

Hemolytic stem cell disorder (Intermittenthappening)

Defective platelets, granulocytes anderythrocytes

Acquired

Arises from one abnormal clone of cells

X-linked gene PIG-A (phosphatidyl glycanprotein

A) = abnormal anchor proteins on RBCs andgranulocyte membrane make them susceptible tolysis by complement


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HEMOGLOBINURIA

Chronic hemolytic anemia

Insiduous

Mild to lethal in form

Hemoglobinuria (red brown urine) at irregular

intervals

-initiated by blood transfusion, infection,surgery

- 40% have venous thrombosis, occurs in

legs/lower extremities


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HEMOGLOBINURIA

Renal failure , hypertension

Budd chiari syndrome

May need thrombocytic therapy/ anticoagulation

Very fatal if it occurs after delivery


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HEMOGLOBINURIA

Treatment

Bone marrow transplant

Eculizumab ( anti-body that inhibit complemnt

activation)

Have not been used in pregnant patient

Chemotherapy targeted agent


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HEMOGLOBINURIA

Fatal in 10-20% of pregnant women

Venous thrombosis in 50%of postpartum

women (ask if there is leg pain or difficulty of

breathing)


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SEVERE PREECLAMPSIA-

ECLAMPSIA

Fragmentation

Microangiopathis hemolysis with

thrombocytopenia

HELLP SYNDROME (hemolysis, elevated liver

enzymes, low platelet)


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BACTERIAL TOXINS

Most common pathogens;

Clostridium perfringens

Group A beta hemolytic streptococcus

Gram negative bacteria (lipopolysaccharide)

Cause hemolysis > mild to moderate anemia

Bacteremia from severe pyelonephritis


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HEMOLYTIC ANEMIA DUE TO

INHERITED ERYTHROCYTE DEFECTS

Mild to moderate anemia most common cause is

pyelonephritis, UTI not treated properly goes up to kidneys

Result in destabilization of membrane lipid layer of

erythrocytes

Surface area deficiency

Poorly deformable RBSs

Result in hemolysis

Hereditary spherocytosis

Pyropoikilocytosis

ovalocytosis


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HEREDITARY SPHEROCYTOSIS

Take out the spleen and patient is okay (but

dont do it in pregnancy)

Autosomal dominant -> spectrin

deficiency/ankyrin deficiency/ autosomal

recessive proteins in the membrane


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Autosomal dominant, variably penetrant

spectrin deficiency

Affect rbc membrane proteins

Autosomal recessoive or dde novo gene

mutations

Deficiency of ankyin, protein 4.2 moderate band 3


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Characteristics

Varying degrees of hemolysis

Jaundice

Spherocytosis on blood smear

Reticulocytosis

Inc. osmotic fragility


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CRISIS in H.S

Severe anemia

Accelarated RBC destruction

Spenic sequestration

Splenomegaly

Splenectomy is an option to reduce hemolysis,

anemia and jaundice Parvovius B19 known to cause hemolysis and

suppress bone marrow production


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HEREDITARY SPHEROCYTOSIS IN

PREGNANCY

Do well during pregnancy

Folic acid supplements are recommended

In new born who inherited HS, may exhibit

hyperbilirubinemia and anemia


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RED CELL ENZYME DEFICIENCIES

Permit anaerobic glucose may

Cause hereditary nonspherocytic anemia

Most are autosomal recessive

G6PD however is X-linked

Induced by drugs or infections

Variable hemolysis

Anemia is episodic


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RED CELL ENZYME DEFICIENCIES

Pyruvate kinase deficiency

Autosomal recessive

Variable anemia and hypertension

Iron overload common due to massive

transfusions

Hydrops fetalis is associated

Confirmed by venipuncture


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APLASTIC ANEMIA

Pancytopenia with hypoplastic bone marrow Grave coplication but rare

Linked with autoimmune disease

Induced by drug, infection, chemicals, radiation,leukemia, immunological disorders, fanconianemia, diamond blackfan syndrome

Marked decrease in committed marrow stem

cells Immune mediated

Difficult to manage


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APLASTIC ANEMIA

Hematopoietic stem cell transplantation

Treatment:

Immunosuppressive therapy + bone marrow transplant

75% with good response

Long term survival is seen withantithymocyte globulin

and cyclosporine

Antibiotic for infection and transfusion for anemia

20% HCT is ok for them Anemia caused by chemotherapy: patient may die

because of infection

If acquired in pregnancy, effects are hemorrhage and

infection and 50% is fatal


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APLASTIC ANEMIA IN PREGNANCY

Major risk: hemorrhage and infection

50% mortality rate

Treatment:

Antibiotics

Red cell transfusions

Maintain hct > 20 volume %

Platelet transfusion to control hemorrhage

Favor vaginal delivery section


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BONE MARROW TRANSPLANT

Can result in successful pregnancies

Risk of preterm delivery and hypertension


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CHRONIC AND ACUTE CHANGES IN


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CHRONIC AND ACUTE CHANGES IN

SICKLE CELL DISEASE Osteonecrosis of femoral and humeral head Renal medullary damage

Autosplenectomy in Hgb SS

Splenomegaly in other variants

Hepatomegaly

Ventricular hypertrophy

Pulmonary infarctions

Pulmonary hypertensions

Cerebrovascular accidents

Leg ulcers

Risk of infection and sepsis

RR for death = 4-11x


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SICKLE CELL IN PREGNANCY

Increased OR (odds ratio) for: Renal failure

Gestational hypertension/preeclampsia

Eclampsia

Placental abruption

Preterm delivery

Fetal growth restriction

Cerebrovascular vein thrombosis

Pneumonia

Deep vein thrombosis Pulmonary embolism

Cardiomyopathy

Pulmonary hypertension


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SICKLE CELL TREATMENT

Close observation! Prenatal folic acid 4mg/day

Pain is from intense sequestrationof sickled RBCs withinfarction of other organs

Treat Bacteriuria/ acute pyelonephritis If in pain, suspect crisis already

Advised to be vaccinated as they can get simpleinfections):

Pneumococcal

Flu vaccine Meningococcal vaccine

Acute chest syndrome Pleuritic chest pain, fever, cough, lung infiltrates, hypoxia


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LABOR AND DELIVERY

Similar to management of pregnant women

with cardiac problems (gravidocardiacs)

Comfortable but not heavily sedated

Epidural analgesia

Blood transfusion

Prophylactic red blood cell transfusion


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THALASSEMIAS

Impaired production of one or more of the

normal globin peptide chains

Abnormal synthesis, hemolysis -> anemia

Classified according to globin chain that is

deficient

Alpha or beta thalassemia, major types

Incidence 1 in 300-500 pregnancies


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GENOTYPES AND PHENOTYPES

genotype genotype phenotype

normal aa/aa -

Alpha thalassemia

(heterozygote)

-a/aa aa/-a Silent carrier

Alpha thalassemia

(heterozygote )

Alpha thalassemia

-a/-a

--/aa

Alpha thalassemia minor-

mild hypochromic

microcytic anemis

Compound heterozygousa/a

--/aa Hgb 4 with moderate tosevere hemolytic anemia

Homozygous a thalassemia --/-- Hydrops fetalis


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ALPHA THALASSEMIA

4 alpha globin chains

Severity depends on the combination of synthesis

impairement

Gene loci centered on chr.16 2 main groups:

Alpha deletion of both locci from one chr (--/aa)

Alpha single locus from one allele(-a/aa) or lossfrom each allele(-a/-a)

Hydrops fetalis happens when there is homozygous

alpha thalassemia


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BETA THALASSEMIA

Impaired production of beta globin chains or instabilityof alpha chains

Single nucleotide substitution

Transcription or translation defects

RNA splicing or modification

Frameshift-> unstable hemoglobins can be the cause

Gene cluster is on chr 11

Decrease beta chain production

Excess alpha chains precipitate ->membrane damage

Alpha chain instability


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Anemia in Pregnancy Trans