Hematologic disorders in pregnancy Flashcards
Summary of normal hematologic changes during pregnancy
- Hemodilution
- Decreased hematocrit
- Slightly reduced platelets
- Increase in clotting factors
- Mild leukocytosis
Iron deficiency anemia
Management
- Dietary counseling (heme vs non-heme iron sources)
- 30 mg elemental iron
- ie Ferrous sulfate 325 mg bid-tid, 30 min before meals
- GI side effects: nausea, constipation, diarrhea
- Acid increases absorption → avoid antacids, H2 blockers (+ calcium)
- Consider IV iron if cannot tolerate PO or severe anemia
- small risk for anaphalaxis
- must give several times to see result
- Repeat CBC and ferritin in 4 wks
- if no improvement → test for bleeding and parasites
- Continue supplements for 4-6 months after levels back to normal
Iron deficiency anemia
Diagnosis
- Ferritin levels (status of iron stores) < 41 ng/mL
- MCV < 80 fL
- Decreased H/H
- Serum iron concentration < 60 mg/dL
- single normal serum iron doesn’t r/o iron def
- Transferrin sat < 16%
- Blood smear: microcytic hypochromic cells with some abnormally shaped RBC’s (pencil forms, aniscytosis, and large distribution of RBC size)
- Symptoms:
- Weakness/fatigue
- Dizziness
- HA
- SOB
- Restless leg
- Irritability
- Pica
Iron deficiency anemia
Pathophysiology
- 75% of anemia during pregnancy is secondary to iron deficiency
- Risks:
- Poor dietary iron intake
- Short interval between pregnancies
- Delivery complicated by hemorrhage
- Bone marrow, liver, and spleen iron stores depleted first → serum iron and transferrin sat decrease, TIBC increases (reflects unbound transferrin) → fall in Hgb/Hct → microcytic, microchromic RBCs released
Major food sources of iron
- Heme - more readily absorbed
- Animal products: meat, poultry, fish
- Non-heme - absorption affected by other substances such bovine milk/dairy, calcium and phosphorus, wheat and maize flour, zinc and cadmium, and phosphoprotein in eggs.
- grains, cereal, eggs, vegetables, fruits, and dairy products.
- Avoid coffee, tea, carbonated drinks - inhibits iron absorbtion
- Vitamin C aids in absorbtion
Food sources of folic acid
- Strawberries
- Green veggies
- Peanuts
- Lentils/Beans
- Liver
- Fortified breads and cereals
Folate deficiency anemia
Pathophysiology
- Most common cause of megaloblastic anemia during pregnancy
- Folate demands go up 4x (fetus) and absorbtion decreases (slow GI tract)
- Onset usually not before 3rd tri
Folate deficiency anemia
Diagnosis
- MCV > 100fL
- Serum folate level (shows recently ingested)
- RBC folate (better indicator at tissue level)
- Symptoms
- Symptoms of anemia
- Hyperpigmentation of the skin
- Low-grade fever
- Neurological sx: numbness/tingling in extremities, decreased metal alertness, and memory problems
- vitamin B 12 deficiency can also cause neuro sx so be sure to check level
Suspect folate deficiency if unexplained thrombocytopenia
Folate deficiency anemia
Management
- Diet - strawberries, green leafy vegetables, lentils, beans, peanuts, and fortified breads and cereals
- Supplement 5 mg folic acid/day x 4 months or through end of pregnancy
Sickle cell anemia and trait
Pathophysiology
- Genetic mutation (base pair substitution) causes HgS instead of HbA
- Autosomal recessive (must have HgSS to be affected, HgSA has trait)
- At low oxygen concentrations HgS forms sickle shape → sludging in vessels → occlusion → pain + microinfarctions
- Sickling can also be triggered by: dehydration, hypoxia, or acidosis
Risks of sickle cell disease during pregnancy
- Multiorgandysfunction
- SAB
- PTL
- PPROM
- Antepartum hospitalization
- Post partum infection
- IUGR/LBW
- Stillbirth
SCT - higher risk for UTI during pregnancy, pp endometritis, LBW
Sickle cell disease/trait
Diagnosis
- Hemoglobin electrophoresis
- FOB testing if mom is carrier
- > AA origin (1 in 12 has trait, 1 in 600 with HbSS)
- >Greek, Italian, Turkish, Arabian, Southern Iranian and Asian Indian
- Genetic counseling
Sickle cell disease/trait
Management
- Folic acid 4mg/day
- Acute tx of pain crisis or acute chest
- Supportive care (O2, hydration)
- Pain management
- Exchange transfusion (HbS40%, Hb>10)
Thalassemia
Pathophysiology
- Defect in the rate of globin chain synthesis
- Production/accumulation of abnormal globin subunits → ineffective erythropoiesis → RBC life span
- Ranges from minimal suppression of synthesis of the affected chain to its complete absence
- Can be alpha or beta chain
- Heterozygote often asymptomatic
Thalassemia
Diagnosis
- Hemoglobin electrophoresis
- can’t always detect → need genetic testing
- Screen if MCV is low with no iron deficiency
- MCH distinguishes between thalassemia minor, major, and intermedia
- Ferritin to r/o iron deficiency
- Homozygos alpha thalassemia → Hgb Bart → possible hydrops
- Heterozygous beta thalassemia (most common) → detected by elevated HgbA2 and HgbF
- Homozygous beta thalassemia (thalassemia major) → transfusion dependent, shortened life expectency, rarely become pregnant
- hepatosplenomegaly and bone changes secondary to increased hematopoiesis
Thalassemia
Management
Similar to sickle cell
Do not give iron unless its very necessary → potential for iron overload
Beta thalassemia - folic acid supplementation
Symptomatic thalassemia - need serial growth scans/NSTs