Hematologic disorders in pregnancy Flashcards

1
Q

Summary of normal hematologic changes during pregnancy

A
  1. Hemodilution
  2. Decreased hematocrit
  3. Slightly reduced platelets
  4. Increase in clotting factors
  5. Mild leukocytosis
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2
Q

Iron deficiency anemia

Management

A
  • 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
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3
Q

Iron deficiency anemia

Diagnosis

A
  • 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
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4
Q

Iron deficiency anemia

Pathophysiology

A
  • 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
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5
Q

Major food sources of iron

A
  • 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
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6
Q

Food sources of folic acid

A
  • Strawberries
  • Green veggies
  • Peanuts
  • Lentils/Beans
  • Liver
  • Fortified breads and cereals
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7
Q

Folate deficiency anemia

Pathophysiology

A
  • 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
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8
Q

Folate deficiency anemia

Diagnosis

A
  • 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

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9
Q

Folate deficiency anemia

Management

A
  • 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
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10
Q

Sickle cell anemia and trait

Pathophysiology

A
  • 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
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11
Q

Risks of sickle cell disease during pregnancy

A
  • Multiorgandysfunction
  • SAB
  • PTL
  • PPROM
  • Antepartum hospitalization
  • Post partum infection
  • IUGR/LBW
  • Stillbirth

SCT - higher risk for UTI during pregnancy, pp endometritis, LBW

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12
Q

Sickle cell disease/trait

Diagnosis

A
  • 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
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13
Q

Sickle cell disease/trait

Management

A
  • Folic acid 4mg/day
  • Acute tx of pain crisis or acute chest
  • Supportive care (O2, hydration)
  • Pain management
  • Exchange transfusion (HbS40%, Hb>10)
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14
Q

Thalassemia

Pathophysiology

A
  • 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
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15
Q

Thalassemia

Diagnosis

A
  • 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
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16
Q

Thalassemia

Management

A

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

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17
Q

Discuss laboratory values associated with different anemias

A
18
Q

Common causes of thrombocytopenia

A
  • Gestational thrombocytopenia
  • Severe preeclampsia
  • HELLP syndrome
  • Disseminated intravascular coagulation
19
Q

Thrombocytopenia lab workup

A
  • CBC (exclude pancytopenia) and SMEAR of peripheral blood (rule out clumping~pseudothrombocytopenia)
  • HISTORY (PEC/meds/family)
  • If drugs and medical disorders are excluded- most likely ITP or GTP
    • < 100 x 109/L more likely ITP, <50 almost positive ITP
    • GTP can happen in 1st tri
  • SUDDEN onset in 3rd tri
    • Think PEC, TTP, HUS, AFL or DIC—then ITP
20
Q

Medications that cause thrombocytopenia

A
  • ANALGESICS: ASA, Acetaminophen, Indomethacin
  • ANTIBIOTICS: Ampicillin, PCN, Bactrim
  • Others:
    • Heparin
    • Methyldopa
    • Digitalis
    • Cyclosporin
    • Anticonvulsant therapy
21
Q

Gestational thrombocytopenia

Incidence

A
  • Most common cause of thrombocytopenia during pregnancy (80% of thrombocytopenias)
  • Onset mid-2nd to 3rd tri
  • 5 - 11% of pregnant people
22
Q

Gestational thrombocytopenia

Pathophysiology

A
  • Not merely dilution of platelets with increasing blood volume
  • Also appears to be due to an acceleration of the normal increase in platelet destruction that occurs during pregnancy.
  • Low risk to fetus
23
Q

Gestational thrombocytopenia

Diagnosis

A
  • No test for it besides platelets
  • Most cases are mild (120,000 - 149,000)
    • 1% of cases are 50,000 - 99,000
  • If platelets continue to fall < 50,000 → consider another dx
  • Mean platelet volume (MPV) is increased
24
Q

Immune Thrombocytopenic Purpura

Treatment

A
  • Similar to non pregnant pt
  • Safe in 1st and 2nd tri
    • If plts < 30K, bleeding occurs or procedure required
    • Glucocorticoids (methylprednisolone)
      • Exacerbate GDM, HTN
      • Watch electrolytes
      • If taken for more than 2-3 weeks → may need more sterioids during L&D due to adrenal suppression → be sure to taper off after
    • IVIG (2nd line)
  • Refractory cases → splenectomy
    • can be performed safely in 2nd and 3rd tri
25
Q

Immune Thrombocytopenic Purpura

Patho/Indicence/Dx

A
  • Occurs generally 1st tri (but can be anytime)
  • Fetal complications virtually non-existant
  • Often IgG mediated
  • Occurs often in people 18 - 40
  • 2/3 women only require observation, 1/3 women require tx
  • Diagnosis of exclusion:
    • Isolated thrombocytopenia with unremarkable peripheral smear
    • Only bleeding clinicaly consistent with a depressed platelet count (ie petechiae)
    • Not taking any meds/herbs/ilicit drug that may cause thrombocytopenia
    • No other disease process that can cause thrombocytopenia
26
Q

Neonatal alloimmune

A
  • Like Rh isoimmunization but with platelets
  • Pregnant parent lacks a specific platelet antigen and develops antibodiesto this antigen → if fetus inherits an antigen from FOB and pregnant parent lacks the antige→ parental antibody can develop → cross the placenta→ severe neonatal thrombocytopenia and possibly fetal intracranial hemorrhage.
  • Pregnant parent has normal platelets
  • Most common antibodies noted in these patients is anti–HPA-1a antibodies (others identified)
  • If neonatal alloimmune suspected → send parental blood to reference laboratory with experience in diagnosing neonatal aloimmune thrombocytopenia.
  • Manage in a tertiary care center with experience caring for this rare disorder
27
Q

Describe the process of alloimmunization

A

Fetomaternal hemorrhage (FMH) occurs in the antenatal period or, more commonly, at the time of delivery.

If ABO blood type incompatibility exists between the pregnant parent and fetus, anti-A and/or anti-B antibodies lyse the fetal cells in the parental circulation and destroy the RhD antigen.

28
Q

List reasons for the failure of Rh immunization prevention

A
  • Failure to identify Rh+ fetus in Rh- parent
  • Not treating during bleeding, esp in early pregnancy or with trauma
  • > 30 mL fetal whole blood exposure in delivery and only got 300 iU of Rhogam (standard dose)
29
Q

Rosette + KB test (Kleihauer-Betke)

A
  • Routine screening at delivery for fetalmaternal hemorrhage
  • Rosette test - qualitative test
    • If negative → give standard dose of 300iU Rhogam
    • If positive → KB stain or fetal cell stain using flow cytometry to understand quantitative amount
  • KB - % fetal cells in parental blood
    • used to calculate amount of Rhogam needed
30
Q

Describe the timetable and active agent in the primary and secondary Rh immune response

A
  • Blood type and screen at 1st prenatal visit
  • Any qualifying event up to 13 wks → 50iU (some people just give 300iU)
  • 28-29 wks → everyone gets 300iU of Rhogam for primary immune response (keeps anti-D titer low)
  • Within 72 hrs of delivery → 2nd dose of 300iU for secondary immune response to any fetal blood exosure
    • protective up to 30 mL exposure of fetal whole blood
31
Q

Discuss the management plan of the pregnancy complicated by Rh isoimmunization

A
  • Typically 1st gestations after sensitization involves minimal disease → gets worse with subsequent pregnancies
  • Sensitization detected → anti-D tites q month until 24 wks → then q 2 wks
  • Test paternal RhD →
    • if negative or cordocentesis shows - fetus → no further testing
    • if positive → watch maternal anti-D titers (usually to 32) → MCA dopplers q 1 - 2 wks → if > 1.5 MOM cordocentesis
  • Previous affected pregnancy → send straight to specialist → amnio at 15 wks for fetal Rh status
32
Q

Reasons to give Rhogam

A
  • SAB or TAB
  • Threatened AB
  • Ectopic
  • Hydatidiform mole
  • Amnio/CVS
  • Fetal blood sampling
  • Placenta previa c bleeding
  • Abruption
  • IUFD
  • Blunt trauma to abdomen
  • External cephalic version
  • After admin of Rh+ blood product
33
Q

Describe the most common causes of alloimmunization

A
  • Fetalmaternal hemorrhage
  • Exposure in any way to + if -
  • Abruption
  • Trauma
  • Invasice procedure
  • blood transfusion
34
Q

Discuss principles of management and CNM/NP role in a pregnancy complicated by alloimmunization

A
  • Make sure all Rh - parents get Rhogam at 28 wks and within 72 hours postpartum and with any episodes of bleeding
  • ID abnormal early and refer
  • Check on Rhogam admin in prior pregnancies
35
Q

Hemolytic disease of the newborn

A
  • Rh antibodies cross the placenta in alloimmunization → fetal anemia, hyperbilirubinemia, hydrops
  • Blood smear of the fetus shows large % of circulating immature cells, erythroblasts
  • Also causes hypoxia, exsanguination, fetal death if w/FMH
36
Q

Describe the difference between the direct and indirect Coomb’s test and its role in identifying alloimmunization

A
  • Direct - used to detect Ab that have bound to RBC surface antigen in vivo
    • to check for immune mediated hemolytic anemia
    • Can be alloimmunity (HDN/RhD), autoimmune (lupus, etc), drug induced
    • Tests for HDN
  • Indirect - used to detect in-vivo antibody-antigen reactions
    • used for all blood transfusions detections of Ab and in pregnancy to detect anti-D Abs that cause HDN
    • Identifies Ab that cross placenta
    • Early identification of alloimmunized
37
Q

Von Willebrand’s Disease

Identify the incidence and etiology of von Willebrand’s disease

A
  • Up to 1% of population
    • Type 1: autosomal dominant
    • Type 2/3: recessive
  • Deficiency of vWF - carrier protein for factor VIII → binds glycoptrotein 1b receptor on platelets to initiate platelet adhesion to damaged blood vessel walls
    • Needs to be activated to be able to bind to GP 1b receptor on platelets
  • Diminished platelet aggregation → prolonged bleeding time
38
Q

Von Willebrand’s Disease

Labs

A
  • Decreased:
    • Platelets
    • Factor VIII
    • vWF (usually increases in pregnancy so may have delayed diagnosis)
  • Increased:
    • PT/PTT
39
Q

Discuss perinatal management and risks to the pregnant patient with von Willebrand’s disease

A
  • PPH CAN OCCUR WITH ANY TYPE
    • Also need to consider inherited vs. acquired
    • vWF levels <50% postpartum can have significant bleeding
    • Involvement of heme and MFM for delivery planning
    • Consider Desmopressin (DDAVP) vs. factor replacement
  • Type 1 rarely requires treatment
  • Type 2b worse in 3rd trimester, abn lvWF binds plts (thrombocytopenia)- NO DDAVP
  • Type 3 requires factor replacement
40
Q

Iron deficiency anemia

Risks to pregnancy

A
  • LBW
  • Preterm delivery
  • Perinatal mortality
  • Severe anemia is associated with impaired fetal oxygenation
    • Fetal RBC production is not impaired