Hematologic disorders in pregnancy Flashcards
1
Q
Summary of normal hematologic changes during pregnancy
A
- Hemodilution
- Decreased hematocrit
- Slightly reduced platelets
- Increase in clotting factors
- Mild leukocytosis
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
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
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
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
6
Q
Food sources of folic acid
A
- Strawberries
- Green veggies
- Peanuts
- Lentils/Beans
- Liver
- Fortified breads and cereals
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
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
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
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
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
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
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)
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
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
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
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
Immune Thrombocytopenic Purpura
Patho/Indicence/Dx
* 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
Neonatal alloimmune
* 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
Describe the process of alloimmunization
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
List reasons for the failure of Rh immunization prevention
* 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
Rosette + KB test (Kleihauer-Betke)
* 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
Describe the timetable and active agent in the primary and secondary Rh immune response
* 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
Discuss the management plan of the pregnancy complicated by Rh isoimmunization
* 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
Reasons to give Rhogam
* 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
Describe the most common causes of alloimmunization
* Fetalmaternal hemorrhage
* Exposure in any way to + if -
* Abruption
* Trauma
* Invasice procedure
* blood transfusion
34
Discuss principles of management and CNM/NP role in a pregnancy complicated by alloimmunization
* 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
Hemolytic disease of the newborn
* 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
Describe the difference between the direct and indirect Coomb's test and its role in identifying alloimmunization
* **_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
Von Willebrand's Disease
Identify the incidence and etiology of von Willebrand's disease
* 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
Von Willebrand's Disease
Labs
* Decreased:
* Platelets
* Factor VIII
* vWF (usually increases in pregnancy so may have delayed diagnosis)
* Increased:
* PT/PTT
39
Discuss perinatal management and risks to the pregnant patient with **_von Willebrand's disease_**
* 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
**Iron deficiency anemia**
Risks to pregnancy
* LBW
* Preterm delivery
* Perinatal mortality
* Severe anemia is associated with impaired fetal oxygenation
* Fetal RBC production is not impaired
