ANAEMIA IN PREGNANCY.ppt

ANEMIA
IN
PREGNANCY
M.mounika
Scon

Definition of Anemia during Pregnancy.
 Anemia is reduction in the oxygen carrying
capacity of the blood, which may be due to :
- reduced number of red blood cells
- low concentration of hemoglobin, or
- combination of both
WHO:11gm/dl or less

Incidence
 40-80% in tropics
 10-20% in developed countries

Degree of anemia
Mild – between 8-10g%
Moderate - < than 8-7g%
Severe - < than 7g%

causes of Anemia
 Iron loss : sweat, repeated pregnancy, hookworm
infestation and malaria
 Faulty absorption mechanism : due to high
incidence of intestinal infestation, there is intestinal
injury
 Faulty diet habit : rich carbohydrate and high
phosphate in diet reduce absorption of iron

 Increase iron demand
 Diminished intake of iron
 Disturbed metabolism( depressed erythropoietic
function)
 Pre-pregnancy health status
 Excess demand(multiple pregnancy, rapid recurring
pregnancy, teen pregnancy)

Classification
 Physiologic
 Pathologic:
a. Deficiency: Iron, Folic Acid, Vitamin B12
b. Hemorrhagic: APH, Hookworm
c. Hereditary: Thalassemia, Sickle cell haemoglobinopathies ,
Hereditary Hemolytic Anemia
d. Bone Marrow Insufficiency: Aplastic Anemia
e. Infections: Malaria, TB
f. Chronic Renal Diseases or Neoplasm.

Concept of Physiologic Anemia
 Disproportionate increase in plasma vol, RBC
vol. and hemoglobin mass during pregnancy
 Marked demand of extra iron during
pregnancy.

Criteria for Physiologic Anemia
 Hb: 10gm%
 RBC: 3.2 million/mm3
 PCV: 30%
 Peripheral smear showing normal morphology
of RBC with central pallor
 Erythropoesis
 Iron requirement in pregnancy

Iron Deficiency Anaemia
Causes:
 poor intake:
-diet deficient in iron
 poor absorption:
-vomiting in pregnancy affects absorption
-increased ph of gastric juices
-ferric ions in gut instead of ferrous
-lack of vitamin c

 increaed utilization:
-demands of pregnancy
multiple pregnancy
grand multiparity
pregnancies close together
vegetarians

Clinical features:
Symptoms:
 fatigue
 drowsiness
 Weakness
 Dizziness
 Headache
 Malaise
 Pica
 Poor appetite
 Changes in mood
 Change in sleep pattern

Signs:
 pallor
Jaundice
Orthostatic hypertension
Peripheral edema
Pale mucous membrane and nail beds
Smooth and sore tongue
Glossitis
Stomatitis
Spleenomegaly
Tachycardia or flow murmur
Tachypnea,Dyspnea on exertion

Investigation
Hematological values
 Haemoglobin (low less than 10g%)
 Total red cell count (low <4million /mm3)
 PCV(<30%)
 MCV decreased <75um3)
 MCH decreased <25 pg
 MCHC decreased <30%
 Sr. iron decreased < 30ug per 100 gm

 Sr. ferritin decreased < 15 ug/l
 Sr. folate normal
 Marrow decreased iron store
Blood film(peripheral blood smear stained with leishman
stain)
red cells :
Size normal
Hypochromia
anisocytosis +
poikilocytosis+
White cells normal

 Examination of stool (helminthic (hook worm
)infestation
 Urine for protein ,sugar ,pus cells, culture, colony
count >10 .5/ml infection
 Chest X ray(PTB)
 SR. protein (hypoproteinemia or osmotic fragility
in hereditary spherocytosis or heamoglobinopathic
disorders

Treatment
Preventive:-
 Regular iron bearing food in diet
 Animal(red meat, white meat , fish,egg)
 Plant(lentils, dark green leafy vegetables, beans, whole wheat ,green
plantains, onion stocks, jaggery.
 Iron and folic acid supplements
 Avoid frequent child birth
 Eradicate hookworm infestation, treat dysentery, malaria, bleeding
piles and UTI
 Early detection of falling hb

 Curative:
 general treatment:
 diet rich in iron, protein and vitamins
 acid pepsin tds (improves appetite and digestion)
 prophylactic antibiotic therapy(avoid septic focus)
 specific therapy:
 oral therapy
 parenteral therapy
 intramuscular therapy
 blood transfusion
 exchange transfusion

Treatment
 Specific therapy
 The principle is to raise the HB level as near to normal as
possible before mother goes in Labour
 Choice of therapy depends on
 Severity of anemia
 Duration of pregnancy
 Associated complicating factors
 Iron Therapy
 Oral Therapy
 Parenteral Therapy

Treatment
 Oral Therapy
 Aim of the treatment is to get the maximum benefit in the
minimum possible time.
 Cap. Ferrous Sulphate 200mg 3 times a day along with food helps in
absorption.
 Disadvantages
 Intolerance ( Evidenced by epigastic pain, nausea, vomiting &
Diarrhea or constipation)
 Unpredictable absorption rate (Small percentage of the iron given is
absorbed and utilized for haemoglobin formation. Antacids, oxalates
& Phosphates will reduce absorption, Ascorbic Acid, lactate & various
amino acids- increase absorption)

Treatment
 Parenteral Therapy:
 It includes IM and IV
 IV therapy includes repeated injections, total dose infusion. (TDI)
 Indications of Parenteral Therapy.
 Contraindications of oral therapy (Intolerance & Severe Anemia)
 Mother is not co-operative to take oral iron
 Severe Anemia
 Advantages
 Increase the iron storage
 Expected rise in the Hb. Concentration after Parenteral therapy is 0.7 to 1gm/100 ml
per week

Treatment
 TDI
 Calculate the Iron deficit.
 Iron dextron 1 ml contains 50 mg of elemental Iron
 The injection should be given slowly
 Taking care not to infiltrate into surrounding tissues
 More than 200 mg at a time is not recommended.

 Advantages
 It eliminates repeated & painful intramuscular injections
 treatment is completed in a day & mother may be discharged
much earlier.
 Less costly compared to the repeated IM therapy.
 Disadvantages
 Maximum Hb. response does not appear before 4 to 9 weeks(
Method is unsuitable if at least 4 weeks time is not available
.Mostly suitable 30-36 weeks of pregnancy)
 Previous history of reaction is contraindicated

 Pre requisites
 Correct Diagnosis
 Adequate Supervision
 Facilities for management of anaphylactic reaction.

 Procedure
 The mother is admitted in the morning for infusion.
 The required iron is mixed with 500 ml of 0.9% saline
 Divide the dose 1st day start with 50 mg ,2nd day 100 mg ,3rd day 200 mg
and from then on every other day 200 mg till the iron deficit is made
good. More than 200mg at a time is not recommended.
 Precautions like those of blood transfusion are to be taken both prior to &
during the infusion process.
 The drip rate should be 10 drops per minute during the first 20 mts. &
there after is increased to 40 drops per mt.
 Any adverse reaction like rigor, chest pain or hypotension – stop the drip

Intramuscular Therapy
 The compounds used are
 Iron dextran (Inferon) 50 mg.
 Iron sorbitol citric acid complex is dextrin (Jectofer) 50
mg
 Total dose to be estimated.

 Procedure for injection
 Test dose 1 ml injection , watch for 20 to 30 mts any anaphylactic
reaction then administered full dose
 Prevent dark staining of skin
 Use ‘Z’ technique
 Oral Iron should be stopped at least 24hrs prior to therapy to avoid
reaction.
 Disadvantage
 The injections are painful
 Chance of abscess formation & discoloration of the skin

Blood Transfusion
Indications:
 To correct anemia due to blood loss
 Mother with severe anemia seen in beyond 36 weeks
 Anemia not responding to either oral or parenteral therapy.
 Advantages
 Increase oxygen carrying capacity of the blood
 Stimulate erythropoieses
 Supplies the natural constituents of blood like proteins,
antibodies etc
 Improvement is seen after 3 days

 Disadvantages
 Premature labor due to blood reaction
 There is increased chance of cardiac failure with
Pulmonary edema.
 Precautions
 Antihistaminic (Phenargan 25mg)
 Diuretics (Frusemide 20mg) IM.
 Drip rate should be 10 drops /mt
 Monitor pulse, respiration

Nursing Management
 Assessment
 Nutritional History
 Client Education
 Nutritional counseling
 Serum Ferrites levels should be obtained after the 20th week. It
should be repeated 6 to 8 weeks intervals.
 7 days diet history is taken to evaluate the pregnant women's
general nutritional status & the quantity of iron available through
nutritional sources

Complications
 Maternal risk during Antenatal period:
 Poor weight gain
 preterm labor
 PIH
 placenta previa
 Accidental hemorrhage
 Eclampsia
 Premature rupture of membrane.

 Maternal complication during Intra-natal
period:
 Dysfunctional labor.
 Intra-natal hemorrhage.
 Shock.
 Anesthesia risk.
 Cardiac failure.

 Postnatal period:
 postnatal sepsis
 Sub involution
 Embolism.

NEONATAL AND FETAL COMPLICATIONS
 Prematurity
 Low birth weight.
 Poor APGAR
 Fetal distress
 Failure to thrive
 Poor intellectual development
 Higher rates of morbidity.

Megaloblastic Anemia
 It is a state where impaired DNA synthesis, results in derangement
in Red Cell maturation with production of megaloblast (abnormal
precussor) from bone marrow.
 It may be due to deficiency of VitB12 or Folic Acid or both.
 Megaloblastic anemia in pregnancy is almost always due to Folic
Acid defeciency.
 Vitamin B12 defeciency is rare in Pregnancy becoz its need is less
in amount and it is met with any diet that contains animal products.

Vitamin B12 deficiency
CAUSES:-
 gastrectomy
 ileal resection(crohn’s disease)
 pernicious anaemia
Addisonian pernicious anemia(auto immune disease –lacks
intrinsic factor –lack of vitamin B12 absorption)

Folic acid deficiency
Definition:-
Leads to reduction in cell proliferation due to lack of
nucleic acid formation.
Causes:-
Inadequate intake
- diet deficient in folates
- vomiting in pregnancy
Increased utilization
- demands of pregnancy
- rapid growth of fetal, placental and uterine tissues.

Diminished absorption
-gastro – intestinal upsets
-oral antibiotics
- intestinal malabsorption syndrome(gluten induced enteropathy i.e.
coeliac disease.
Excessive demand
- multiple pregnancy
- multiparity
- rhesus incompatibility(fetal hemolysis)
- infection(reduces life span of red cellsand increases demand of folic
acid)
-maternal haemorrhagic condition(peptic ulcer, hookworm infestation

-maternal hemolytic condition(malaria, sickle cell anemia,
thalassaemia
Diminished utilization
-analgesics
-antibiotics
-anticonvulsant drugs
-sulfasalazine
-methotrexate
Diminished storage
-hepatic disease
-vitamin c deficiency,Iron deficiency anemia

Sign and symptoms
 Insidious onset, mostly in last trimester
 Tired, breathlessness, oedema, protracted vomiting
 Anorexia and occasional diarrhoea
 Pallor of varying degree
 Ulceration in mouth and tongue
 Hemorrhagic patches under the skin and conjunctiva
 Enlarged liver and spleen(jaundice)

Blood values
 Hb<10gm%
 Blood film(any two)
 Hypersegmentation of neutrophils
 Macrocytosis and anisocytosis
 Giant polymorphs
 Megaloblast
 Howell-jolly bodies
 MCV>100micrometer3
 MCH>33pg, but MCHC is Normal
 Serum Fe is Normal or high

TIBC is low
Leucopenia
Thrombocytopenia
Sr. folate is less than 3ng/ml
Sr.B12 < 90pg/ml
Sr.bilirubin raised
Bone marrow-megaloblastic erythropoiesis

Treatment
 Prophylactic
- all woman of reproductive age should be given 400mcg of
folic acid daily
 Curative
-daily administration of Folic acid 4mg orally for at least 4
wks following delivery
-vitamin B12 100ug im/day
-ascorbic acid 100mg

complications
Megaloblastic anemia:-
Abortion
Dysmaturity
Prematurity
Abruptio placentae
Fetal malformation
Heart failure
Pancytopenia(low WBC & platelet count)

Vitamin B12 deficiency:-
Neuropathy involving peripheral nerves and spinal
cord
Psychiatric disturbances
Visual disturbance
Fetal neural tube defects

Dimorphic anemia
Definition:-
anemia that results from deficiency of both iron & folic
acid or vitamin B12(poly deficiency state)
Causes:-
-dietary inadequacy
-intestinal malabsorption

Investigations:-
Red cells-
macrocytic/normocytic
hypochromic/normochromic
Bone marrow
-megaloblastic
Treatment:-
iron and folic acid in therapeutic doses

Aplastic anemia
Definition :-
it is a condition where bone marrow does not produce sufficient new cells to replenish
blood cells resulting in marked decrease in marrow stem cells(i.e.production of erythrocytes,
WBC’s, platelets fails)
Causes:-
Acquired:
 unknown
 immunologically mediated
 autosomal recessive inheritance

Exposure to ionizing radiation
Chemical agents
Idiosyncratic reactions to drugs (chloramphenicol or quinacrine)
Infections –viral or bacterial(infectious mononucleosis, infectious
hepatitis, cytomegalovirus infections & miliary tuberculosis)
Pregnancy
Paroxysmal nocturnal hemoglobinuria
Others- preleukemia and carcinoma
Congenital
Fanconi’s anemia

pathophysiology
Reduction or depletion of hematopoietic precursor stem cells
leads to peripheral pancytopenia. due to:-
-quantitative or qualitative damage to pleuri potent stem
cells
-abnormal hormonal stimulation of stem cell proliferation
-defective bone marrow micro environment
-cellular or humoral immunosuppression of hematopoiesis

Clinical features
Fatigue
Heart palpitations
Pallor
Infections
Petechiae
Mucosal bleeding
Tachycardia
Fever
Painful ulceration of throat

Investigations
Blood:
Pancytopenia(anemia, leucopenia, thrombocytopenia)
 lymphocytosis
Normocytic,normochromic RBCs
Anisocytosis
Poikilocytosis
Decreased RBC
Hypocellular bone marrow
Biopsy:
empty bone marrow

Treatment
Repeated blood transfusion(to maintain hct >20)
Granulocyte transfusion(combat infection)
Platelet transfusion(control bleeding)
Packed red blood cells
Glucocorticoid therapy(corticosteroids)
Bone marrow or stem cell transplantation
Antithrombocyte antibody
Immunosuppressive agents

complications
Increased fetal wastage
Prematurity
Intrauterine fetal demise
Increased maternal morbidity
Death due to infection and haemorrhage

Haemolytic anemia
Definition :-
it is abnormal breakdown of red blood cells
(RBCs) either in blood Vessels (intravascular
hemolysis) or else where in the body (extravascular)
Classification:
hereditary(inherited)
acquired

causes
Hereditary:-
 defects in haemoglobin production(thalassemia and sickle
cell disease
 defects of red blood cell membrane production(hereditary
spherocytosis & hereditary elliptocytosis)
 defective red cell metabolism(G6PD & pyruvate kinase
deficiency)

Acquired:-
immune mediated
transient factors – mycoplasma pneumoniae infection(cold agglutinin
disease)
permanent factors – autoimmune(SLE, chronic lymphocytic
leukemia)
Hyperspleenism(portal hypertension)
burns
Infection
Runners(footstrike hemolysis) venous destruction of RBC at foot.

Clinical features
Pallor
Fatigue
Shortness of breath
Heart failure
chronic hemolysis( excretion of bilirubin
–gallstones)
Continuous release of haemoglobin (PHT- Syncope, chest pain,
breathlessness-RHF,ascites, peripheral edema)

Investigation
 Peripheral smear microscopy
 Fragments of red blood cells(schistocytes)
 RBC smaller and rounder(spherocytes)
 Elevated reticulocytes
Elevated unconjugated bilirubin
Increased LDH
Decreased haptoglobin
Positive direct coomb test

Urine testing
 Presence of hemosiderin
 Urobilinogen

Treatment
 Stop use of offending drug
 Corticosteroids(prednisone)
 Iv immunoglobulin infusion
 Immuno suppressive(azathioprine &
cyclophosphamide)
 Erthyropioetin( to increase RBC production)
 Splenectomy(extra vascular hemolysis)

Hemoglobinopathies
 An inherited mutation of the globin genes
leading to a qualitative or quantitative
normality of globin synthesis.

Classification
 Mutation causing qualitative
abnormality(sickle cell anemia)
 Quantitative abnormality(Thalassemias)

Abnormal hemoglobin synthesis
 Production of structurally normal but decreased amount of globin
chains(Thalasemia)
 Production of structurally abnormal globin chains(hemoglobin s, c
and e)
 Failure to switch globin chain synthesis(herditary persistence of
HBF)
- Autosomal co-dominant disorders

Thalassaemia
 Hereditary abnormality of hemoglobin production where the
primary difficulty is quantitative deficiency-either beta globin
leading to beta thalassaemia or alpha globin leading to alpha
thalassaemia i.e genetic decrese in globin chain synthesis.

Alpha thalassaemia
 Deletion of one or more alpha genes from
chromosome 16.

Beta thalassaemia
 B chain production is decreased and excess of alpha
chains precipitate to cause red cell membrane damage
i.e only two globin genes one on each chromosome
11.
 B + gene mutation cause partial block in B chain
synthesis
 B zero gene mutation causes absence of B chain
production.

Sickle cell Hemoglobinopathy
 Hbs comprises 30-40% total Hb
 There is substitution of Lysine for glutamic acid at the sixth
position of B chain of Hb
 Red cells in oxygenated state behave normally, but in
deoxygenated state it aggregates, polymerises and distort red
cells to sickle.
 These cells are more fragile and increased destruction leads to
hemolysis, anemia and jaundice.

Effects on pregnancy
 Increase incidence of abortion, prematurity, IUGR
and Fetal loss.
 Perinatal mortality is high.
 Incidence of pre-eclampsia, postpartum hemorrhage
and infection is increased.

Management
 Careful antinatal supervision
 Air travelling in unpressurised aircraft to be avoided.
 Prophylatically Folic A. 1gm daily.
 Regular blood transfusion at approx. in 6 weeks
interval

ANAEMIA IN PREGNANCY.ppt

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ANAEMIA IN PREGNANCY.ppt