Ova and cysts

1. ANAEMIA IN PREGNANCY
ABDUL HAMID
CAESAR MAKARA
FIDELIS HEBULEY
KENNETH KIBET

2.  Anemia in pregnancy is often defined as a hemoglobin
measurement below 10 g/dL or hematocrit below 30%.
 Anemia in non-pregnant women is defined as hemoglobin
concentration less than 12 g/dL
 Centers for Disease Control defined anemia as less than 11
g/dL in the first and third trimesters, and less than 10.5 g/dL
in the second trimester.
 Any condition in which the number of red blood cells per
mm3, the amount of hemoglobin in 100 ml of blood, and/or
the volume of packed red blood cells per 100 ml of blood
are less than normal
DEFINITIONS

3.  Anemia is a significant maternal problem during
pregnancy.
 A hemoglobin of less than 11 g/dL or a hematocrit of
less than 33% should be investigated and treated to
avoid blood transfusion and its related complications
 A pregnant woman will lose blood during delivery and
the puerperium, and an anemic woman is therefore at
increased jeopardy.

4.  With normal pregnancy, blood volume increases, which results in
a concomitant hemodilution.
 During pregnancy, the blood volume increases by about 50% and
the red blood cell mass by about 25%
 This physiologic hydremia of pregnancy will lower the hematocrit
but does not truly represent anemia.
 Although red blood cell mass increases during pregnancy, plasma
volume increases more, resulting in a relative anemia.
 This results in a physiologically lowered hemoglobin (Hb) level,
hematocrit (Hct) value, and red blood cell (RBC) count, but it has
no effect on the mean corpuscular volume (MCV).
PHYSIOLOGY OF PREGNANCY

5.  Pregnancy-induced hypervolemia has several
important functions:
 To meet the demands of the enlarged uterus with its
greatly hypertrophied vascular system.
 To protect the mother, and in turn the fetus, against the
deleterious effects of impaired venous return in the
supine and erect positions.
 To safeguard the mother against the adverse effects of
blood loss associated with parturition.

6. Anaemia
Acquired
Iron Deficiency Anemia
Acute Blood loss
Anaemia of
Inflammation/Malignancy
Acquired hemolytic anemia
Aplastic/hypoplastic anemia
Hereditary
Thalassemias
Sickle-cell
hemoglobinopathies
Other
hemoglobinopathies
Hereditary hemolytic
anemias
ETIOLOGY

7.  The two most common causes of anemia during
pregnancy and the puerperium are iron deficiency
and acute blood loss
 Iron deficiency is responsible for about 95% of the
anemias during pregnancy, reflecting the increased
demands for iron
IRON DEFICIENCY ANAEMIA

8.  A woman who is pregnant often has insufficient iron stores
to meet the demands of pregnancy.
 Poor nutritional status frequently is associated with iron-
deficiency anemia
 Malabsorption of iron.
 Many women enter pregnancy with low iron stores
resulting from heavy menstrual periods, previous
pregnancies, breast feeding, or poor nutrition.
 Physiological increase in iron requirements.
 True anemia is common, mainly because of the demands of
the developing fetus on iron and folic acid, particularly
during the later months of pregnancy.
 It is difficult to meet the increased requirement for iron
through diet, and anemia often develops unless iron
supplements are given.
ETIOLOGY OF IDA

9.  Red cells may not become hypo-chromic and
microcytic until the hematocrit has fallen significantly.
(fall in MCV and MCH)
 When this occurs, a serum iron level below 40 ug/dL
and a transferrin saturation less than 10% suggest iron
deficiency anemia
 Clinical symptoms of iron deficiency anemia include
fatigue, headache, and pica (in extreme situations).
PATHOGENESIS/CLINICAL FEATURES

10.  Simple iron compounds: ferrous sulfate, fumarate, or gluconate
 The most appropriate oral iron therapy is use of a tablet containing ferrous
salts, such as:
 Ferrous fumarate — 106 mg elemental iron/tablet
 Ferrous sulfate — 65 mg elemental iron/tablet
 Ferrous gluconate — 28 to 36 mg iron/tablet
 Treatment consists of a diet containing iron-rich foods and 60 mg of
elemental iron (e.g. 300 mg of ferrous sulfate) three times a day with meals
 The recommended daily dose for the treatment of iron deficiency in adults is
in the range of 150 to 200 mg/day of elemental iron; there is no evidence
that one iron preparation is more effective than another.
 As an example, a single 325 mg ferrous sulfate tablet taken orally three
times daily between meals provides 195 mg of elemental iron per day.
 This regimen should lead to a modest reticulocytosis beginning in
approximately seven days and a rise in the hemoglobin concentration of
approximately 2 g/dL over the ensuing three weeks.
TREATMENT

11.  A liquid preparation, the dose of which (44 mg elemental
iron per 5 mL) can be easily titrated by the patient
 To replenish iron stores, oral therapy should be continued
for 3 months or so after the anemia has been corrected.
 Iron is best absorbed if taken with a source of vitamin C
(raw fruits and vegetables, lightly cooked greens).
 All pregnant women should take daily iron supplements.
 If the woman cannot or will not take oral iron preparations,
then parenteral therapy is given
 Iron dextran (INFeD, Dexferrum), which contains 50 mg of
elemental iron/mL can be given either IM or IV.
 Dosage: Ferrous sulfate 325mg bid-tid

12.  In the "classic" case of vitamin B12 (cobalamin) or folic acid
deficiency, the patient presents with a severe macrocytic
anemia (RBC MCV >100 fL, and often >115 fl), a low to low-
normal absolute reticulocyte count, and a characteristic
blood smear showing macroovalocytes, occasional
megaloblasts, and hypersegmented neutrophils
 Folic acid deficiency anemia is the main cause of
macrocytic anemia in pregnancy, since vitamin B12
deficiency anemia is rare in the childbearing years.
 The daily requirement of folic acid doubles from 0.4 mg to
0.8 mg in pregnancy.
FOLIC ACID ANEMIA

13.  Twin pregnancies
 Infections
 Malabsorption
 Use of anticonvulsant drugs such as phenytoin can
precipitate folic acid deficiency.
ETIOLOGY OF FOLIC ACID DEF.
ANEMIA

14.  The anemia may first be seen in the puerperium
owing to the increased need for folate during
lactation.
 The diagnosis is made by finding macrocytic red cells
and hypersegmented neutrophils in a blood smear
PATHOGENESIS

15.  Because the deficiency is hard to diagnose and folate intake is
inadequate in some socioeconomic groups, 0.8-1 mg of folic acid is
given as a supplement in pregnancy; the dose in established
deficiency is 1-5 mg/d
 Folate deficiency is treated with folic acid (1 to 5 mg/day PO) for one
to four months, or until complete hematologic recovery occurs.
 A dose of 1 mg/day is usually sufficient, even if malabsorption is
present.
 Good sources of folate in food are leafy green vegetables, orange
juice, peanuts, and beans.
 Cooking and storage of food destroys folic acid.
 Strict vegetarians who eat no eggs or milk products should take
vitamin B12 supplements during pregnancy and lactation.
TREATMENT

16.  Pernicious anemia (PA) is typically treated with parenteral (i.e.
intramuscular) Cbl, in a dose of 1000 µg (1 mg) every day for one
week, followed by 1 mg every week for four weeks and then, if
the underlying disorder persists, as in PA, 1 mg every month for
the remainder of the patient's life.
 Treatment of vitamin B-12 deficiency includes 0.1 mg/d for 1 week,
followed by 6 weeks of continued therapy to reach a total
administration of 2 mg
 Folate deficiency is much less common than iron deficiency;
however, taking 0.4 mg/d to reduce the risk of neural tube
defects is recommended to all women contemplating pregnancy.
 Patients with a history of neural tube defect should take 4 mg/d.

17.  Due to a genetic substitution of valine for glutamic acid at codon
6 of the globin chains.
 1 in 400 births in blacks has SCD.
 Affects about 0.2% of blacks.
 8–10% of blacks carry the sickle cell trait.
 Normal Hb made up of 4 subunits. Each subunit = a globin chain
+ an attached heme. A heme = a porphyrin ring + Fe2+
 From 6 months of age, 95–97% of the total haemoglobin is
haemoglobin A (HbA).
 HbA = ά2ß2
 HbF = ά2 ‫ﻻ‬
2
SICKLE CELL ANEMIA

18.  Vasoocclusive
 Sequestration
 Aplastic (assoĉ parvovirus B19 Infx)
 Painful
 Hemolytic
 Acute chest syndrome
SICKLE CELL CRISES

19.  ↑risk of sickle cell crises, infections (bacterial pneumonia, UTI),
PET and thromboembolic events.
 ↑rates of maternal morbidity and mortality. Maternal mortality
1-2%.
 Hydroxyurea contraindicated in pregnancy.
 Early fetal wastage
 Stillbirth
 Preterm delivery
 Fetal growth restriction
 Non-immune hydrops fetalis
 placental abruption
PROBLEMS IN PREGNANCY

20.  Assess for frequency of crises, previous transfusion
endorgan damage (e.g nephropathy, heart failure and
pulmonary hypertension).
 Folate 5mg O.D started 3-6mons before conception.
 Hydroxyurea stopped 3-6mons before conception.
PRECONCPTION CARE

21.  Hx of crises and drug use.
 Pregnancy dating, since ♀ with SCD have ↑risk of IUGR and may
need early delivery.
 FBC, LFTs, Renal fn tests.
 Folate supplementation, antibiotic prophylaxis.
 Remain well hydrated and avoid heavy physical exertion, a cold
environment and stress.
 Multidisciplinary care by obstetrician and hematologist.
 Serial obstetric scans in 3rd trimester to r/o IUGR
 Painful crises Mx: pain relief, treatment of infections,
oxygenation, correcting metabolic acidosis and maintaining an
adequate haemoglobin level.
ANTENATAL MANAGEMENT

22.  In the presence of IUGR, recurrent painful crises and
other complications, induce labour at 34-37 weeks.
 During labour avoid dehydration (rehydrate), hypoxia (O2
by mask), sepsis and acidosis; GXM and save blood.
 Adequate analgesia.
 FHR monitoring.
LABOUR AND INTRAPARTUM CARE

23.  There is an increased risk of PPH, hypovolaemia, tissue hypoxia,
infections, thromboembolism and vaso-occlusive crises.
 AMTSL ( Active Mx of 3rd Stage of Labour).
 Antibiotic prophylaxis.
 Early ambulation, thromboembolic deterrent stockings,
appropriate hydration and oxygenation are encouraged.
 Thromboembolic prophylaxis:daily sc heparin (e.g. 40 mg
enoxaparin).
 Adequate hydration and pain relief.
 Breastfeeding encouraged.
 Cord blood for Hb electrophoresis.
POST PARTUM CARE

24.  During labour and operative deliveries, precipitating
factors for sickle crisis include immobilisation,
hypoxia, acidosis, infection, dehydration,
hypertension and blood loss. Take measures to
prevent or reduce these.
 Regional block is preferable to general anaesthesia
because it largely avoids the risk of iatrogenic
hypoxia.
 Prophylactic heparin in operative deliveries.
CRISES PREVENTION

25.  With its attendant haemolysis increases folate
demand leading to megaloblastic anaemia.
 Natural acquired immunity is lowered in pregnancy
leading to excessive destruction of RBCs in some
cases.
MALARIA INFESTATION

26.  Chronic parasite infection affects millions of women
of reproductive age in developing countries.
 Lives in the duodenum - the site of optimal iron
absorption, therefore interfering with the latter by
their attachments to the duodenal mucosa besides
sucking blood from the patient (0.05 – 0.1ml per
worm/ day), and leads to iron deficiency.
HOOKWORM INFESTATION

27.  Other helminthes and parasites e.g E. histolytica
 Haemoglobinopathes e.g. thalasaemia and glucose 6-
phosphate dehydrogenase deficiency.
 Chronic diseases e.g. TB, HIV, Brucellosis, scistosomiasis,
UTI, chronic liver and renal dx, and protein deficiency.
 Demands of pregnancy parse; Extra demands to the
haemolytic factors increased red cell mass plus demands
of the growing foetus = increase in the total number of
rapidly dividing cell leads to increased requirement of folic
acid).
OTHER CAUSES

28.  Characteristically insidious in onset
 Presentation usually non-specific and depends on the
severity of anaemia, duration of disease and causative
factors.
 Diagnosis depends on history, physical examination
and various lab tests done based on aetiological
factors.
 In the early stages it may only be detected by routine
HB estimation in the ANC.
CLINICAL FEATURES

29. - General weakness, malaise, fatigue, lethergy or
lassitude
- Dizziness
- Dyspnoea on slight exertion
- Breathlessness
- Swelling of legs feet and face (oedema)
SYMPTOMS

30.  palour (conjunctiva, tongue, palms and nail beds, sole
of the feet etc),
 jaundice (or tinge of),
 Moderate tachycardia at rest,
 Haemic murmur,
 low grade fever without obvious cause is common
plus or minus hepatosplenomegaly in haemolytic
anaemia e.g. of malaria (endemic) and SCD,
SIGNS

31.  Orthorpnoea and other signs of cardiac failure e.g.
engorged neck veins in the semi-upright position,
congestion of lung bases, enlarged tender liver,
increased pulse pressure, and may be present in very
severe cases
 Albuminuria is common

32.  In the terminal phase acute pulmonary oedema may
supervene and cerebral anoxia may produce
excitement and mental confusion followed by loss of
consciousness.

33.  A slightly increased risk of preterm birth with midtrimester
anemia.
 Anemia may be associated with fetal growth restriction,
this may lead to adult cardiovascular disease .
 Maternal anemia influences placental vascularization by
altering angiogenesis during early pregnancy.
 According to the World Health Organization, anemia has
been implicated as contributory in up to 40 percent of
maternal deaths in third-world countries
 Increased risk of postpartum infections
EFFECTS OF ANEMIA IN PREGNANCY

34.  H’gram + PBF+ BS for MPs
 Stool: O/C
 Hb electrophoresis/ sickling test
 LFTs for serous proteins as in chronic liver disease and
hypoproteinaemia
 U/Es + Cr + U.A to rule out underlying nephrosis
 CXR- to r/o intercurrent chronic chest infection
INVESTIGATIONS

35.  Mainly directed at the cause
 Supportive care is similarly important e.g.
administration of haematinics or blood transfusion or
both – depending on the degree of anaemia and the
gestational age at the time of diagnosis.
TREATMENT

36.  Protein intake- Should be adequate – at least
100grams per /day, 50% of which should preferably be
animal protein
 Chronic diarrhoeas – should be treated as they
interfere with folic acid and B12 absorption
 Hookworm – should be treated with non-toxic
antihelminthics
GENERAL MEASURES

37. 1). Oral iron therapy; in Fe def. anaemia of moderate
degree in the first and second trimester
2). Parenteral iron therapy; in more severe cases
particularly those seen for the first time near term to
achieve quicker response as well as for those not able
to tolerate oral Fe due to gastric symptoms and also
those not responding due to malabsorption.
SPECIFIC TREATMENT

38. 3). Suplementary Folic Acid
4). Malaria treatment – when confirmed or suspected
5). Steroid therapy – in excessive haemolysis
6). Vit. B12 – for megaloblastic anaemia unresponsive to
folic acid or when B12 def.is confirmed

39. 7).Cardiac failure - treated appropriately with antifailure
regime (digoxine, aminophyline, O2 etc
8). Blood transfusion – for impending CCF, patient in
labour with severe anaemia
- watch for overload
- Packed RBCs is preferred
- Transfuse slowly (not more than 500mls in at
least 6-8 hrs

40.  Labour and the first 2wks of the puerperium are the
periods of greatest danger to the anaemic mother.
 Most deaths occur in the first 12hrs after delivery
 O2 should be delivered in labour by mask to reduce
the risk of foetal asphyxia
MANAGEMENT OF LABOR AND
PUERPERIUM

41.  Aseptic techniques to be employed due to decreased
immunity
 2nd stage should be shortened by assisted vacuum
extraction or low forceps delivery
 Antibiotic prophylaxis in the puerperium
 Specific treatment for anaemia to continue for at
least 6wks after delivery (puerperium) to accelerate
recovery

42.  Finally before discharge warn the mother of
possibility of recurrence in subsequent pregnancies
therefore to present as soon as they become
pregnant for prophylaxis

43. a) Correct faulty dietary habits e.g. overcooking
vegetables and meat (important sources of folic
acid)
b) Increase production and consumption of foods
which contain the raw materials of erythropoesis.
c) Antimalarial prophylaxis
PREVENTION

44. d) Reduction of hookworm loads
e) Prophylactic medication – haematinics
f) Early detection of anaemia in pregnancy by
screening all pregnant women (ANP) – first and
last visits

45.  CCF= death in pregnancy or soon after delivery or
during labour
 Low resistance = infections e.g. pneumonias,
puerperal sepsis etc
 IUGR
 Late abortions (20 – 28 wks)
 Premature labour
SEQUALE OF ANEMIA IN
PREGNANCY

46.  IUFD/ neonatal death (perinatal death) due to
intrapartum asphyxia
 Infantile anaemia 2-3 months post delivery due to
deficient iron storage in the last trimester.

47.  Prevention of anaemia is difficult in developing
countries due to its multfactorial origin:
- Poor SES
- Poor health facilities
- Socio-cultural factors
- Poor utilization and scarcity of FP and ANC services
 However prophylactic use of haematinics and
antimalarials has reduced the severity of anaemia in
the tropics.
CONCLUSION