Case Report: Aplastic Anaemia in Pregnancy - Management and Follow-up

 
APLASTIC ANAEMIA IN
PREGNANCY
 - 
A CASE
REPORT
 
 
Dr.Sofia.K (Fellow in Reproductive medicine)
Dr.V.Geetha  ,Dr.Lakshmi , Dr.Kundavi
Institute of reproductive medicine,
Madras medical mission
Monday,15
th
 February 2021(online)
 
CASE REPORT
 
23 year old primi presented to IRM at 7weeks +4days
for antenatal care with  an history of recently diagnosed
aplastic anemia.
 
H
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Patient was married at 23 years
 
3 months after marriage  Developed UTI associated with
chills and rigor.
 
 Evaluated at private hospital and Routine laboratory tests
showed pancytopenia
          Haemoglobin of 7gm/dl,
          Platelet – 37000 &
          TC-3,600 & 3 units of PRBC transfused
 
I
N
V
E
S
T
I
G
A
T
I
O
N
S
 
 
Hematologist opinion was obtained
        Iron
        Ferritin
        TIBC
 
Bone marrow aspirate:
      Hypocellular marrow
      Dyserythropoiesis
      Absent iron storage
 
A bone marrow biopsy confirmed the diagnosis of aplastic
anemia
.
 
Normal
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
H
I
S
T
O
R
Y
 
Menstrual History
:
 Regular menstrual cycles
 
Medical History
: 
Evaluated for giddiness at 20 year and found to have mild
anemia and vitamin B12 deficiency treated with vitamin B12 injection
 
 
Surgical History
: 
NIL
 
Family History
:  
NIL
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
H
I
S
T
O
R
Y
 
Obstetric History 
:
   
NT scan
 
   
First trimester screening
   
Anomaly Scan
   
serial growth scans
 
 Her pregnancy was managed with multidisplinary approach .
 
NORMAL
 
I
N
V
E
S
T
I
G
A
T
I
O
N
S
 
Repeat bone marrow done at early gestation –
 
   
Hypocellular marrow particles
   
Normoblastic erthyropoiesis
 
   
Mildy suppressed megakaryopoiesis
 
 
Myelodysplastic syndrome panel by FISH – Negative
 
 
 
Chromosomal analysis – Normal female karyotype 46XX
 
HAEMATOLOGIST ADVICE
 
 
Advised blood count every 2 weeks
 
 
Haemoglobin < 8gm/dl -  2 units of packed red blood cells
 
Platelet count < 20,000 – 4 units of platelets
 
 
According to the Hematologists advice patient was
managed accordingly.
 
H
A
E
M
A
T
O
L
O
G
I
C
A
L
 
P
R
O
F
I
L
E
 
 
M
A
N
A
G
E
M
E
N
T
 
 
According to hematologist advise patient was transfused with PRBC and
platelets
 
 
 
Haemoglobin > 8gm/dl
 
 
 
          platelet  > 20,000,
 
To prevent the serious consequences of thrombocytopenia and anemia
of the mother and fetus  .
 
M
A
N
A
G
E
M
E
N
T
 
At  35 weeks + 3 days of gestation  decision to LSCS was made.
 2 days before  the  lscs patient was Haemoglobin was 9gm and platelets 40,000
patient was transfused with 4 units of random  platelets & 1 unit of PRBC
   
                              Platelet refractoriness checked
   
                              platelets after one hour -80,000
Antenatal steroids given for fetal lung maturity
On the day of LSCS Haemoglobin - 9.9 gm/dl
                                     Platelet - 70,000
 
D
E
L
I
V
E
R
Y
 
 
Patient underwent Elective lscs at 35 weeks and 5 days with 4 units of platelets on
flow under antibiotic coverage
        
B
        
A
        
B
        
Y
.
 
Histopathology of placenta 
-: Umblical cord - Three blood vessel
 
      
        Membranes - No specific lesion
 
     
                  placenta  -  Mild congestion
 
Alive male
2.470 kgs
9/10,9/10
 
P
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t
 
o
p
e
r
a
t
i
v
e
 
p
e
r
i
o
d
 
Post operative period was uneventful
 
          Patient was discharged in stable condition  on 4
th
 POD.
 
   
     Haemoglobin - 9gm
 
   
     platelets -1 lakh
 
.
 
W
H
A
T
 
I
S
 
A
P
L
A
S
T
I
C
 
A
N
E
M
I
A
?
 
Aplastic anemia is a rare disease caused by destruction of pluripotent stem
cells in bone marrow with an annual incidence of 2 to 6/10,00,000.
 
 In contrast to the term 'aplastic anemia', suggesting suppression of
erythropoetic cell lines, all cell lines may be affected .
 
Depending  on affected cell lines, aplastic anemia is associated with
fatigue, bleeding due to thrombocytopenia and recurrent infections due to
neutropenia .
 
The diagnosis 'aplastic anemia' is confirmed by hypocellularity of the bone
marrow. The remaining cells are morphologically unaffected without
malignant infiltration.
 
APLASTIC ANEMIA IN PREGNANCY
 
The first report of Aplastic anemia in Pregnancy  was publised by Ehrlich in 1888
 Pathophysiology of pregnancy associated AA – high levels of hormones during
pregnancy
The level of placental lactogen ,erythropoietin- stimulate the function of
hemopoiesis
Increased estrogen  during pregnancy -  inhibits erythropoiesis
 
Aitchison RG, Marsh JC, Hows JM, Russell NH, Gordon-Smith EC. Pregnancy associated aplastic anaemia: a report of five cases and review of
current management. Br J Haematol. 1989;
73
:541–545. doi: 10.1111/j.1365-2141.1989.tb00294.x. [
PubMed
] [
CrossRef
] [
Google Scholar
]
 
APLASTIC ANEMIA IN
PREGNANCY
 
 
Haemorrhage and   sepsis due to pancytopenia are the major reasons
for death in pregnant  women with aplastic anemia
 Immunosuppressive agents or hemopoietic stem cell transplantation
are contraindicated during pregnancy.
 Supportive care remains the first line treatment for pregnant women
 
C
l
a
s
s
i
f
i
c
a
t
i
o
n
 
o
f
 
A
A
:
 
c
a
m
i
t
t
a
 
c
r
i
t
e
r
i
a
 
 
C
A
U
S
E
S
 
O
F
 
A
P
L
A
S
T
I
C
 
A
N
E
M
I
A
 
 
INHERITED-
Fanconi's anemia
Dyskeratosis congenita
Shwachman-Diamond syndrome
Reticular dysgenesis
Amegakaryocytic thrombocytopenia
Familial aplastic anemias
Preleukemia (monosomy 7, etc.)
Nonhematologic syndrome (Down, Dubowitz, Seckel)
 
C
A
U
S
E
S
 
O
F
 
A
P
L
A
S
T
I
C
 
A
N
E
M
I
A
 
 
ACQUIRED-
Radiation
Drugs and chemicals
Viruses (non-A, non-B, non-C Hepatitis, EBV, Parvovirus B19,
HIV-1)
Immune diseases (Eosinophilic fasciitis, Thymoma,
Hyperimmunoglobulinemia, Graft-versus-host disease)
Paroxysmal nocturnal hemoglobinuria, Pregnancy
Idiopathic
 
P
A
T
H
O
P
H
Y
S
I
O
L
O
G
Y
 
 
Bone marrow failure results from severe damage to the
hematopoietic cell compartment.
 
There is replacement of the bone marrow by fat.
 
An intrinsic stem cell defect exists for the constitutional aplastic
anemias
 
Extrinsic damage to the marrow follows massive physical or
chemical insults such as high doses of radiation and toxic
chemicals
 
Immune mediators like Helper T cells, TNF, IFN-
ϒ
 may be
involved in the pathogenesis.
 
C
L
I
N
I
C
A
L
 
P
R
E
S
E
N
T
A
T
I
O
N
 
E
f
f
e
c
t
s
 
o
f
 
a
n
e
m
i
a
 
i
n
 
p
r
e
g
n
a
n
c
y
 
m
a
t
e
r
n
a
l
 
c
o
m
p
l
i
c
a
t
i
o
n
s
 
 
During
pregnancy 
:
-Preterm labour
-Pre eclampsia
-Cardiac failure
 
During labour
-Uterine inertia
-Post partum
Hemorrhage
-Shock
Puerperium
-Sub involution
-Puerperal
sepsis
-Failing
lactation
-Pulmonary
embolism
 
Neonatal complications
 
Prematurity
Intra uterine growth retardation
Low birth weight
Poor APGAR score
Fetal distress
Neonatal Anemia
 
I
N
V
E
S
T
I
G
A
T
I
O
N
S
 
BLOOD
CBC
     Peripheral smear
     Reticulocute count
     B 12/folate
     LFT
     Virology
FLOW CYTOMETRY FOR PNH
BONE MARROW ASPIRATE AND BIOPSY
 
 
 
 
 
 
 
 
 
 
 
 
 
L
A
B
 
F
I
N
D
I
N
G
S
 
Severe pancytopenia with  relative lymphocytosis
Normochromic ,normocytic RBCs
Mild to moderate  anisocytosis and poikilocytosis
Decreased reticulocyte count
Hypocelullar bonemarrow with > 70% yellow marrow
 
B
M
 
B
I
O
P
S
Y
 
 
H
Y
P
O
C
E
L
L
U
L
A
R
,
 
I
N
C
R
E
A
S
E
D
 
F
A
T
 
S
P
A
C
E
S
 
 
N
O
R
M
O
C
E
L
L
U
L
A
R
 
B
O
N
E
 
M
A
R
R
O
W
 
 
D
I
F
F
E
R
E
N
T
I
A
L
 
D
I
A
G
N
O
S
I
S
 
 
Paroxysmal noctural hemoglobinuria
 
Inherited marrow failure
 
Myelodysplastic syndrome(MDS)
 
M
A
N
A
G
E
M
E
N
T
 
 
1. Identification and elimination of underlying
cause
 2.supportive therapy
 
3.Hemotopoietic stem cell transplantation
 
4.Immunosuppressive treatment
 
5.Androgens
 
6.Growth  factors (GM,CSF,G-CSF,EPO)
 
 
S
U
P
P
O
R
T
I
V
E
 
T
H
E
R
A
P
Y
 
              Supplementation of blood products
             Prevention and treatment of haemorrhage
              Prevention and treatment of infection
 
 
B
O
N
E
M
A
R
R
O
W
 
T
R
A
N
S
P
L
A
N
T
A
T
I
O
N
 
Treatment of choice
Correction of haematopoetic defect
The best therapy for the younger patient with fully
histocompatible sibling donor.
Long term survival rates :80-90%
Donor stem cells > 4 x 10
5-15% risk of graft failure in multitransfused patients
 
 
I
M
M
U
N
O
S
U
P
P
R
E
S
S
I
O
N
 
As most of patients lack suitable donor, it is the treatment of
choice for them.
Antithymocyte globulin (ATG)
Antilymphocyte globulin (ALG)
Cyclosporin
Intensive immunosuppression :
    
       cyclophosphamide
corticosteroids
 
I
M
M
U
N
O
S
U
P
P
R
E
S
S
I
O
N
 
 
Increasing age and the severity of neutropenia are the most
important factors weighing in the decision between transplant
and immunosuppression in adults who have a matched family
donor.
 
 
Older patients do better with Anti thymocyte globulin  and
cyclosporine, whereas transplant is preferred if granulocytopenia
is profound.
 
 
 
M
A
N
A
G
E
M
E
N
T
 
O
F
 
A
A
 
-
 
P
R
E
G
N
A
N
C
Y
 
 
Little research has been published about therapy for aplastic
anemia during pregnancy. In fact, only case reports and
series with small sample sizes are available.
 
 
 In young non-pregnant patients first choice therapy for
aplastic anemia is allogenic stem cell transplantation with a
five-year survival of 70 to 80%
 
 
However, stem cell transplantation is not feasible during
pregnancy because of the teratogenic effects of the
immunotherapy and radiotherapy for the unborn child
 
Aitchison RG, Marsh JC, Hows JM, Russell NH, Gordon-Smith EC. Pregnancy associated aplastic anaemia: a report of five cases and review of
current management. Br J Haematol. 1989;
73
:541–545. doi: 10.1111/j.1365-2141.1989.tb00294.x. [
PubMed
] [
CrossRef
] [
Google Scholar
]
 
 
 
 
 
.
 
M
A
N
A
G
E
M
E
N
T
 
O
F
 
A
A
 
-
 
P
R
E
G
N
A
N
C
Y
 
 
Pregnancy termination to start bone marrow
transplantation was not recommended because of
the relatively good prognosis for both mother and
child.
 
 
During pregnancy supportive therapy with
erythrocyte and platelet transfusions is a widely
used, reasonable alternative
 
C
O
N
C
L
U
S
I
O
N
 
 
Aplastic anaemia is a serious condition which may manifest
during pregnancy.
 
The seriousness depends on the degree of bone marrow
suppression.
 
Most pregnant patients will have full-term pregnancies with
a healthy child with supportive care
 
Fortunately,aplastic anaemia has a low mortality due to
treatment
 
C
O
N
C
L
U
S
I
O
N
 
 
As described in this case,the benefit of transfusions to
prevent bleeding should be weighed against the likelihood
of developing HLA antibiodies and hemochromatosis in the
mother.
 
In case the patient responded insufficiently to supportive
therapy, immunotherapy with ATG,CsA  or
methylprednisolone can be started.
 
patient with severe AA was treated throughout the course of
pregnancy with haemopoietic growth factor in combination with
an immunosuppressive agents and supportive transfusion
undefined
During severe aplastic anemia or complications caused by
supportive therapy (PRBC and platelet tranfusion) ATG,
cyclosporine can be used
undefined
Conservative transfusion management
is critical to prevent alloimmunization.
undefined
 
P
R
O
P
H
Y
L
A
C
T
I
C
 
M
E
A
S
U
R
E
S
 
 
Prophylactic platelet transfusion at delivery.
 
Prophylactic analgesics and antibiotic coverage during
delivery.
 
Assisted second stage of labour in cases of vaginal delivery.
 
In post-partum period,perineal infection should be avoided.
 
T
A
K
E
 
H
O
M
E
 
M
E
S
S
A
G
E
 
 
 
A multidisplinary - team  approach to the management of aplastic
anemia in pregnancy  involving the obstetrician ,the hematologist
,Anaesthetist and  neonatologist is necessary to
                                              Coordinate  antenatal care
 
                                             Optimize maternofetal outcomes &
 
                                             Plan peripartum interventions
 
 
Good supportive care and blood transfusion resulted in successful
outcome in our patient.
 
 
Obstetrics,Haematologist,Neonatologist ,Anaesthetist & lab services,
Madras Medical Mission
undefined
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A 23-year-old primigravida with recently diagnosed aplastic anemia presented for antenatal care. History of UTI, pancytopenia, and transfusions were noted. Hematologist confirmed aplastic anemia with hypocellular marrow. Despite challenges, pregnancy was managed with multidisciplinary approach including repeat bone marrow evaluations. Hematologist advised regular blood counts and transfusions as needed. Close monitoring ensured optimal management throughout pregnancy.

  • Case Report
  • Aplastic Anaemia
  • Pregnancy Management
  • Hematologist Advice
  • Antenatal Care

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  1. APLASTIC ANAEMIA IN APLASTIC ANAEMIA IN PREGNANCY PREGNANCY - - A CASE REPORT REPORT A CASE Dr.Sofia.K (Fellow in Reproductive medicine) Dr.V.Geetha ,Dr.Lakshmi , Dr.Kundavi Institute of reproductive medicine, Madras medical mission Monday,15th February 2021(online)

  2. CASE REPORT 23 year old primi presented to IRM at 7weeks +4days for antenatal care with an history of recently diagnosed aplastic anemia.

  3. History of presenting illness History of presenting illness Patient was married at 23 years 3 months after marriage Developed UTI associated with chills and rigor. Evaluated at private hospital and Routine laboratory tests showed pancytopenia Haemoglobin of 7gm/dl, Platelet 37000 & TC-3,600 & 3 units of PRBC transfused

  4. INVESTIGATIONS INVESTIGATIONS Hematologist opinion was obtained Iron Normal Ferritin TIBC Bone marrow aspirate: Hypocellular marrow Dyserythropoiesis Absent iron storage A bone marrow biopsy confirmed the diagnosis of aplastic anemia.

  5. HISTORY HISTORY Menstrual History: Regular menstrual cycles Medical History: Evaluated for giddiness at 20 year and found to have mild anemia and vitamin B12 deficiency treated with vitamin B12 injection Surgical History: NIL Family History: NIL

  6. HISTORY HISTORY Obstetric History : NT scan First trimester screening NORMAL Anomaly Scan serial growth scans Her pregnancy was managed with multidisplinary approach .

  7. INVESTIGATIONS INVESTIGATIONS Repeat bone marrow done at early gestation Hypocellular marrow particles Normoblastic erthyropoiesis Mildy suppressed megakaryopoiesis Myelodysplastic syndrome panel by FISH Negative Chromosomal analysis Normal female karyotype 46XX

  8. HAEMATOLOGIST ADVICE Advised blood count every 2 weeks Haemoglobin < 8gm/dl - 2 units of packed red blood cells Platelet count < 20,000 4 units of platelets According to the Hematologists advice patient was managed accordingly.

  9. HAEMATOLOGICAL PROFILE HAEMATOLOGICAL PROFILE Date GA Hb platelet WBC Blood transfusion 3/12/19 7+4wks 12.7 37000 20/12/19 10 wks 10.6 45000 3840 2/1/20 12 wks 9.1 58000 2670 14/1/20 13+3 wks 7.1 60000 4000 2 PRBC 5/2/20 16+4 wks 7.7 50000 3900 2PRBC 19/2/20 18+4 wks 8.3 50000 3800 28/2/20 19+6 wks 6.8 50000 4000 2 PRBC 29/3/20 23 wks 6.7 38000 4500 2 PRBC 8/4/20 25+4 wks 7.5 26000 4200 1PRBC 15/4/20 26+4 wks 7.2 1 PRBC 27/4/20 28+2 wks 6.5 30000 3900 2 PRBC

  10. MANAGEMENT MANAGEMENT According to hematologist advise patient was transfused with PRBC and platelets Haemoglobin > 8gm/dl platelet > 20,000, To prevent the serious consequences of thrombocytopenia and anemia of the mother and fetus .

  11. MANAGEMENT MANAGEMENT At 35 weeks + 3 days of gestation decision to LSCS was made. 2 days before the lscs patient was Haemoglobin was 9gm and platelets 40,000 patient was transfused with 4 units of random platelets & 1 unit of PRBC Platelet refractoriness checked platelets after one hour -80,000 Antenatal steroids given for fetal lung maturity On the day of LSCS Haemoglobin - 9.9 gm/dl Platelet - 70,000

  12. DELIVERY DELIVERY Patient underwent Elective lscs at 35 weeks and 5 days with 4 units of platelets on flow under antibiotic coverage B A B Y . Alive male 2.470 kgs 9/10,9/10 Histopathology of placenta -: Umblical cord - Three blood vessel Membranes - No specific lesion placenta - Mild congestion

  13. Post operative period Post operative period Post operative period was uneventful POD Hb Platelet TC POD -0 9.9 1,00,000 7100 POD- 1 9.0 1,00,000 5700 POD-2 8.9 1,00,000 6200 POD-3 9.2 1,10,000 5500 Patient was discharged in stable condition on 4th POD. Haemoglobin - 9gm platelets -1 lakh

  14. WHAT IS APLASTIC ANEMIA? WHAT IS APLASTIC ANEMIA? . Aplastic anemia is a rare disease caused by destruction of pluripotent stem cells in bone marrow with an annual incidence of 2 to 6/10,00,000. In contrast to the term 'aplastic anemia', suggesting suppression of erythropoetic cell lines, all cell lines may be affected . Depending on affected cell lines, aplastic anemia is associated with fatigue, bleeding due to thrombocytopenia and recurrent infections due to neutropenia . The diagnosis 'aplastic anemia' is confirmed by hypocellularity of the bone marrow. The remaining cells are morphologically unaffected without malignant infiltration.

  15. APLASTIC ANEMIA IN PREGNANCY The first report of Aplastic anemia in Pregnancy was publised by Ehrlich in 1888 Pathophysiology of pregnancy associated AA high levels of hormones during pregnancy The level of placental lactogen ,erythropoietin- stimulate the function of hemopoiesis Increased estrogen during pregnancy - inhibits erythropoiesis Aitchison RG, Marsh JC, Hows JM, Russell NH, Gordon-Smith EC. Pregnancy associated aplastic anaemia: a report of five cases and review of current management.Br J Haematol. 1989;73:541 545. doi: 10.1111/j.1365-2141.1989.tb00294.x.[PubMed] [CrossRef] [Google Scholar]

  16. APLASTIC ANEMIA IN PREGNANCY Haemorrhage and sepsis due to pancytopenia are the major reasons for death in pregnant women with aplastic anemia Immunosuppressive agents or hemopoietic stem cell transplantation are contraindicated during pregnancy. Supportive care remains the first line treatment for pregnant women

  17. Classification of AA: Classification of AA: camitta camitta criteria criteria

  18. CAUSES CAUSES OF APLASTIC ANEMIA APLASTIC ANEMIA INHERITED- Fanconi's anemia Dyskeratosis congenita Shwachman-Diamond syndrome Reticular dysgenesis Amegakaryocytic thrombocytopenia Familial aplastic anemias Preleukemia (monosomy 7, etc.) Nonhematologic syndrome (Down, Dubowitz, Seckel)

  19. CAUSES CAUSES OF APLASTIC ANEMIA APLASTIC ANEMIA ACQUIRED- Radiation Drugs and chemicals Viruses (non-A, non-B, non-C Hepatitis, EBV, Parvovirus B19, HIV-1) Immune diseases (Eosinophilic fasciitis, Thymoma, Hyperimmunoglobulinemia, Graft-versus-host disease) Paroxysmal nocturnal hemoglobinuria, Pregnancy Idiopathic

  20. PATHOPHYSIOLOGY PATHOPHYSIOLOGY Bone marrow failure results from severe damage to the hematopoietic cell compartment. There is replacement of the bone marrow by fat. An intrinsic stem cell defect exists for the constitutional aplastic anemias Extrinsic damage to the marrow follows massive physical or chemical insults such as high doses of radiation and toxic chemicals Immune mediators like Helper T cells, TNF, IFN- may be involved in the pathogenesis.

  21. CLINICAL PRESENTATION CLINICAL PRESENTATION Low RBC Low platelets Low WBC (Anemia) (Thrombocytopenia) (Leukopenia) Pallor Fatigue Dyspnoea Dizziness Chest pain Bleeding is the most common early symptom Easy bruising petechie epistaxis heavy menstrual flow Infections Fever. Flu- like illness

  22. Effects of anemia in pregnancy Effects of anemia in pregnancy maternal complications maternal complications During pregnancy : -Preterm labour -Pre eclampsia -Cardiac failure During labour -Uterine inertia -Post partum Hemorrhage -Shock Puerperium -Sub involution -Puerperal sepsis -Failing lactation -Pulmonary embolism

  23. Neonatal complications Prematurity Intra uterine growth retardation Low birth weight Poor APGAR score Fetal distress Neonatal Anemia

  24. INVESTIGATIONS INVESTIGATIONS BLOOD CBC Peripheral smear Reticulocute count B 12/folate LFT Virology FLOW CYTOMETRY FOR PNH BONE MARROW ASPIRATE AND BIOPSY

  25. LAB FINDINGS LAB FINDINGS Severe pancytopenia with relative lymphocytosis Normochromic ,normocytic RBCs Mild to moderate anisocytosis and poikilocytosis Decreased reticulocyte count Hypocelullar bonemarrow with > 70% yellow marrow

  26. BM BIOPSY BM BIOPSY HYPOCELLULAR, INCREASED FAT SPACES HYPOCELLULAR, INCREASED FAT SPACES

  27. NORMOCELLULAR BONE MARROW NORMOCELLULAR BONE MARROW

  28. DIFFERENTIAL DIAGNOSIS DIFFERENTIAL DIAGNOSIS Paroxysmal noctural hemoglobinuria Inherited marrow failure Myelodysplastic syndrome(MDS)

  29. MANAGEMENT MANAGEMENT 1. Identification and elimination of underlying cause 2.supportive therapy 3.Hemotopoietic stem cell transplantation 4.Immunosuppressive treatment 5.Androgens 6.Growth factors (GM,CSF,G-CSF,EPO)

  30. SUPPORTIVE THERAPY SUPPORTIVE THERAPY Supplementation of blood products Prevention and treatment of haemorrhage Prevention and treatment of infection

  31. BONEMARROW TRANSPLANTATION BONEMARROW TRANSPLANTATION Treatment of choice Correction of haematopoetic defect The best therapy for the younger patient with fully histocompatible sibling donor. Long term survival rates :80-90% Donor stem cells > 4 x 10 5-15% risk of graft failure in multitransfused patients

  32. IMMUNOSUPPRESSION IMMUNOSUPPRESSION As most of patients lack suitable donor, it is the treatment of choice for them. Antithymocyte globulin (ATG) Antilymphocyte globulin (ALG) Cyclosporin Intensive immunosuppression : cyclophosphamide corticosteroids

  33. IMMUNOSUPPRESSION IMMUNOSUPPRESSION Increasing age and the severity of neutropenia are the most important factors weighing in the decision between transplant and immunosuppression in adults who have a matched family donor. Older patients do better with Anti thymocyte globulin and cyclosporine, whereas transplant is preferred if granulocytopenia is profound.

  34. MANAGEMENT OF AA MANAGEMENT OF AA - - PREGNANCY PREGNANCY Little research has been published about therapy for aplastic anemia during pregnancy. In fact, only case reports and series with small sample sizes are available. In young non-pregnant patients first choice therapy for aplastic anemia is allogenic stem cell transplantation with a five-year survival of 70 to 80% However, stem cell transplantation is not feasible during pregnancy because of the teratogenic effects of the immunotherapy and radiotherapy for the unborn child Aitchison RG, Marsh JC, Hows JM, Russell NH, Gordon-Smith EC. Pregnancy associated aplastic anaemia: a report of five cases and review of current management. Br J Haematol. 1989;73:541 545. doi: 10.1111/j.1365-2141.1989.tb00294.x. [PubMed] [CrossRef] [Google Scholar]

  35. MANAGEMENT OF AA MANAGEMENT OF AA - - PREGNANCY PREGNANCY . Pregnancy termination to start bone marrow transplantation was not recommended because of the relatively good prognosis for both mother and child. During pregnancy supportive therapy with erythrocyte and platelet transfusions is a widely used, reasonable alternative

  36. CONCLUSION CONCLUSION Aplastic anaemia is a serious condition which may manifest during pregnancy. The seriousness depends on the degree of bone marrow suppression. Most pregnant patients will have full-term pregnancies with a healthy child with supportive care Fortunately,aplastic anaemia has a low mortality due to treatment

  37. CONCLUSION CONCLUSION As described in this case,the benefit of transfusions to prevent bleeding should be weighed against the likelihood of developing HLA antibiodies and hemochromatosis in the mother. In case the patient responded insufficiently to supportive therapy, immunotherapy with ATG,CsA or methylprednisolone can be started.

  38. patient with severe AA was treated throughout the course of pregnancy with haemopoietic growth factor in combination with an immunosuppressive agents and supportive transfusion

  39. During severe aplastic anemia or complications caused by supportive therapy (PRBC and platelet tranfusion) ATG, cyclosporine can be used

  40. Conservative transfusion management is critical to prevent alloimmunization.

  41. PROPHYLACTIC MEASURES PROPHYLACTIC MEASURES Prophylactic platelet transfusion at delivery. Prophylactic analgesics and antibiotic coverage during delivery. Assisted second stage of labour in cases of vaginal delivery. In post-partum period,perineal infection should be avoided.

  42. TAKE HOME MESSAGE TAKE HOME MESSAGE A multidisplinary - team approach to the management of aplastic anemia in pregnancy involving the obstetrician ,the hematologist ,Anaesthetist and neonatologist is necessary to Coordinate antenatal care Optimize maternofetal outcomes & Plan peripartum interventions Good supportive care and blood transfusion resulted in successful outcome in our patient.

  43. Obstetrics,Haematologist,Neonatologist ,Anaesthetist & lab services, Madras Medical Mission

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