Clinical Cases in Obstetrics and Gynecology Haresh U Doshi
Page numbers followed by f refer to figure, fc refer to flowchart, and t refer to table
Abnormal uterine bleeding 208, 226
acute 226
anovulatory 232
chronic 226
clinical evaluation 227
examination 228
history 227
incidence 226
investigations 228
management of 233
ovulatory 233
symptoms of 227t
treatment of 229
Abortion 61, 105, 115, 275
Abruption placenta 132, 132t
Abscess 164
Absorption 5, 13
Acanthosis nigricans 254
Acid-fast bacillus 147
Acidophilic erythroblast 6
Acidosis 119
Acids 6
Acne 254, 258
Acquired immunodeficiency syndrome 161
Activated partial thromboplastin time 127
Acyclovir 176
Add-back therapy 250
Adenocarcinoma 194, 195
Adenoma, pituitary 235
Adenomyosis 213, 229, 252
differential diagnosis 252
management 253
physical examination 252
symptoms 252
ultrasound 252
Adjuvant therapy 119
Adnexal mass during pregnancy, differential diagnosis of 280
Aedes aegypti 152, 154
Agenesis 106
Aggressive insulin therapy 109
Air embolism 119
Albumin antibodies 115
Alkalies 6
Alloimmunization, ultrasonography classification of 118
Alopecia 254
Alphadopa 6
Alpha-thalassemia 16
Amenorrhea 254, 261
primary 261
secondary 261
types of 261fc
Amiodarone 180
Amniocentesis 115, 117, 183
Amnioinfusion 78, 94
antenatal 184
Amnioreduction 183
Amnioscopy 83
Amniotic fluid 81, 84
index 83, 92, 118
volume 83
Amnisure 76
Amsel's criteria 286
Anastrozole 250
Androgen 211, 233
Anemia 3, 8, 21, 61, 67, 142, 143, 178
addisonian pernicious 14
aplastic 3
causes of 8, 8
chronic hemolytic 19
congenital 115
correction of 133
degree of 3, 7
diagnosis of 7
dimorphic 15
hemolytic 8
hemorrhagic 15
megaloblastic 8
microcytic 8
nutritional 4, 15t
severe 20, 70
sideroblastic 8
Anencephaly 106
examination under 199
general 116
Aneuploidies, screening for 59
Ankles, edema of 6
Ankylostoma duodenale 4
Anorectal atresia 106
Anorexia 6, 199
Antacids 6
Antenatal management 52, 121f
Antepartum 63, 151
bleeding, active 134
distress 111
surveillance 110
management 92, 124
Anterior vaginal wall
cyst 220
prolapse 220
Antibiotics 73
prophylactic 157
formation, mechanism of 115
types of 115
Anticardiolipin antibodies 101
Anticoagulants 127
Anticonvulsants 32
Antifibrotic agent 214
Antihypertensive management 34
Anti-Müllerian hormone 101
Antiphospholipid antibody 101
syndrome 25, 28, 90, 98, 101, 102
Antiprogesterones 210
Antiprogestins 249
Antiretroviral drugs 165
Antithyroid drugs, side effects of 180
Antiviral drugs 159
Anuria 26
Aorta, coarctation of 126
Aortic isthmic Doppler 93
Aortic stenosis 125
Aplasia cutis 180
Aplastic crisis 19
Apnea, recurrent 74
Appendicitis, acute 68
Aromatase inhibitors 250
Arrhythmias, cardiac 123, 127
Ascites 117
Ascorbic acid 6
Asoprisnil 214
Asphyxia 31
endometrial 229
pneumonia 31
Aspirin, low dose 27, 92
Assisted breech delivery 43
Assisted hatching 243
Assisted reproductive technology 25, 242, 243
Asthma 67
Atosiban 72
injection, steps of 72t
Atresia, esophageal 182
Atrophic vaginitis 287
Atrophy, postmenopausal 218
Attack, acute 143
Azithromycin 159
Azoospermia 243
obstructive 241
Backache 7
low dull 68
Bacterial vaginosis 68, 286
clinical features 286
diagnosis 286
treatment 286
Bacteriuria, asymptomatic 8, 68, 144
Baden walker halfway system 216
Ball sign 185
Barker's hypothesis 95
Barrier contraceptives 111
Bartholin's glands 285
Basal body temperature 238
Basophilic erythroblast 6
Betamethasone 73, 92
Beta-mimetics 70
mechanism of action of 71
Beta-thalassemia 16, 18
intermedia 17
minor 17
Bethesda system 195
revised 195t
Bilirubin, serum 8
Biochemical methods 91
Biophysical profile 82, 85, 92
cervical 199
endometrial 229
Biparietal diameter 84
asphyxia 74, 81, 94
weight 61
Bladder 208, 281
Blake's cyst 155
Bleeding 131
first trimester 84
pathophysiology of 130
vaginal 54
Blind spots 26
Blindness 26, 27
temporary 31
components 293
pressure 25, 31
fasting 101
postlunch 101
transfusion 11, 12, 134
massive 12
prophylactic 21
urea nitrogen 26
volume changes 3f
Body iron, distribution of 5t
Body mass index 58, 188, 245
pre-pregnancy 25
Bone marrow examination 8
Bonney's clamp 212
Bracht maneuver 45
Bradyzoites 169
Breastfeeding 119, 166
exclusive 166
Breath, shortness of 165
Breech 38, 39
complete 39, 39t
etiological factors of 38t
incidence 38
types 38
Burns-Marshall method 44, 45f
Buserelin 250
Cachexia 199
carbonate 6
citrate 6
salts 6
supplement 27
Cancer cervix, effects of pregnancy on 278
albicans 162, 285
tropicalis 285
Candidial vulvovaginitis 285
clinical features 285
diagnosis 285
treatment 285
Candidiasis, recurrent 286
Carbimazole 180
Carbohydrates, complex 113
Carbonyl iron 9
Carboxymethylcellulose 212
cervix 193, 278
etiology 193
FIGO staging 200t
macroscopic appearance 194
mode of spread 194
pathology 194
in situ 195
ovarian 279
peritoneal 272
Cardiac disease 68, 70
Cardiac dysfunction 178
Cardiac failure 6, 7, 31, 119
Cardiac surgery 127
Cardinal ligaments 217
Cardiomyopathy, peripartum 123, 126
Cartridge-based nucleic acid amplification test 147
Cellulose, oxidized regenerated 212
Centchroman 231
Center for Disease Control 3
Central nervous system 106
Cephalopelvic disproportion 49, 53, 188
artery, middle 93, 117
spinal fluid 31
venous thrombosis 31
precursors 194
screening, methods of 195, 196t
cerclage 69
erosion 288
factor 241
fibroid 199
infections, treatment of 69
intraepithelial neoplasia 195, 198
length assessment 68
papilloma 199
pessary 70
polyp 199
stump, carcinoma of 205
weakness 99
Cervicitis 287
acute 287, 288
chronic 288
clinical features 289
management 289
Cervilenz 74
Cervix 84
carcinoma of 193, 198, 199, 201, 205
elongated 220
funneling of 68f
hardening of 199
malignant lesions of 195
premalignant lesions of 194, 195
tuberculosis of 199
visual inspection of 198
Cesarean delivery 134
elective repeat 48
Cesarean section 42, 93, 94, 115
lower segment 41, 59
role of 74
Chemoprophylaxis 143
Chemoradiation 205
Chemotherapy 205
hyperthermicintraperitoneal 273
intraperitoneal 273
neoadjuvant 273
Chlamydia trachomatis 162, 193, 288
Chloroquine 143
Chocolate cyst 247
Cholelithiasis 149
Cholestasis, intrahepatic 149
Chorioamnionitis 70
Chorionic villus sampling 59
Chorionicity, determination of 57
Chorioretinitis 173
congenital toxoplasmosis of 170
Choroid plexus cyst 155
Chromopertubation 239
Cimetidine 6
Ciprofloxacin 6
Cirrhosis 149
Citric acid 6
Clindamycin 286
Clomiphene citrate 241, 258
Clonus 26
Clot observation test 138
Clotrimazole 286
Clue cells 286, 287f
Coagulation disorder 27, 31
clinical screening for 228t
Coccyx, borders of 217
Cold coagulation 201
Colitis, necrotizing 119
Collagen matrix 208
Collascope 74
Colpocleisis, complete 224
Colpoperineorrhaphy 223
anterior 223
posterior 223
Colposacropexy 224
Colposcopy 197
abnormal 197
cervicography 197
guided biopsy 199
indications 197
method 197
unsatisfactory 197
Coma, stage of 30
Combined hormonal contraceptives 249
Combined oral contraceptive 230, 233
Complete androgen insensitivity syndrome 264
Complete blood count 26, 228
Cone biopsy 199
types of 202
Congenital rubella 171, 172
high risk of 172
investigations 172
manifestations 172
mode of transmission 171
prevention 172
risk of transmission 172
treatment 172
Conjoined twins 63
Conjunctiva 22
Conjunctivitis 22, 159
Contraception 21, 111, 125
injectable 111
oral 211, 268
pills 194
Contraction stress test 83
Convulsion, differential diagnosis of 31t
Coomb's tests 8
Copper deficiency 8
compression 81
problems 81, 94
Cordocentesis 115, 118
Corona virus 158f
Coronary artery disease 123, 127
Corpus luteal cyst 280
Corticosteroids, antenatal 133
Cough 165
Covaxine 159
COVID-19 158
clinical features 158
management 159
mode of infection 158
symptoms 159
treatment of 159
Covishield 159
Cramps, abdominal 68
Crisis 19
hemolytic 19
megaloblastic 20
painful 19
treatment of 20
Crown-rump length 59, 84
Cryoablation 232
Cryoprecipitate 293
Cul de sac obliteration 246
Cyanocobalamin 14
Cyst, simple 279
Cystadenocarcinoma, bilateral serous 267f
Cystectomy 251
Cystic degeneration 276
Cystitis 144
Cystoscopy 201, 248
Cytomegalovirus 149, 173
clinical manifestation 173
congenital 173
epidemiology 173
etiopathogenesis 173
fetal infection 174
human 173
investigations 174
maternal infection 174
modes of transmission 173
perinatal infection 173
prevention 174
treatment 174
Daily fetal monitoring chart 84
Daily fetal movement count 82, 85
chart 92
Danazol 231, 250
Dawn phenomenon 112
D-chiro-inositol 257
Deafness, sensorineural 172
Death, causes of 31
Dehydration 81
Delivery, mode of 93, 118
fever 152, 154
clinical course of 153f
critical phase 152
diagnosis 154
febrile phase 152
prevention 154
recovery phase 153
signs 152
symptoms 152
treatment 154
warning signs 153
infection 152, 154
severe 152, 153
uncomplicated 153
virus 152, 152f
Dengvaxia 154
Deoxyribonucleic acid 13, 101
Desmopressin 233
Dexamethasone 72, 73, 92
Dhall-Mittal scoring, modified 53t
Diabetes 68, 83, 90
effects of pregnancy on 105
hybrid forms of 104
mellitus 49, 53, 99, 104
gestational 25, 104106
pregestational 25, 105
treatment of 240
types of 104
Diazepam 32, 33
Dienogest 249
Diet 63
Disproportionate intrauterine growth intervention trial 95
Disseminated intravascular coagulation 12, 31
Divalent metal transporter 1 5
Dizziness 6, 26
Docetaxel 274
Donor twin, hydrops of 60
Doppler studies 83, 92, 93
Down syndrome 18, 186
screening for 187
Drowsiness 26
Drugs 6, 68
Dry Cusco's bivalve speculum 196
Ductusvenosus 93
Duodenal atresia 106, 182
Duplex ureter 106
Dysmaturity syndrome 81
Dysmenorrhea 208, 246
Dyspepsia 6
Dysphagia 6
Dysplasia 194
Dyspnea 6
Dystocia 275
Eclampsia 24, 31, 32, 149
complications of 31
Edema 6, 22, 25, 36, 164
cardiogenic pulmonary 26
non-cardiogenic pulmonary 26
pulmonary 25, 27, 31
Ederson hypothesis classification 104
Efavirenz 165, 166
Eflornithine 259
Eisenmenger's syndrome 126
Ejaculatory disturbance 241
Ejection systolic murmurs 22
Elderly primigravida 186
labor 187
management 187
pregnancy 186
puerperium 187
Electrodiathermy 201
Elkin's maneuver 46
Embryo transfer 242
Embryonic chromosomal abnormalities 98
Encephalitis 176
herpetic 175
Encephalopathy, hypoxic ischemic 91
Endocervical curettage 199
Endocervical gel 186
Endometrial ablation techniques 231
Endometrioma 249f
Endometriosis 245
classification 245
complications 248
diagnosis 245
differential diagnosis 248
extragenital 252
invasive testing 248
investigations 247
management 248
physical examination 247, 247t
risk of malignancy 248
sites of 245
management 250
treatment of 250
symptoms of 246, 246t
Endothelial cell activation 152
Entercolitis, necrotizing 94
Enterocoele repair operations 224
Epilepsy 31
Episiotomy, generous mediolateral 44
Epithelial cell abnormalities 195
Epithelial ovarian cancer 267
FIGO staging of 270f
guidelines for staging in 271
endocervical 283
squamous 198
Epstein-Barr virus 149
Erythrocyte 6
Erythropoiesis 5, 6
Erythropoietin 11
Estrogen 233
Ethambutol 148
Ethamsylate 230
Etoposide 274
Exchange transfusion 12, 119
Excretion 5
External cephalic version 41, 115
changes 26
complications 31
defects 172
Fadrozole 214
Failing lactation 7
Fallot tetralogy 126
Famicyclovir 176
Fatigue 6, 13
Favipiravir 159
Feeding difficulties 74
Femoral length 89
Fenticonazole 286
Ferric carboxymaltose 10
Ferric iron 5, 6
Ferric pyrophosphate 9
Ferrous ascorbate 9
Ferrous bisglycinate chelate 9
Ferrous fumarate 9
Ferrous gluconate 9
Ferrous iron 6
Ferrous salts 9
Ferrous succinate 9
Ferrous sulfate 9
acoustic stimulation test 82
anomalies 67
assessment 133, 134
blood sampling 18
breathing movements 69, 83
complications 61
death 31
distress 70
echogenic bowel 91
fibronectin 68
growth restriction 89
rate, reactive 83
sound 39, 41
infection 156
monitoring 109
movements 84
absence of 185
ponderal index 94
risks 50
surveillance 84
thyroid agenesis 179
tone 83
vessels, Doppler studies of 92
well-being assessment 82, 92
Fetomaternal bleed 116
Fetoscopy 115
Fetus, acardiac 62
Fibrin degradation products 27
Fibrinogen 27
Fibristal 214
Fibroid 207
classification 207
clinical features 208
diagnosis 209
etiology 207
hysteroscopy 209
multiple 213f
pathology 208
polyp 220
pregnancy 275
clinical diagnosis 276
effects of 209, 275
risk factors for 207t
signs 209
symptoms 208
type of 207, 207f
Fibromyoma 207
Fibrous tissue 208
FIGO classification 208f
Finasteride 259
Finger compression 212
Flamm Geiger scoring system 52
Flamm score 52t
Flaviviridae 152, 154
Flavivirus 152, 154
Fluid 81
leaking per vagina 68
Fluorescent microscopy 142
Flutamide 259
Foley's catheter 186
Folic acid 14t, 20
deficiency anemia 13
supplements 13, 19
Follicle-stimulating hormone 259
Formiminoglumatic acid excretion test 13
Fothergill-Manchester operation 222
Frank breech 38, 39, 39t
Freda's grading 117
Free erythrocyte protoporphyrin 8
Free tri-iodothyronine 101
Fresh frozen plasma 293
grip 39
height 91
Gamete intrafallopian transfer 243
Gastric delivery system 9
Gastroenteritis 68
Gastrointestinal tract 163
Gemcitabine 274
Genital herpes infection 176
Genital prolapse 215
differential diagnosis 220
etiology 218
examination 219
investigations 220
prevention 220
symptoms 218
treatment 220
Genital tract 163, 262
infection, treatment of 240
Gestational age 77, 84
small for 89
Gestational diabetes mellitus 25, 104106
maternal complications of 107
prevalence of 104
screening for 107
Gestrinone 250
Giant polymorphs 14
Giddiness 6
Glandular cell 195
Glomerular filtration rate 26
Glossitis 6, 22
Glucocorticoids 72
Glucose tolerance test 107t
Glucose-6-phosphate dehydrogenase screening 8
Glycosylated fructosamine level 113
Gonadotoxic factors, avoidance of 240
Gonadotropin 241, 258, 291
releasing hormone
agonists 250
analogs 211
Goodall-Power modification 223, 224
Goserelin 211, 250
Grand multipara 187
labor 188
management 188
pregnancy 187
puerperium 188
Great vessels, transposition of 106
monitoring 63
restriction intervention trial 95
Gynecology diseases 275
disease, severe 157
infection 156, 159
influenza A 157
virus 156f
Head 41
circumference 89
Headache 6, 26, 31, 159
abnormalities 172
disease 123
congenital 59, 123, 126
types of 123
failure 27
Hellins rule 57
Hematocrit 13
Hematuria 8, 26, 54
Heme iron 6
Hemoglobin 3, 16
Hemoglobinopathies 3, 8, 15
Hemolysis, elevated liver enzymes, low platelets syndrome 25, 27, 34, 34
Hemorrhage 127
accidental 27, 136
acute 15
antepartum 43, 53, 61, 67, 90, 115, 130, 130t, 132
cerebral 31
chronic 15
intracranial 27
postpartum 6, 27, 61, 130, 165, 275
Hepatic failure 31
A 149
B 149
C 149
chronic 149
D 149
E 149
serological markers 150t
viral 149
viruses 149t
Hepatorenal failure 31
Hepatotoxic drugs 149
Hernia, congenital diaphragmatic 59
Herpes infection, neonatal 176
Herpes simplex virus 149, 174
clinical manifestations 175
diagnosis 175
infection 176
types of 174
mode of transmission 175
neonatal infection 175
prevention 176
transmission of 175
vaccine 176
High performance liquid chromatography 20
Hirsutism 254, 258
Hormone therapy 241
Howell-Jolly body bodies 14
Human chorionic gonadotropin levels 291
Human immunodeficiency virus infection 164, 193
in pregnancy 161, 162
clinical manifestation 161
diagnosis 162
effect of 162
epidemiology 161
etiology 161
fetal complications 163
major signs 162
minor signs 162
modes of transmission 161
pathogenesis 161
testing 162
Human leukocyte antigen 101
Human papilloma virus
DNA testing 197
infection 193
vaccines 205
Human placental lactogen 86, 104
Hydralazine 28
hydrochloride 28
Hydramnios 61, 113, 182
degrees of 183t
Hydration 143
Hydrocephalus 170
Hydrops fetalis 115, 182
Hydrothermal ablation 232
Hydroxychloroquine 159
Hyperandrogenic anovulation 256
Hyperbilirubinemia 94, 106
Hyperemesis gravidarum 112, 149
Hyperglycemia 104, 106
Hyperkalemia 119
Hyperplasia, congenital adrenal 265
Hyperprolactinemia 99
Hyperpyrexia 31, 68, 143
Hyper-reflexia 26, 31
Hypertension 24, 25, 29
acute 28t
chronic 24, 25, 30, 30t, 90
gestational 24, 25
masked 25
mild 26
pregnancy-induced 41, 53, 68, 83
severe 43, 90
white-coat 25
Hypertensive disorders 24, 24t
classification of 25
Hyperthermia 156
Hyperthyroidism 68, 70, 179, 180
etiology 180
exacerbation of 180
incidence of 179
role of surgery in 180
treatment 180
Hypervascularity 135
Hyperviscosity 94, 106
Hypocalcemia 74, 94, 106
Hypofunction, adrenocortical 81
Hypoglycemia 74, 81, 94, 106, 112
symptoms of 112t
Hypotension 54
Hypothermia 74, 94, 106
Hypothyroidism 99, 178, 181
congenital 179
diagnosis of 179
effects of pregnancy on 178
etiology 178
subclinical 179
treatment 179
Hypovolemia 81
Hypoxia 81
Hysterectomy 213, 213f, 232
abdominal 213
radical 202, 203, 203f
total 251
vaginal 222
Hysteria 31
Hysterosalpingography 239
differential diagnosis 210
management 210
secondary changes 210
Icterus gravis neonatorum 115
Idiopathic hypertrophic subaortic stenosis 126
Iliococcygeus fixation 224
Imferon 11
Imidazole 285
Immune antibodies, production of 115
Immunity 141
Immunosuppression 120
Immunotherapy 273
Impaired liver function 25
In vitro fertilization 242, 258
Indomethacin 72
Infection 6, 12, 20, 68, 101, 105, 173
acute 169
genital 176
intrauterine 68, 86
Infectious disease syndromes 173
Infertile couple, treatment protocol of 240fc
Infertility 235, 246, 247
cervical factor 239
etiology 235, 235t
evaluation 236
female partner 237
incidence 235
male partner 236
ovarian factor 238
treatment 240
tubal factor 239
unexplained 243
uterine factor 239
A 156
B 156
C 156
viruses 156
Infravaginalsacropexy 224
Inherited thrombophilic defects 100
Injuries 31
Inorganic iron 6
Inositols 257
Insomnia 6
like growth factor binding protein-1 69
sensitizers 257
therapy 108
International Society for Study of Hypertension in Pregnancy 25
Intracranial calcification 170
Intracytoplasmic sperm injection 242, 243
Intrapartum 61, 63, 109, 151
fetal distress 81, 91, 111
management 52, 85, 93, 124
Intrauterine fetal death 105, 184
complications 185
diagnosis 185
etiology 184
incidence 184
investigations 185
management 185
ultrasonography 185
Intrauterine growth restriction 7, 27, 41, 43, 84, 89
diagnosis of 91
Doppler studies in 92
early onset 93
etiology of 90t, 92
late onset 93
types of 89t, 93
Intrauterine insemination 242
Intrauterine transfusion 60, 118
Intravenous immunoglobulin therapy 120
Invasive cancer 271
management of 202
Iodine 180
Iron 13, 19
absorption 6
factors affecting 6t
cycle 5f
deficiency 3, 6, 15
anemia 4, 8
dextran 11
excess 6
food factors influencing absorption of 4t
intake, low 4
intoxication 11
metabolism 5
polymaltose complex 9
salts 6
serum 20
sorbitol citric acid complex 11
sucrose 10
therapy 8
Isoimmunization 115
Isoniazide 148
Isonicotinic hydrazide 148
Jaundice 74
Jaw flexion shoulder traction 44
Jeffcoate's classification 216
Joshi's single dose magnesium sulfate 31, 32
Kallaman's syndrome 235, 265
Kartagener's syndrome 236
Kejel's exercises 221
Kelly-Paterson syndrome 21
Ketoacidosis 112
Khanna's operation 222
Kidney disease 25
Klebsiella pneumoniae 144
Kleihauer-Betke-test 120
Klinefelter syndrome 235
Knee reflex 32
Koilonychia 6, 22
Kristeller maneuver 44
Labetalol 28
Labor 277
active management of third stage of 54
and delivery, management of 165
augmentation of 53
induction of 50, 53
management in 12
onset of 67
premature 132, 275
prolonged 81
stress 81
Lacunar flow 135
Lamivudine 165, 166
Lanreotide 214
Laparoscopic sling operations 222
Laparoscopy 239, 248
Laser vaporization 201
Last menstrual period 80, 91
Latent tubercular infection 147
Latzko-Okabayashi-Meigs operation 203
L-carnitine 241
Le Fort's operation 223
Le Fort's partial colpocleisis 224
Lead poisoning 8
Legs, edema of 22
Leiomyoma 207, 229
pathological variants of 208
Lethal malformation 70
Letrozole 241, 257
Leukorrhea 219, 283
pathological 283
physiological 283
Leuprolide 250
depot 211
Levatorani 217
Levator plication-vault fixation 224
Levodopa 6
Levonorgestrel intrauterine
device 249
system 230
Levothyroxine 179
Ligaments 217
Liposomal doxorubicin 274
Lithium 180
disease 68
enzymes, elevation of 231
function test 27
Lochia 165
Lopinavir 159, 165
Lovsetmaneuver 44
Low birth weight 89
Low mean corpuscular volume 17
Lower uterine segment
scar, ultrasonography monitoring of 51
wall thickness 51
Low-molecular-weight heparin 28, 127
Lugol's iodine, application of 198
injury, acute 12
problems 81
Luteal phase defect 100, 238
Lycopene 241
Lymphadenectomy, para-aortic 204
Lymphocytosis 147
Lymphogranuloma venereum 288
Lytic cocktail regimen 32, 33
MacFeeJhonson expectant treatment 133
MacKenrodt's ligament 217
Macropolycytes 14
Macrosomia 81, 106, 111, 113
sulfate 32, 71, 92
toxicity, serum levels of 33t
Magnetic resonance imaging 132
Malaria 8, 68, 141, 142
effects of pregnancy on 142
Malignant epithelial neoplasms, treatment of 272
Malpresentation 61, 67, 132
Marfan's syndrome 126
age 25, 90, 97
assessment 133, 134
death 31
distress 105
infection, primary 170
mortality 50
weight 97
Mauriceau-Smellie-Veit technique 44, 45f
Mayour-Rokitansky-Kuster-Hauser syndrome 264
McCall culdeplasty 224
Mean corpuscular
hemoglobin concentration 7, 13, 15
volume 7, 13, 15
Meconium 81, 94
aspiration 81
syndromes 91
problems 82f
Medical nutrition therapy 107
Medroxyprogesterone acetate 230, 249
Mefenamic acid 230
Membranes, preterm premature rupture of 40, 67
Meningitis 175
Menorrhagia 8
Menstrual blood loss 227
Menstrual cycle, during 283
Menstrual irregularity 254, 257
Mental confusion 26
Mersilene tape 222
Metabolic disorders 262
Metabolic syndrome 106, 255, 259
Metaplasia, immature 198
Metformin 257
Methimazole 180
Methyldopa 28
Metrogyl 286
Metronidazole 286
Microepididymal sperm aspiration 243
Microinvasive carcinoma, management of 202
Micro-ophthalmia 173
Microwave thermal ablation 231
Mifepristone 185, 231
Minerals 292
Minimally invasive surgery 231
Miscarriage 97
recurrent 97
threatened 90
Misoprostol 186
Mississippi classification 34
Mitral stenosis 123
Modified biophysical profile 92
Molecular biology 142
Molimina, premenstrual 227
Monoamniotic twins 63
Monosomy X 99
Monozygotic twins 57
types of 57t
Moschowitz operation 224
Motile spermatozoa 242
Mucinous cyst adenoma 269
Mucous membrane 6, 22
Multifetal gestation 25, 57, 58, 60, 62
Multiparity 194
Murmurs, hemic 22
Mycoplasma hominis 286
Myoinositol 257
Myolysis, laparoscopic 213
Myoma 207
enucleated 212
submucous 211
Myomectomy 211
abdominal 212
hysteroscopic 211
laparoscopic 212
vaginal 213
Nails 22
Naked eye single tube red cell osmotic fragility test 8
National High Blood Pressure Education Program, working Group of 24
National Vector Borne Disease Control Programme 141
Nausea 26, 31
Necatoramericans 4
Nephropathy, diabetic 111
Neural tube defects 182
Neurectomy, presacral 251
Nevirapine 166
New York Heart Association 124
functional classification 124t
Newborn prophylaxis 166
dose 166
duration 166
Nifedipine 28, 72
Nitric oxide donors 72
Nitroglycerin 28
Non-descent vaginal hysterectomy 232
Nonheme iron 6
Noninvasive prenatal testing 59, 60
Nonnucleoside reverse transcriptase inhibitors 165
Nonsteroidal anti-inflammatory drugs 154, 249
Nonstress test 20, 82, 82f, 85
Norethindrone acetate 249
Norethisterone 230
Nuchal translucency 61, 187
Nucleic acid
amplication testing 174, 284
test 162
Nucleoside reverse transcriptase inhibitors 165
Nulliparity 25
Obesity 188
labor 189
management 189
pregnancy 189
puerperium 189
Obstructive sleep apnea 25
Oligohydramnios 76, 81, 82f, 92, 183
causes of 81, 183
complications 184
cord compression 81
diagnosis 183
management 184
Oligomenorrhea 254
Oliguria 26
Oocytes 169
Optic atrophy 173
Oral antidiabetic drugs 108
Oral contraceptive 211, 268
pills 257
Oral iron 10, 11
preparations 9t
side effects of 10
therapy 8
Oral pills 125
Oral progesterones 230
Organic iron 6
Ormeloxifene 231
Orogenital sexual practices 174
Orthomyxoviridae 156
Oseltamivir 157, 159
Osteoporosis 211
maternal 127
Ovarian cancer 267
borderline 272f
diagnosis 269
differential diagnosis 270
epidemiology 267
etiology 267
familial 268
incidence 267
mode of spread 270
pathology 271
prevention 268
risk factors for 268t
screening for 268
signs 269
staging 270
symptoms 269
true hereditary 268
Ovarian carcinogenesis, concepts of 267
Ovarian endometrioma 245
management 251
Ovarian epithelial cancers 270
Ovarian hyperstimulation syndrome 244
Ovarian reserve 244
Ovarian tumor 279, 280
effects of pregnancy on 279
benign 279
borderline 271
Ovulatory dysfunction 230
treatment of 230
Packed cell volume 7, 11
Paclitaxel 274
Pain 208
causes of 247
complication of 46
epigastric 31
Palm Coein classification 208
Palpitation 6
Papanicolaou's classification 194, 194t
Papanicolaou's smear 195
procedure 196
Papovaviridae 193
Paracervical ligaments 222
Parasitology 141
Parenteral iron therapy 10
Partial androgen insensitivity syndrome 265
Partial thromboplastin time 27
diaphragm 217
endometriosis, superficial 245
examination 238
floor muscles 217, 220
exercises 221
grip 39
organ prolapse 215
pain 213, 247
pressure 199
feeling of 68
tumors 280
veins 208
Pelvis, contracted 49
Per abdomen examination 39
Per vaginal examination 39
Percutaneous balloon mitral valvotomy 124
Percutaneous epididymal sperm aspiration 244
Perinatal complications 31, 107
Perinatal deaths 7
Perinatal switch 59
Perineal body 218
Peripheral smear 7, 15
Peritoneal implants 251
Phenobarbitone 119
Phenytoin 32
sodium regimen 33
Phototherapy 119
Pirfenidone 214
Placenta 25
accreta 136
spectrum disorder 132, 135
manual removal of 116, 275
previa 130132, 134, 135, 187
asymptomatic 133
differential diagnosis of 132t
Placental abruption 178
Placental alpha macroglobulin-1 69
Placental growth factor 26
Placental insufficiency 81
Placental migration 131
folate 13
protein A
pregnancy associated 187
serum pregnancy-associated 26
Plasmapharesis, maternal 120
Platelet 293
count 27
Plummer-Vinson syndrome 21
Pneumonia 31, 156
Polychromatophilic erythroblast 6
Polycystic ovarian syndrome 100, 101, 238, 254, 258
evaluation 255
manifestations 254
differential diagnosis 256
management 256
pharmacological treatment 257
physical examination 255
pregnancy in 259
Polycythemia 81
Polyhydramnios 67, 105, 182
causes 182
complications 183
diagnosis 182
investigations 182
management 183
signs 182
symptoms 182
types 182
Polymenorrhea 247
Polyp 229
Polyposis colonic cancer 269
Polytetrafluoroethylene 212
POP-Q classification 215
Post-coital test 239
Posterior intravaginalslingoplasty 224
Posterior vaginal wall 220
Postmaturity 80, 81
Postpartum 61, 111
hemorrhage 6, 27, 61, 130
management of 135
Post-term pregnancy 80
management of 85
prevention of 87
Post-transfusion care 119
Potter's syndrome 184
Pouch of Douglas 223
Prague maneuver 45
Pre-eclampsia 20, 24, 25, 28, 30, 61, 90, 105, 178, 183
atypical 29
differential diagnosis of 30t
prediction of 25
severe 27, 29, 149
superimposed 24
ultimate cure of 28
Pregnancy 3, 6, 123, 127, 141
acute fatty liver of 149
after previous cesarean section 48
biochemical 243
early 58, 280
ectopic 115
effects of 14, 150
anemia in 6
diabetes on 105
tuberculosis on 146
iron requirement during 4t
late 280
loss 97, 97f
recurrent 97, 101, 176
morbidity 98
multiple 57, 67
postdate 80
precious 84
prolonged 80
teenage 188
termination of 172
test 228
thyroid disorders in 178
Prematurity 7, 27
care 109
counselling 124
Pressure effects 208
Preterm birth 61
Preterm labor 67, 70, 142
etiology 67
incidence 67
prediction of 68
prevention 69
Previous scar thickness 51
Primary amenorrhea 261
causes 261
evaluation 262
examination 262
history 262
investigation of 263, 265, 266fc
management 263
Primigravida 186
Pritchard's regimen 32
Procidentia, complete 216
Proerythroblast 6
Progesterone 69, 72, 111, 210
only pill 111
serum 229
Progestogens 249
high-dose 233
Progressive preterm labor, management of 74
Propylthiourasil 180
Prostaglandin 53
Prosthetic valves 123, 126
Protease inhibitors 165
Proteins, serum 8
Proteinuria 24, 25, 29
Prothrombin time 27
Pruritus 164
Psychosis, postpartum 31
Pteroylglutamic acid 14
Pubertal changes, Tanner's staging of 263t
Pubic hair growth 263
Pubocervical ligament 217
Puborectalis 217
Puerperal sepsis 7, 31
Puerperium 7, 12, 109, 277
Pulsatility index 93
Purandare'scervicopexy 222
Purandare's modification 203
Pyelonephritis 19, 145
Pyrazinamide 148
Pyrexia 141
Pyrimethamine 170
Quinine 68
Quintero's classification system 62
external beam 204
intracavitary 204
Radioactive iodine 181
Radiotherapy 204
Rapid diagnosis tests 142
Red blood cell 13
Red cell osmotic fragility test 8
Reifenstein's syndrome 235
Renal damage 31
Renal disease 68, 90
Renal failure 31
Renal function test 20, 26
Renal insufficiency 25
Repeat exchange transfusion, indications of 119
Resistant ovary syndrome 265
Respiratory illness, severe acute 159
Respiratory tract 163
infections 145, 146
Reticulocyte 6
Reticuloendothelial system 5
Retinal artery spasm 26
Retinal edema 26
Retinopathy, diabetic 112
Retroverted gravid uterus 280
diagnosis 281
differential diagnosis 281
effects on pregnancy 281
etiology 280
signs 281
symptoms 281
treatment 281
Reverse transcriptase-polymerase chain reaction 154
Revised American Fertility Society classification 246t
Revised National TB Control Programme 147
Rh incompatibility 84
Rh isoimmunization 67, 114
prevention of 116
Rheumatic heart disease 123
Ribavirin 159
Rifampicin 148
Ritodrine 71
Ritonavir 165
Robert's sign 185
Rotterdam criteria 255
Rubber tourniquet 212
Rubella 171
clinical manifestations 171
etiopathogenesis 171
infection 171
organism 171
Sacral ligament, anterior 224
Sacrocolpopexy, laparoscopic 224
Sacroposterior breech 41
Sacrospinous fixation 224
Saline antibodies 115
Savage syndrome 265
abdominal 185
dehiscence 53, 54f
endometriosis 252
rupture 53
tenderness 54
Schauta's radical vaginal hysterectomy 203
Schuardt's incision 203
Scotoma 26
Seizures, tonic-clonic 24
Selective fetal growth restriction 60
Semen, normal 237t
Senile vaginitis 287
Sepsis 74, 119
Sertoli cell 235
Serum folate 8
Serum glutamic
oxaloacetic transaminase 27
pyruvic transaminase 27
Sexual dysfunction 236
Shaw's classification 216
Shaw's operation 224
Shirodkar's sling 222
Shock 6
postpartum 31
Siamese twins 63
Sickle cell
anemia 18, 19
disease 18
syndromes 8
trait 18, 19
Sickle test 8, 20
Sickling 19f
crisis 20
syndromes 18
tests for 20
Siderophilin 5
Sims-Huhner test 239
manifestations 164
pallor of 6, 22
Sliding test 248
Sling operations, abdominal 221
feredetate 9
ferric gluconate 11
Somogyi phenomenon 112
Sonosalpingography 239
Spalding's sign 185
transport, impaired 236
vitalizing therapy 241
Spermatogenesis, defective 235
Spherocytosis, hereditary 8
Spina bifida 106
Spiramycin, dosage of 170
Spironolactone 258
Splenic sequestration crisis 20
Sporozoites 169
Squamous cell carcinoma 194, 195
Squamous intraepithelial lesion, low-grade 193, 195
Stabilization 134
Statins 257
Status eclampticus 31
Stem cells 6
Stenosis, pulmonary 126
Steroids 72, 92
administration 63
Stillbirths 91
Stomatitis 6
Strawberry cervix 284
Strawberry vagina 284
Stress 98
incontinence 219, 221
Subfertility therapy 58
Submucous fibroids 209
classification of 209, 210t
Sulphadiazine 170
abdominal 68
adjuvant 251
bariatric 259
cytoreductive 273
exenteration 203
Swine flu 156
Symphysial fundal height 58
Systemic lupus erythematosus 25
Systemic maternal endocrine disorders 99
Tachycardia 6, 22, 54
Tachypnea, transient 49
Tamoxifen 241, 258
Tanner's staging 262
Tennessee classification 34
Tenofovir 166
disoproxilfumarate 165
Terbutaline 71
Testicular sperm extraction 244
Tetany 119
Tetraploidy 99
Thalassemia 8, 12
facies 17
syndromes 15, 16
Thermal balloon ablation 231
Thiopentone sodium 33
Thrombocytopenia 25
heparin-induced 127
Thrombophilia 25
hereditary 101, 102
Thrombosis, heparin-induced 127
binding globulin 178
disease, treatment of 240
dysfunction of 262
function test 179, 229
stimulating hormone 101
storm 180
Thyroiditis, postpartum 181, 181t
Thyrotoxicosis 181
Thyroxine 179
Tissue cyst 169
Tocolysis 70
agents 70t
prophylactic 70
Tongue 22
bite 31
Topotecan 274
TORCH infections 169
Torsion 275
Torulopsis glabrata 285
Total iron-binding capacity 6
Toxoplasma gondii 169
Toxoplasmosis 169
clinical manifestation 169
congenital 169171
etiopathogenesis 169
mode of infection 169
prevention 171
serological tests 170
transmission of infection 169
treatment 170, 171
Trachelectomy, radical 204
Traditional surrogate 244
Tranexamic acid 230, 233
Transabdominal sonography 132
Transfusion reaction 12, 12t
Transvaginal sonography 101
Transvaginal ultrasonography 269
Trauma, abdominal 115
Trichomonas vaginalis 162, 284, 284f
Trichomoniasis 284, 287
clinical features 284
diagnosis 284
treatment 284
Tricuspid valve diseases 125
Triploidy 99
Triptorelin 211, 250
Trisomy 21 18
Trophoblastic disease, gestational 24
Trophozoite 169
Truffle study 95
Tuberculin test 147
Tuberculosis 68
effects of pregnancy on 146
pulmonary 146
Tumors, atypical proliferative 271
Turner's syndrome 262, 263
classical features of 263, 264t
Twin peak sign 58
Twin-twin transfusion syndrome 59
Ulipristal acetate 214
Ultrasonography 18, 39, 51, 80, 83, 9092, 132
Ultrasound 117
monitoring, indications for 58
Umbilical artery 93
Umifenovir 159
Upper respiratory tract infections 146
Ureaplasma urealyticum 286
Ureter 208
Urethra 281, 285
Urethritis 144
Urinary tract infection 8, 19, 143, 163
analysis 26
examination 8
pregnancy test 84
Urogenital diaphragm 218
Uterine 207
activity 54
anomalies, congenital 67
artery 92, 93
embolization 213
pulsatility index 26
factor 241
hypertonus 184
inertia 6, 185, 275
malformations, congenital 99
prolapse 220
classifications 215
healing of 49
rupture 49
sounding 209
supports 217
Uterocervical length 219
Uterosacral ligaments 217
Uterus 182, 215, 238, 281
couvelaire 138
during pregnancy, prolapse of 277
enlargement of 183
examination 185
inversion of 220
overdistension of 67
prolapse of 221
supports of 217
surgical treatment, prolapse of 222t
Vagal stimulation 81
Vagina 215, 283
absence of 263
middle 217
prolapse of 221
shortness of 219
supports of 217
Vaginal bleeding, abnormal 199
Vaginal breech delivery 43
Vaginal contraceptive ring 249
Vaginal delivery 50, 63
Vaginal discharge 68, 199
abnormal 283
Vaginal examination 54
Vaginal infections, treatment of 69
Vaginal prolapse 216
Vaginal supports 217
Vaginal walls 219
Vaginitis 283, 287t
Valacyclovir 176
Varicocele 240
Vasa previa 139
Vascular disease 90
Vascular thrombosis 98
Vasectomy 125
permanent contraception 111
Vault prolapse operations 224
Vibroacoustic stimulation test 82
Viral antigen 154
detection 162
Viral infections, newer 152
Virkud's composite sling operation 222
isolation 154
mononucleosis 173
blurred 26
dimness of 31
Visual disturbances 25, 31
Visual inspection, advantages of 198
B12 14t
deficiency 3, 14
serum 8
fat-soluble 292
water-soluble 292
Vomiting 26
von Willebrand factor 233
Vulvovaginitis 287
Warfarin 127
Warm saline, amnioinfusion of 94
Weight gain 91
abnormal 26
low maternal 90
Wertheim's radical hysterectomy 203
Wharton's jelly 81
Whiff test 286
White classification, modified 104
Whole blood transfusion 11
Williams-Richardsons operation 224
World Health Organization 48, 104
classification, modified 128
X-ray, chest 147
Zahara prediction score 128
Zanamivir 157
Zidovudine 165
Zika virus 154, 155, 155f
infection 154, 155
antenatal management 158
chemoprophylaxis 157
clinical features 156
complications 155
diagnosis 155, 157
investigations 157
management in pregnancy 157
perinatal 156
pregnancies complicated with 155t
prevention 155, 157
signs 155
symptoms 155
transmission 154
treatment 155
vaccination 157
syndrome, congenital 155
Zuspan regimen, Sibai modification of 32
Zygote intrafallopian tube transfer 244
Chapter Notes

Save Clear

  1. Anemia in Pregnancy
  2. Hypertensive Disorders in Pregnancy
  3. Breech
  4. Pregnancy after Previous Cesarean Section
  5. Multiple Pregnancy
  6. Preterm Labor
  7. Post-term Pregnancy
  8. Intrauterine Growth Restriction
  9. Recurrent Pregnancy Loss
  10. Diabetes in Pregnancy
  11. Rh Isoimmunization
  12. Pregnancy with Heart Disease
  13. Antepartum Hemorrhage
  14. Pregnancy with Pyrexia
  15. Newer Viral Infections in Pregnancy
  16. HIV in Pregnancy
  17. TORCH Infections in Pregnancy
  18. Thyroid Disorders in Pregnancy
  19. Special Cases2

Anemia in PregnancyCHAPTER 1

HU Doshi
Anemia is the most common medical disorder encountered during pregnancy. 40–90% of pregnant women in India are suffering from anemia. As per NFHS-4 (2015–2016)1 incidence in pregnant women on an average is 50.4%.
Anemia is defined as decrease in the oxygen carrying capacity of the blood due to decrease in amount of RBCs or hemoglobin (Hb) or both. In adult female <12 g Hb% in peripheral blood is called anemia.
Causes of Anemia during Pregnancy
  • Physiological
  • Nutritional: Iron deficiency folate and/or vitamin B12 deficiency dimorphic
  • Hemorrhagic: Acute or chronic
  • Hemoglobinopathies
  • Hemolytic: Congenital or acquired
  • Aplastic anemia.
Due to physiological hemodilution during pregnancy fall in Hb occurs. There is 2.5–3 times increase in plasma volume as compared to RBC mass. Maximum increase occurs in 2nd trimester. Blood volume changes during pregnancy are shown in Figure 1.1.
Due to this, anemia in pregnancy is considered as per center for disease control (CDC) modified WHO definition as follows:
<11.0 g% in 1st and 3rd trimester
<10.5 g% in 2nd trimester
Degrees of anemia
10–10.9 g%
9–10.9 g%
7–9.9 g%
7–8.9 g%
4–6.9 g%
<7 g%
Very serve
<4 g%
<10 g%
zoom view
Fig. 1.1: Blood volume changes during pregnancy.
Nutritional Anemia
In India 90% of anemia in pregnancy are of nutritional origin. Iron deficiency is by far the most common cause of nutritional anemia.
Iron Deficiency Anemia
Iron is the essential element of heme pigment of the Hb. Deficiency of iron during pregnancy in our country is due to following reasons:
  • Low iron intake: As iron cannot be produced in the body, it is essential to eat food that contains iron. Dietary sources rich in iron are mentioned in Table 1.1. Cooking in iron utensils is helpful.
  • Increased nutrient demand: There is increased demand of iron during pregnancy. Each pregnancy needs approximately 1 g (1,000 mg) of extra iron as shown in Table 1.2.
    Most of this is required in second half of pregnancy. Although iron absorption increases during pregnancy (20–30% from normal 10%) the average vegetarian diet does not contain enough iron (10 mg average) to fulfil this demand.
    So, if woman has depleted iron stores, she requires 6–7 mg iron/day during second half of pregnancy, while woman with good iron stores 3–4 mg/day is sufficient. Thus iron supplement during pregnancy is must for an Indian mother.
    Table 1.1   Dietary sources rich in iron.
    Green leafy vegetables, spinach, mustard, fenugreek
    Whole wheat, bajra, jowar
    Green peas, beans, groundnuts, lentils
    Apple, banana are medium sources
    Jaggery, dates
    Liver, meat (fish and egg are medium sources)
    Table 1.2   Iron requirement during pregnancy.
    Expansion of RBC
    400–500 mg
    Fetus (80 mg/kg)
    200–250 mg
    Placenta and cord
    80–100 mg
    Basal losses
    220–250 mg
    900–1,100 mg
    Average 1,000 mg (1 g)
    Saving of iron due to amenorrhea during pregnancy (25 × 8 = 200 mg) compensates for blood loss at delivery (150–200 mg).
  • Poor absorption and utilization: The Indian diet which is predominantly vegetarian contains many substances which inhibit iron absorption. The factors influencing iron absorption are mentioned in Table 1.3.
    Also the bioavailability of nonheme iron (vegetarian diet) is poor and is slowly absorbed as compared to heme iron (5–10% vs 35–40%).
  • Poor reserve: Normal iron store in adult female is 300–500 mg. An average Indian woman enters her first pregnancy with inadequate or poor iron stores. This is due to inadequate nutrition during adolescent period because of gender bias, poverty, and less education.
    In parous women repeated pregnancies at short intervals (<2 years) and prolonged lactation (without iron supplement) also leads to depletion of iron stores.
  • Increased loss: The increased loss is due to high incidence of malaria and hookworm infestation. In rural areas hookworm infestation is common. This leads to average blood loss from 0.03 (Necator americans) to 0.2 mL (Ankylostoma duodenale) per parasite/day. In heavy infestation daily loss of iron can be up to 5 mg. Excessive menstrual loss (before pregnancy) and sweating are also responsible.
Table 1.3   Food factors influencing the absorption of iron.
  • Phytates in cereals
  • Tannins in tea. Polyphenols in coffee
  • Oxalates in vegetables
  • Phosphates in egg yolk
  • Proteins
  • Ascorbic acid—vitamin C
  • Organic acids, such as citric acid, lactic acid
  • Sprouted and fermented food
  • Meat, fish
Total body iron depends upon age, sex (more in male) and body weight of the person. In an adult female it is 2.0–2.5 g (35–40 mg/kg). It is distributed in the body as shown in Table 1.4.
  • Exact mechanism of absorption is still not known.
  • Iron is mainly absorbed from duodenum.
  • Nonheme iron (vegetarian diet) is mostly in ferric (Fe+++) form. It has to be reduced to ferrous (Fe++) form for absorption.
  • Due to acidic pH of the stomach and other reducing agents Fe+++ is reduced to Fe++.
  • A transporter protein called divalent metal transporter 1 (DMT 1) of enterocytes transports Fe++ iron from duodenal lumen to inside the enterocyte. With the enzyme peroxidase it is converted to ferric (Fe+++) iron.
  • Ferric iron can have one of the two fates: (1) Iron combines with apoferritin to form ferritin which is deposited in the intestinal cells and eventually excreted on their desquamation. (2) Iron which is not combined with apoferritin is absorbed and circulated in the plasma as ferric form combined with transferrin.
  • Heme iron is in Fe++ form so its absorption is 2–3 times more than nonheme iron. Heme iron is present in hemoglobin and myoglobin (i.e., nonveg diet).
  • Absorption of heme iron is not decreased by other foods simultaneously ingested.
Table 1.4   Distribution of body iron.
Percentage of total body iron
Stores (ferritin, hemosiderin)
Myoglobin + enzymes (catalase, cytochromes, peroxidase)
Plasma iron (bound to transferrin)
  • Fe+++ is taken up by transferrin (siderophilin), an iron-binding protein present in the blood for transportation to various parts of the body.
  • Transferrin receptors present in the various cells of the body including RBCs (erythropoiesis) recognize transferrin leading to the entry of complex into the cell. Iron is released intracellularly. While transferrin is released back into the circulation to carry fresh load of iron.
  • Iron from the breakdown of senescent RBCs in the reticuloendothelial system (RES) is also transported by transferrin for recycling in erythropoiesis.
  • Some iron is stored in the RE cells in the liver, spleen and bone marrow as ferritin (major portion) and hemosiderin.
    Fe+++ + Apoferritin = Ferritin
    Aggregate of ferritin = Hemosiderin
  • Ferritin can accommodate up to 4,500 of iron atoms. Ferritin is water-soluble while hemosiderin is not. Stores are mobilized to provide iron as and when need arises. In iron deficiency first the stores are depleted.
  • About 0.8–1.0 mg of lost iron is daily through exfoliated gastrointestinal (GI) mucosal cells, skin and in stool, urine, and sweating. In female approximately 1.0 mg/day should be added for menstrual loss during reproductive age group.
    zoom view
    Fig. 1.2: Iron cycle.
    Iron cycle is mentioned in Figure 1.2. As there is no physiological mechanism for 6iron excretion, which is almost constant; iron content of the body is regulated by absorption alone. The amount of iron absorbed from the diet depends upon iron stores and requirement for erythropoiesis. Factors affecting iron absorption are mentioned in Table 1.5 (food factors affecting the absorption of iron are already mentioned in Table 1.3).
  • Drugs, such as Alphadopa, Levodopa, Ciprofloxacin, and Cimetidine interfere with iron absorption.
Table 1.5   Factors affecting iron absorption.
Factors favoring
Factors reducing absorption
Iron deficiency
Iron excess
↑↑ Erythropoiesis
↓ ↓ Erythropoiesis
Inorganic iron
Organic iron (diet)
Ferrous iron (iron salts, heme iron)
Ferric iron (nonheme iron)
Acids: HCl, ascorbic acid, citric acid
Calcium citrate, calcium carbonate
Other calcium salts
Iron deficiency occurs in three stages
First stage:
Depleted iron stores.
Second stage:
Decrease in serum iron and increase in total iron-binding capacity (TIBC). There is deficient erythropoiesis.
Third stage:
Iron deficiency anemia.
Thus decrease in Hb represents very late stage of iron deficiency.
RBCs are formed in the red bone marrow situated in the ends of long bones, from nucleated cells known as stem cells or hemocytoblasts.
Stem cells → Proerythroblast → Basophilic erythroblast (early normoblast) → Polychromatophilic erythroblast (intermediate normoblast) → Acidophilic erythroblast (late normoblast) → Reticulocyte → Erythrocyte (RBC)
From proerythroblast to reticulocyte it takes 7 days. From reticulocyte to mature RBC it takes 2 days. Erythropoiesis is stimulated by the hormone erythropoietin secreted from the kidney. Erythropoiesis is stimulated if there is tissue anoxia or if the red cell count goes down.
Clinical Features
  • Fatigue, weakness, lassitude, impaired work capacity
  • Dizziness, giddiness, headache, insomnia
  • Dyspnea on exertion, palpitation
  • Anorexia, dyspepsia
  • Edema of ankles.
  • Pallor of skin and mucous membrane. In severe anemia there is even loss of color in the palmar creases.
  • There may be glossitis, stomatitis and dysphagia.
  • Koilonychia (changes in nails: Initially brittleness and dryness, later there is flattening and finally concavity, i.e., spoon-shaped nails).
  • Tachycardia.
Effects of Anemia in Pregnancy
  • Increased susceptibility to infection.
  • Cardiac failure at 30–34 weeks of pregnancy if severe anemia.
  • Pre-eclampsia may be related to malnutrition.
  • Preterm labor (3 times greater risk).
  • Uterine inertia.
  • Postpartum hemorrhage—even moderate blood loss can lead to collapse.
  • Cardiac failure
  • Shock7
  • Cardiac failure
  • Puerperal sepsis
  • Subinvolution
  • Failing lactation
  • Chronic ill health, backache.
Fetus and Neonate
  • Prematurity
  • Intrauterine growth restriction (IUGR) (3 times increased risk).
  • Increased perinatal deaths.
  • Decreased iron stores in neonate (Hb level in the fetus or neonate is not affected in anemic mother but soon infant can develop anemia due to deficient iron store).
Table 1.6   Hematological values.
Normal values in female
Iron deficiency anemia in pregnancy
12.0–16.0 g%
<11.0 g%
RBC count
4–5 million/mm3
<3.2 million/mm3
75–100 cubic micron
<75 μ3
25–33 pg
<25 pg
Serum iron
60–120 μg/dL
<60 μg/dL
300–350 μg/dL
>400 μg/dL
Percentage saturation
20–45% (1/3rd average)
Serum ferritin
15–200 μg/L (ng/mL)
<12 μg/L
Transferrin receptors
2–4 mg/L
0–35 μg/dL
Stainable bone marrow
Although clinical history and examination (pallor) are suggestive, following investigations are done. Investigations are carried out for:
  • Diagnosis and degree of anemia: Clinical estimation can be erroneous. Hb estimation is used for diagnosis. Hb below 11.0 g% suggests pathological anemia. Value of mild, moderate and severe degrees are already mentioned before.
    RBC count <3.2 million and packed cell volume (PCV) <30% suggest anemia.
  • Type of anemia:
    • Peripheral smear (PS): To study the morphology of RBCs. It shows microcytic hypochromic picture in iron deficiency anemia. RBCs are smaller in size with central pallor. Also there is anisocytosis (variation in size) and poikilocytosis (variation in shape). PS may also help in diagnosing malarial parasites. Reticulocyte count may be slightly raised. Occasionally target cells are present.
    • Hematological indices: These are mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), and mean corpuscular hemoglobin concentration (MCHC). Their values in iron deficiency anemia as compared to normal are mentioned in Table 1.6.
    • Specific investigations for iron deficiency include serum iron, TIBC, percentage saturation (serum iron/TIBC), serum ferritin level (Table 1.6). In fact decreased ferritin level is the first feature of iron deficiency.8
      Free erythrocyte protoporphyrin (FEP) and transferrin receptor levels are not routinely carried out. They increase early in case of iron deficiency and are more sensitive than even ferritin.
      Bone marrow examination: This is not routinely done. It is only indicated in—(1) refractory anemia and (2) aplastic/hypoplastic anemia. In iron deficiency anemia iron stores are absent. The absence of stainable iron is ‘gold standard’ for IDA.
  • Cause of anemia: For diagnosing the cause, detailed history is also important, e.g., food habits, obstetric history (multipara, short intervals), gynecologic history (menorrhagia), history of malaria or worms.
    • Urine examination: Routine and microscopy (culture studies if indicated) are done for diagnosing urinary tract infection (UTI), asymptomatic bacteriuria, hematuria, etc.
    • Stool examination: Ova (eggs), cysts and for occult blood. Eggs of hookworm are segmented (4 blastomeres) and float in saturated solutions of common salt.
    • Serum proteins: Hypoproteinemia.
      Special tests may be carried out in megaloblastic and other rare anemias.
      Serum folate, RBC folate—megaloblastic anemia
      Serum vitamin B12
      Serum bilirubin—hemolytic anemia.
      Coomb's tests—autoimmune hemolytic anemia
      Sickle test—sickle cell syndromes
      Hb electrophoresis—hemoglobinopathies.
Naked eye single tube red cell osmotic fragility (NESTROF) test2—beta thalassemia trait. Glucose-6-phosphate dehydrogenase (G6PD) screening,
Red cell osmotic fragility test—hereditary spherocytosis.
Causes of microcytic anemia:
  • Iron deficiency anemia
  • Thalassemia
  • Anemia of chronic disease
  • Sideroblastic anemia
  • Lead poisoning
  • Anemia associated with copper deficiency
  • Alcohol use.
General preventive measures are:
  • Screening of adolescent girls in school and giving iron supplements.
  • Education and motivation for taking diet rich in iron (Table 1.1).
  • Change in food habits, i.e., avoiding tea or coffee for at least 2 hours after meals.
  • Prevention of hookworm and malaria. For hookworm, Albendazole 400 mg stat or Mebendazole 100 mg BID for 3 days is recommended. For malarial prophylaxis weekly 2 tablets of Chloroquine (300 mg base) are given from 2nd trimester onwards in endemic areas.
  • Keeping adequate interval between pregnancies (>2 years minimum) and avoiding prolonged lactation without iron supplement.
  • Fortification of food by iron, i.e., 30–36 mg iron should be added per kg of wheat flour.
  • Fortification of common salt by iron.
  • Cooking in iron utensils is helpful.
Govt of India (Ministry of Health and Family Welfare) has recommended 100 mg of elemental iron + 0.5 mg FA/day for 100 days to every pregnant woman in our country as prophylaxis from second trimester onwards and postpartum for 6 months. Dose is to be doubled if there is mild anemia.
Apart from treatment of the cause, iron therapy for correction of anemia as well as to replenish the iron store is essential.
Iron Therapy
  • Oral iron therapy: It is indicated in all mild and moderate iron deficiency cases. It is cheap, safe and effective in most of the cases. 100–200 mg elemental iron per day 9is recommended. Different common iron salts with their elemental iron content is mentioned in Table 1.7.
    • Ferrous salts are 3 times readily absorbed than ferric salts.
    • Ferrous sulfate is the cheapest and well absorbed form of iron.
    • Ferrous gluconate is well tolerated but it has low iron content (36 mg in 320 mg tablet).
    • Ferrous fumarate is the most commonly used salt in commercial preparations.
    • Ferrous ascorbate is a synthetic molecule of ascorbic acid, iron and as ascorbate makes stable chelate with iron there is no dissociation in GI tract, so there is no action of food inhibitors. Tablets containing 100 mg elemental iron is available for use.
    • Carbonyl iron: Newer market preparation contain this. Carbonyl refers to manufacturing process where iron is obtained by thermal decomposition of iron pentacarbonyl which when heated to above its boiling point decomposes to give iron and carbon monoxide. Iron thus obtained has high purity (>98%), very fine spherical size (<5 μ) and uniform particle size. It is easily absorbed and less toxic than ionized forms of iron, such as iron sulfate. It has a high safety range.
      Table 1.7   Oral iron preparations.
      Elemental iron
      Ferrous sulfate
      200 mg
      60 mg (30%)
      Ferrous fumarate
      200 mg
      66 mg (33%)
      Ferrous gluconate
      320 mg
      36 mg (12%)
      Ferrous succinate
      100 mg
      35 mg (35%)
      -Ferric ammonium
      125 mg
      25 mg (17–22%)
      Ferrous ascorbate
      100 mg
      100 mg
      Carbonyl iron
      90 mg
      Sodium feredetate
      231 mg
      Ferric pyrophosphate
      30 mg
    • Sodium feredetate: It contains ferric sodium EDTA. It contains iron in a unionized form. It is not astringent and does not discolor teeth. Its absorption is less affected by food inhibitors, such as phytates.
      Ferric pyrophosphate: It is relatively newer iron preparation with advance microsomal technology. It leads to lower GI side effects than conventional oral iron preparation.
      Faster rise of Hb is claimed by manufacturer.
    • Micronization of iron and encapsulation with liposomes increases bioavailability.
      Ferrous bisglycinate chelate: It is a chelated form of iron, where two molecules of amino acid glycine are bound to a molecule of iron. It does not cause gastric irritation and constipation. Absorption of bisglycinate is not affected by phytates in food.
    • Iron polymaltose complex (IPC): It is ferric hydroxide polymaltose complex. It is nonionic and it does not stain the teeth. There is no metallic taste and no interaction with food or other drugs. Initially claimed high therapeutic results were not found in clinical practice, so it is less used now.
    • Sustained-release (SR) or time release (TR) preparations have less GI side effects but lesser iron is released in the main absorptive area, i.e., duodenum and upper jejunum and so less is absorbed.
    • Gastric delivery system (GDS) contains ferrous sulfate in a gel forming polymer matrix, so the tablet floats in the stomach for 5–12 hours releasing small amount of iron to the main absorptive area (i.e., duodenum). It is claimed that 3 times more iron is absorbed with less side effects.
    Iron prescription:
    • More than 2 tablets/day is not favored as it increases the side effects without therapeutic benefits.10
    • If there is swallowing problem or intolerance use liquid preparation (less side effects but staining of teeth may be a problem).
    • Iron should be taken on empty stomach with fruit juice for better absorption, i.e., 1 hour before or 2 hours after meals. Due to stomach upset it is usually taken with the meals.
    • Tea, coffee avoided for 2 hours after taking iron.
    • Taking vitamin C helps in absorption.
    • Calcium salts (except calcium carbonate and calcium citrate) and antacids should be avoided.
    • Reticulocyte count increases by 7–10 days.
    • Hb% rises at 10–14 days. About 1 g%/week rise in Hb occurs from 2nd week onwards.
    Side effects of oral iron: Upper GI tract—nausea, gastric discomfort, loss of appetite and eructation. Staining of teeth particularly in liquid preparation.
    Lower GI tract—constipation, diarrhea, and flatulence.
    Nonresponse to oral iron: Reasons can be:
    • Noncompliance due to intolerance or otherwise.
    • Poor absorption
    • Wrong diagnosis another etiology of anemia.
    • Continued loss of iron.
  • Parenteral iron therapy: It is indicated when:
    • Intolerance to oral iron.
    • Noncompliance to oral iron.
    • Poor absorption of oral iron (malabsorption syndrome, dysentery, etc.)
    • No response to oral iron after 4 weeks in a confirmed case of iron deficiency anemia.
    • Some cases of moderate anemia (6–8 g Hb) very late in pregnancy.
    • Iron sucrose: It is available as 20 mg/mL in 5 mL (100 mg) or 10 mL (200 mg) ampoules.
    • Ferric carboxymaltose (FCM) available as 50 mg/mL in 5 mL or 10 mL vials.
    Iron sucrose:
    • It is category B drug.
    • Dose calculation is total iron = 2.4 × weight in kg × deficit of Hb in g. 500 mg should be added for pregnancy.
    • It is safer, effective and well tolerated.
    • Test dose is not recommended. However, some authorities prefer to give test dose.
    • It can be given undiluted IV slowly 1 mL/min OR diluted 100 mg in/100 mL of normaI saline and given IV over 15 minutes.
    • Maximum 200 mg per dose is given repeated up to three times a week.
    • Iron sucrose is dissociated by the reticuloendothelial (RE) system into iron and sucrose. The released iron increases Hb. 75% sucrose is excreted by kidney in 24 hours.
    • It is claimed that there is rapid rise of Hb than oral iron, i.e., after 1 week and also rapid buildup of iron stores.3
    • It cannot be given IM due to alkaline pH (>10) as it causes muscle damage.
    • It is not stable in dextrose, so it cannot be diluted in dextrose.
    Ferric carboxymaltose (FCM):
    • It is newer parenteral iron where ferric hydroxide core is stabilized by carbohydrate shell so there is controlled release of iron leading to decreased oxidative stress.
    • It was initially recommended only for postpartum use but now safety during pregnancy is established.
    • Dose is calculated as per standard formula and single dose is given in not <15 minutes in 250 mL saline.
    • Dose should not exceed 15 mg/kg body weight and if required 2 doses are given 7 days apart.11
    • Minor adverse reactions in the form of injection site redness, swelling or nausea, vomiting, headache may occur in few patients.
    • It elevates Hb level and restores iron stores faster than oral iron or even IV iron sucrose.4
    Iron sorbitol citric acid complex:
    • 0.5 mL (25 mg) test dose should be given.
    • 100 mg/day is given daily or on alternate days (75 mg Jectofer).
    • It is given deep IM by “Z” technique to prevent skin staining.
    • Side effects are: (1) it is painful; (2) discoloration of skin; (3) injection abscess; (4) sarcoma is reported in rats (Imferon) but not in humans.
    Iron dextran (Imferon):
    • It was used in past. It was given IM or IV after test dose.
    • Side effects include: Thrombophlebitis at IV site, malaise, fever, arthralgia, urticaria, lymphadenopathy.
    • Anaphylaxis is the real risk. Rarely deaths also have been reported. So total dose Imferon is not practiced at present.
  • Iron intoxication: Wrong diagnosis of iron deficiency anemia or there is already iron overload (thalassemia).
  • Advantages of IV over IM therapy are: (1) it is less painful; (2) complacency is better—complete treatment is ensured; and (3) less hospital stay.
  • Oral iron should be stopped for at least 48 hours before parenteral therapy to prevent intoxication.
  • Sodium ferric gluconate:
    • It is given IV 10 mL (125 mg) diluted in 100 mL normal saline (available 12.5 mg/mL).
    • It is mainly used for iron deficiency in hemodialysis patients.
    • Side effects include nausea, vomiting, hypersensitivity reaction and hypotension.
  • Erythropoietin: Recombinant human erythropoietin is mainly useful for anemia in patients with renal disease and on cancer chemotherapy. In pregnancy as such erythropoietin levels are increased. It is given 150 IU/kg subcutaneous (SC) thrice a week with iron supplements.
Blood Transfusion
It is indicated in iron deficiency anemias in following cases:
  • Severe anemia (Hb <7.0 g) at any gestational age.
  • Moderate anemia beyond 36 weeks and when there is failure of response to iron therapy.
Blood transfusion is also indicated in many obstetric situations:
  • Severe hemorrhage—antepartum hemorrhage (APH), PPH, rupture uterus at cesarean section, severe first trimester hemorrhage.
  • Thalassemia and sickling disorders in pregnancy.
As per RCOG guidelines PCV is given during pregnancy as follows:
  • <34 weeks. If Hb <5 g with or without cardiac failure or hypoxia; 5–7 g in presence of impending failure.
  • >34 weeks. If Hb <7 g even without cardiac failure or hypoxia.
Whole blood transfusion should not be used. Packed cells volume (PCV) transfusion is better than whole blood as patient will have less—(1) volume overload, (2) less transfusion reactions and (3) components separated from whole blood can be used for other patients. Properly grouped, typed and “X” matched PCV should be used. 1 unit increases hematocrit by 3–4% or Hb by 0.8–1.2 g% depending upon blood volume of the patient and Hb level of PCV transfused.
Steps of PCV transfusion
  • Patient's sample is collected in plain and EDTA (2–3 cc each) and sent to blood bank after proper labeling with requisite form for grouping and ‘x’ matching.
  • Patient's consent is taken for blood transfusion.12
  • Demand is sent for supply of unit of PCV when required.
  • PCV bag is released from blood bank after proper grouping and ‘x’ matching with standard form having all details.
  • PCV bag supplied is doubly checked with blood bank form and patient's case paper.
  • Identification at bedside is advisable.
  • There is no need to warm the bag or to bring it to room temperature.
  • Rate of transfusion is 15 drops/min initially for half an hour to check for any immediate adverse reaction.
  • Then the rate is increased and whole unit is transfused taking 4 hours.
  • Vitals are recorded before starting the blood and then after half hourly.
  • Few cc of blood is left behind in the bag.
  • The empty bag with necessary form is always returned to blood bank.
  • Diuretic may be given at the end of transfusion to prevent overload.
Exchange transfusion
  • This particularly indicated in severe anemia with congestive cardiac failure (CCF).
  • PCVs are transfused (minimum 3 units) through one antecubital vein and simultaneously whole blood is withdrawn from opposite femoral vein.
  • Blood withdrawn should be 200 mL more than the amount transfused, i.e., keeping negative balance.
Adverse reactions to blood transfusion
  • Transfusion reactions: The most dangerous is acute hemolytic reaction due to mismatched transfusion which can be fatal. They are mentioned in Table 1.8.
  • Infections: Viral: Hepatitis B, hepatitis C, human immunodeficiency virus (HIV), human T-cell lymphotropic virus (HTLV), cytomegalovirus
    Bacterial: Syphilis, gram-negative bacteria
    Parasitic: Malaria.
  • Volume overload: If whole blood is transfused in chronic severe anemia and if diuretic is not used.
  • Others: These include hypothermia, citrate toxicity, hyperkalemia secondary to increased potassium in stored cells, hypocalcemia (secondary to binding of calcium by citrate based anticoagulant), iron overload (in thalassemia) and disseminated intravascular coagulation (DIC)(dilution coagulopathy in massive blood transfusions) and rarely air embolism.
Table 1.8   Transfusion reaction.
Risk per unit
Acute fatal hemolytic
Delayed hemolytic
1: 1,000
Febrile (nonhemolytic)
Allergic (urticarial)
(TRALI: transfusion related acute lung injury)
As per RCOG guidelines PCV is given during pregnancy as follows:
  • <34 weeks If Hb <5 g with or without cardiac failure or hypoxia.
  • >34 weeks Hb <7 g even without cardiac failure or hypoxia.
Management in labor
  • Mild sedation or pain relief is done.
  • Oxygen is given by mask if dyspnea occurs.
  • Strict asepsis is ensured.
  • PCV should be kept ‘x’ matched and ready.
  • In severe anemia digitalization may be required if CCF occurs.
  • Second stage should not be prolonged and prophylactic forceps (preferred) or vacuum should be done.
  • Active management of 3rd stage of labor should be done, as these patients may not tolerate even mild PPH (10 units IM oxytocin).
  • Adequate rest is ensured with early ambulation.
  • Prophylactic antibiotics are given.
  • One should be vigilant for CCF due to overloading from redistribution of blood, diagnose and treat it adequately.13
  • Fatigue, weakness, feeding problems are common.
  • Iron and folic acid (FA) supplements should be continued for 6 months.
Folic Acid Deficiency Anemia
FA along with vitamin B12 is required for synthesis of thymidine in the body, which is a necessary precursor of deoxyribonucleic acid (DNA) synthesis and red blood cell (RBC) formation, so their deficiency leads to impaired growth, maturation of RBC and anemia known as megaloblastic anemia.
Pure folic acid deficiency anemia is hardly 3–4%, but it is usually associated with cases of iron deficiency anemia causing dimorphic anemia. With increased awareness and routine supplement of folic acid during pregnancy it is decreasing nowadays.
  • Increased demand due to pregnancy and lactation, poor intake (low socioeconomical class, alcoholics) and malabsorption (tropical sprue, celiac disease) are the main causes.
  • It is more common in multiple pregnancy, multigravida patients and also in chronic hemolytic states.
  • Dietary rich sources of FA are dark green vegetables (the word folic acid comes from Latin word ‘folium’ means leaf), nuts, sprouts, sweet potatoes, fruits. Vegetables include spinach, broccoli, asparagus, lentil, legumes, and mushroom.
    Liver and kidney are rich nonveg sources.
  • FA absorption or metabolism may be impaired by drugs, such as oral contraceptives, pyrimethamine, primidone, phenytoin, barbiturates and sulfa + trimethoprim.
  • Prolonged cooking leads to loss of vitamins and lack of raw food in diet also leads to deficiency.
Absorption and storage: FA is mainly absorbed from the proximal jejunum. In the circulation it may be free or loosely bound to plasma protein β-globulin. The liver is the principle storage depot. It stores 6–10 mg of folic acid.
Clinical features: Anemia usually develops in late pregnancy or early puerperium. General symptoms as mentioned in iron deficiency anemia are present. In long standing cases glossitis, dry lips and roughness of skin are more evident. Intense anorexia aggravates the dietary deficiency.
Diagnosis: Apart from low Hb other hematological diagnostic parameters are mentioned in Table 1.9. Formiminoglumatic (FIGLU) acid excretion test diagnostic of FA deficiency is not useful in pregnancy because there is increased utilization of histamine by fetus as pregnancy advances.
Earliest morphological change is hypersegmentation of neutrophils.
Term megaloblastic represents bone marrow picture. Only in severe cases megaoblasts appear in peripheral blood. Megaloblastic is viewed as unbalanced growth between cytoplasm and nucleus, due to improper and defective synthesis of nucleoprotein.
For diagnosis of megaloblastic anemia at least 2 of the following features must be present in the films of buffy coat layer.
  • >4% neutrophils must have >5 lobes.
  • Presence of orthochromic macrocytes (diameter >12 um).
  • Nucleated RBCs are found (i.e., normoblasts showing premature hemoglobinization for their stage of nuclear development).
Table 1.9   Hematology in FA deficiency.
FA deficiency
Peripheral smear
75–100 μ3
>100 μ3
Plasma folate
5–20 ng/mL
<3 ng/mL
RBC folate
>150 ng/mL
<80 ng/mL
(MCV: mean corpuscular volume; MCHC: mean corpuscular hemoglobin concentration; RBC: red blood cell) *Other causes of macrocytic anemia are myxedema, liver disease and leukemia but they have normoblast bone marrow.
  • 14Howell–Jolly body bodies (residual nuclear inclusion bodies within RBCs).
  • Macropolycytes (giant polymorphs) present.
Effects on pregnancy: Apart from megaloblastic anemia FA deficiency was believed to cause abruptio placenta, spontaneous abortion and IUGR but it is not definitely proved. The only proved association of FA deficiency in first trimester is that it causes open neural tube defects, e.g., anencephaly, spina bifida, etc., in the fetus. Fetus otherwise is not anemic. It effectively extracts folate from maternal circulation.
Management: Prophylaxis—along with iron, folic acid 0.5 mg/day is recommended to every pregnant mother. Conventional hematinic preparation contains 0.5–1.5 mg FA along with iron and other micronutrients. For prevention of neural tube defects higher doses, i.e., 5 mg/day is given and it is started 3 months preconceptional.
  • 1–5 mg/day orally is usually given.
  • Injection FA is rarely required, i.e., in presence of GI disorders, such as sprue, or rarely for deficiency diagnosed late in pregnancy.
Vitamin B12 Deficiency Anemia
  • As mentioned previously along with folic acid it is required for DNA synthesis.
  • It has very little daily requirement and long storage life.
  • In pregnancy its deficiency can occur in strict vegetarians. It can also occur in patients with history of gastrointestinal surgeries, inflammatory bowel disease and helminthic infestation.
  • Severe deficiency is usually associated with infertility.
  • Common dietary sources are meat, fish, poultry, and dairy products.
  • It is absorbed in the ileum, bound to intrinsic factor. Intrinsic factor is secreted in the stomach by the parietal cells.
  • Main storage site is liver.
  • Addisonian pernicious anemia (lack of intrinsic factor) is rare in pregnancy due to: (1) patients are usually infertile, (2) occurs after 40 years of age, and (3) not common in India.
  • Recommended dietary allowance is mentioned in Table 1.10. Hematology is same as seen in FA deficiency anemia except that plasma and RBC folate levels are normal and vitamin B12 level is <100 pg/mL (Normal: 150–950 pg/mL).
Comparison of folic acid and vitamin B12 are mentioned in Table 1.11.
Effects on pregnancy: It produces megaloblastic anemia so effects on pregnancy are those of anemia. Subacute combined degeneration of spinal cord due to vitamin B12 deficiency is almost uncommon in pregnant patient.
Table 1.10   Recommended dietary allowance (RDA).
No pregnant
15 mg
30 mg
15 mg
180 μg
400 μg
280 μg
Vitamin B12
2.0 μg
2.2 μg
2.6 μg
Table 1.11   Comparison of folic acid and vitamin B12.
Folic acid
Vitamin B12
Chemical name
Pteroylglutamic acid
Required for DNA synthesis
For DNA as well as RNA synthesis
Rich sources
Green leafy vegetables
Animal food, dairy products
Proximal jejunum
Body store
6–10 mg
2–5 mg
Time over which deficiency develops
3–4 months
2–10 years
Serum level normal deficiency
5–20 ng/mL
<3 ng/mL
150–900 pg/mL
<100 pg/mL
Table 1.12   Nutritional anemia.
Iron deficiency
<75 cubic micron
>100 μ3
>100 μ3
Microcytic hypochromic
Macrocytic normochromic
Macrocytic hypochromic
Serum iron
Serum ferritin
Serum folate/vitamin B12
(MCV: mean corpuscular volume; MCHC: mean corpuscular hemoglobin concentration; PS: peripheral smear)
  • Oral preparations have unreliable absorption properties and are inadequate for long-term treatment.
  • Injection vitamin B12 1,000 μg (1 mg) IM once a week is recommended for 6–8 weeks.
  • Most of the oral hematinic preparations include FA + vitamin B12 along with iron.
Dimorphic Anemia
Combined defect of hematopoietic factors is common than isolated defect so, nutritional anemia, in upto 40% of cases are dimorphic anemia, i.e., iron + folic acid (rarely vitamin B12) deficiency.
  • Dietary inadequacy and intestinal malabsorption are the common causes.
  • Clinical features will depend upon the relative proportion of the deficient factors apart from degree of anemia.
  • Different hematological parameters are mentioned in Table 1.12.
  • Hematological features will also depend upon the relative deficiency. When one deficiency is predominating it may mask the expression of other deficiency.
  • Macrocytic hypochromic picture suggest both deficiency. Low serum iron and serum ferritin as well as low serum folate/vitamin B12 levels are seen.
Hemorrhagic anemia: Hemorrhage can be acute or chronic. In pregnancy acute hemorrhage is common.
  • Acute hemorrhage: Rapid and severe blood loss may be associated with:
    • Abortion, ruptured ectopic or gestational trophoblastic diseases in early pregnancy.
    • Antepartum hemorrhage in late pregnancy.
    • Intra- and postpartum due to PPH, rupture uterus and some cases of cesarean section.
  • Chronic hemorrhage: This may be due to piles, peptic ulcer, worm infestation, dysentery and drugs (not with low dose aspirin).
It is a collective term used for genetic (autosomal recessive) disorders affecting the globin portion of hemoglobin molecule. Hemoglobin consists of heme (haem) + globin. Globin is made up of 2 pairs of peptide chains each attached to heme complex.
The composition of different Hb and their percentage in adult are mentioned in Table 1.13.
Hemoglobinopathies are further divided into:
  • Thalassemia syndromes: Reduced or absent synthesis of structurally normal globin chains (quantitative defect).
Table 1.13   Different Hb in adult.
Hb type
Globin chains
Percentage in adult
Hb A (normal adult)
Alpha 2 Beta 2 (α2 β2)
Hb A2
Alpha 2 Delta 2 (α2 δ2)
Hb F (fetal Hb)
Alpha 2 Gama 2 (α2 γ2)
* In fetus 3 other Hbs are also seen Gover I, Gover II and Parkland.
  • 16Hemoglobin variants: Structural abnormality of globin chains, e.g., sickle cell syndromes (qualitative defect).
  • Greek word Thalassic means sea. depending upon which synthesis is affected it is called oc thalassemia or β thalassemia. The incidence of thalassemia in pregnancy for all races is 1 in 300–500.
  • Alpha thalassemia: High incidence is found in Far East, Malaysia, South China and also in South East Asia. The genes for OC globin chain are present on chromosome 16. It is in pair inherited from each of the parent. So normal individual genotype is OCOC/OCOC. The defect in OC thalassemia is of deletion type. The disease severity increases as the deletion of gene increases. Different types of OC thalassemia are mentioned in Table 1.14. OC 0 thalassemia is characterized by deletion of both genes from one chromosome (– –/OCOC). It is also known as Alpha thal-1. It is more seen in Asian population. OC + Thalassemia is characterized by loss of single gene from one chromosome, i.e., OC/OC – and OC –/OC –. It is also known as alpha thal-2. It is more seen in African population.
Table 1.14   Different OC thalassemia.
Deletion of genotype
Clinical picture genes
Silent carrier
OC–/OC –
OC thalassemia minor
––/OC OC
Mild hemolytic anemia
––/OC –
HbH disease, tetramer of β chains (β4). Moderate to severe hemolytic anemia
––/– –
Homozygous OC thalassemia Hb Barts (tetramer of gamma chains γ4), Hydrops fetalis
Clinical Picture
  • Silent carrier state: No clinical or hematological abnormality is evident.
  • OC thalassemia minor (OC–/OC–, OCOC/– –):
    • Mild microcytic, hypochromic anemia.
    • Hb may be slightly decreased but usually patients tolerate pregnancy well.
    • Oral iron and folic acid are given.
    • Parenteral iron should be given.
    • Blood transfusion may be required.
    • Diagnosis is made by low MCV and MCH but serum iron serum ferritin levels are normal or raised (unlike iron deficiency anemia) and Hb A2 <3.5% on electrophoresis (unlike beta thalassemia).
    • Fetus may inherit the carrier state.
    • If both the parents are minor (OC 0 type) the fetus may be major (25%). Here prenatal diagnosis has a role.
  • HbH disease (OC –/– –):
    • HbH results due to deletion of 3 genes leading to tetramer of beta chains β4.
    • These individuals have normal expectancy but chronic hemolytic anemia of moderate to severe degree exists.
    • In adult, 5–30% of Hb is HbH. Though it is stable and soluble, conditions of oxidant stress causes it to precipitate and hemolysis occurs.
    • Anemia worsens during pregnancy and blood transfusions are often required.
  • Homozygous OC thalassemia (OC thalassemia major) (– –/– –):
    • Due to deletion of all 4 genes, OC chain is not synthesized at all.
    • Tetramer of gamma chains (γ4), i.e., Hb Bart's occurs.
    • Hb Bart's has very increased affinity for oxygen so it does not deliver it to fetus adequately. Fetus suffers from hypoxia and develops hydrops (no immune) and dies in utero. Thus pregnant patient with OC thalassemia major is not seen.
    • Patient can develop severe preeclampsia if fetus is having thalassemia major (hydrops).
      Beta thalassemia: It results from decreased (β+) or absent (β0) synthesis of beta chain. Beta chain synthesis in 17fetal life begins at sixth week of gestation and Hb A (α2γ2) appears at 11th week of gestation. Gene for β chain is located on chromosome 11. Unlike OC chain it is single gene from each parent and not pairs so genotype of normal individual is β/β. Also unlike OC thalassemia the defect is not by deletions of gene but it is by point mutations of the gene.
      Heterozygous β thalassemia—β thalassemia minor. Homozygous β thalassemia—β thalassemia major. Other names for β thalassemia major are—Cooley's anemia, Mediterranean anemia (Thomas Cooley from Detroit first described this condition).
      High incidence is found in Mediterranean area, the Middle East, Indian subcontinent and the Far East. In India it is more found in Kutch people (Gujarat) and in Sindhi, Lohana community.
      • β Thalassemia major: In intrauterine life main Hb is Hb F (α2γ2) so fetus is not much affected (unlike homozygous alpha thalassemia). But after birth, the normal replacement of Hb F by Hb A2 does not occur due to absence of β chain. This leads to increased production of OC chains. Tetramer of OC chains (OC4) occurs which is insoluble and precipitates inside the cell (Heinz bodies) and interferes with erythropoiesis, alters cell membrane function and leads to hemolysis and severe anemia.
        • The child requires repeated blood transfusions. Iron load increases secondary to multiple transfusions and increased absorption from GI tract due to hypoxia. Iron deposition (hemosiderosis) leads to liver, cardiac and endocrinal dysfunction. Growth is stunted. Hyperplastic bone marrows particularly frontal bossing and maxillary prominence gives typical “Thalassemia facies”. They die early due to intercurrent infections and cardiac failure. Survival beyond teens is uncommon. Also they are infertile due to gonadal dysfunction. So pregnancy with β thalassemia major is rare.
        • However with better transfusion facilities and iron chelating therapy (desferioxamine) pregnancy cases have been reported.
        • Due to high maternal mortality in such cases MTP is strongly indicated.
      • β Thalassemia intermedia:
        • This applies to clinical conditions where disease is much less intense than β thalassemia. Major but severe than minor.
        • The several possibilities to explain this intermediate condition are coinheritance of OC thalassemia (OCβ thalassemia). HbE β thalassemia, unusual high levels of HbF synthesis and other rare mutations.
        • Hemolytic anemia requiring intermittent, but not regular, blood transfusion occurs.
      • β Thalassemia minor:
        • May be asymptomatic and may go unrecognized during pregnancy.
        • Mild microcytic hypochromic anemia which does not respond to iron therapy. In such cases Hb electrophoresis should be advised.
        • Diabetes and hypothyroidism are frequently found in these patients.
        • Hb remains around 7–8 g% and occasionally blood transfusion may be required.
        • Parenteral iron should never be given.
        • Mild splenomegaly is common.
        • Low mean corpuscular volume (MCV) (<65), low mean corpuscular hemoglobin (MCH), with normal or high serum iron and serum ferritin will be found.18
        • Hb A2 >3.5% by Hb electrophoresis confirms β thalassemia
        Different Hbs carry different electrical charges so they can be separated and measured by electrophoresis.
        • It is important to check the husband's status and if he is also minor, fetus has 1 in 4 (25%) chances of developing β thalassemia major. So prenatal diagnosis of such fetus and termination of pregnancy is advisable for primary prevention of β thalassemia major.
        • Prenatal diagnosis is done by fetal DNA analysis from trophoblast obtained by chorionic villi sampling (>10 weeks gestation) or from amniotes obtained by amniocentesis (>15 weeks gestation) direct measuring of the relative amounts of globin chain synthesis can be done in fetal blood. Fetal blood sampling is done by ultrasonography (USG) guided cordocentesis (18–20 weeks) but this carries risk of fetal loss.
        • When both the parents are minor, 50% of the fetuses inherit carrier state and 25% will be totally normal.
        • Noninvasive prenatal testing (NIPT): This is new technique to diagnose genetic conditions of fetus. Maternal blood sample is taken after 10 weeks of pregnancy. These types of genetic conditions can be diagnosed—(1) aneuploidy, i.e., extra chromosome, e.g., trisomy 21: Down syndrome, (2) microdeletions, i.e., small deletion in a specific region of a chromosome or (3) single gene disease, i.e., genetic conditions caused by mutations in a gene, e.g., beta thalassemia, sickle cell disease.
        • In utero stem cell transplantation and gene therapy are under research.
Unlike thalassemia, here there is structural defect in globin chain, but its rate of synthesis is normal. Hundreds of Hb variants have been described, those affecting beta chain are more common and sickle cell hemoglobin Hb S is the most common.
Hb S is transmitted by autosomal recessive gene. The heterozygous state is called sickle cell trait (Hb AS), while homozygous state is called sickle cell anemia or sickle cell disease (Hb SS).
The exact defect in different Hb variants are described in Table 1.15. Amongst the sickling syndromes major disorders (clinically severe) include—(1) sickle cell anemia (Hb SS); (2) sickle cell C disease (Hb SC) and (3) sickle cell β thalassemia. The last two are combined heterozygous states. Minor disorders, (clinically mild) include sickle cell trait (Hb AS), sickle cell E disease (HB SE). Hb CC and Hb EE even though homozygous are clinically mild hemoglobinopathies.
Table 1.15   Common hemoglobin variant.
Type of Hb
Structural defect in beta chain of chromosome 11
Geographical distribution
Hb S
Glutamic acid at 6th position replaced by valine
Africa, USA (blacks) Mediterranean countries, Caribbean islands, India*
Hb C
Glutamic acid at 6th position replaced by lysine
West Africa
Hb E
Glutamic acid at 26th position replaced by lysine
South East Asia
Hb D
Glutamic acid at 121st position replaced by glycine
*In India it is found mainly in tribals of Maharashtra, Gujarat and Madhya Pradesh (10–15% incidence)
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Fig. 1.3: Sickling.
Pathophysiology: The name sickle is given because RBCs containing Hb S on deoxygenation assumes the shape of sickle as shown in Figure 1.3.
Hb S is soluble in oxygenated state but in a reduced (deoxygenated) state it gets polymerized (aggregates). This leads to sickle shape of RBC. On oxygenation again DE polymerization occurs. But repeated sickling and DE sickling leads to cell membrane damage and RBC becomes permanently sickled (even in oxygenated state).
The sickle cells are rigid and cannot pass through microcirculation, such as normal RBCs. The blockage of small vessels leads to microinfarcts, painful vaso-occlusive crisis and end organ damage. These abnormal RBCs are filtered in spleen (trapped and destroyed). The life span of such RBCs is hardly 10–20 days (normal 120 days).
In sickle cell anemia (Hb SS) there is no normal Hb A, but in sickle cell trait (Hb AS) >50% is Hb A. So in patients of HB AS clinical manifestations are rare except under conditions of extreme hypoxia. Hb F (α2γ2) has some protective effect to sickling. Hb F present in the same RBC prevents polymerization of Hb S on DE oxygenation and prevents sickling. It is about 2–20% in patients with Hb SS.
Sickle cell trait in pregnancy:
  • No effect on pregnancy. Patients may not be aware of the disease due to its asymptomatic nature.
  • Patients may have mild anemia (normocytic). Hb usually remains between 7–10 g%.
  • Iron and folic acid supplements should be given.
  • Urinary tract infection (pyelonephritis) risk is doubled.
  • People with sickle cell Hb are immune to malaria as malarial parasites are trapped and killed along with sickled RBCs. This is the reason why sickle cell is common in malarial endemic regions, e.g., Africa. Nature offers protection by causing mutagenic change in the gene for globin chain to produce Hb S.
  • If sickle cell trait is diagnosed in mother, counselling is done and husband's Hb is checked for Hb S. If he is also having Hb S trait prenatal diagnosis is offered to couple to detect 25% chances of fetus having sickle cell anemia (Hb SS). Prenatal diagnosis is done as described under thalassemia and if found homozygous state in fetus (Hb SS), MTP is advised.
Sickle cell anemia (Hb SS):
  • It is severe condition with variable clinical manifestations. There are no parameters to judge the severity of the disease and frequency of crisis. The disease starts right from childhood, at 3–6 months of age when Hb F is normally replaced by normal Hb A (here Hb SS).
  • Chronic hemolytic anemia is present with Hb ranging between 6 to 9 g%.
  • Crisis is precipitated by infection, cold, exercise dehydration, acidosis, stress and high altitude.
Different crisis are:
  • Painful crisis: Due to vascular occlusion of various organs by capillary thrombosis resulting in infarction. Severe pain can occur in abdomen, chest, back, bones and joints.
  • Aplastic crisis: It is not infrequent during pregnancy. It may be due to viral or bacterial infection.
  • Hemolytic crisis: Acute hemolysis.
  • 20Splenic sequestration crisis: It is common in children. Autosplenectomy occurs by adulthood. Rapidly enlarging spleen with abdominal pain occurs.
  • Megaloblastic crisis: Due to folate deficiency particularly during twin pregnancy.
Treatment of crisis include oxygenation, narcotic analgesics, hydration by intravenous (IV) fluids, antibiotics and blood transfusion (PCV or exchange transfusion to reduce Hb S <30%).
Plasma expanders and anticoagulant (heparin) are not found useful.
Due to repeated microinfarcts patients may have renal damage, chronic lung disease, cardiac dysfunction, retinopathy, bony deformity, and CNS damage and leg ulcers.
Effects of disease on pregnancy:
  • Severe anemia: Due to extra burden of pregnancy on a chronic hemolytic state.
  • Sickling crisis: Increased, but severity and frequency are unpredictable.
  • Pre-eclampsia: Increased incidence (15%). It may be due to placental ischemia and endothelial injury due to sickling.
  • Infections: Pyelonephritis, pulmonary infections and puerperal sepsis are more common.
(1) Abortion, (2) Prematurity, (3) IUGR—due to severe anemia or poor perfusion of placenta, (4) Stillbirth.
Overall perinatal mortality increases by 7 times.
Effects of pregnancy on disease:
As such there is no direct effect, but patients are more likely to have crisis during late pregnancy, delivery and puerperium.
Maternal mortality can be as high as 25%.
Antenatal management:
  • Counseling of the patient regarding disease and risk of complications.
  • Hematologist should be consulted.
  • Frequent antenatal visits: Every 2 weeks in 2nd trimester and every weekly in third trimester.
  • Folic acid 5 mg is given to all. Iron is only indicated if deficiency is confirmed.
  • Fetal surveillance should begin at 32–34 weeks by serial USG and weekly nonstress tests (NSTs).
  • Routine pregnancy investigations.
  • Peripheral smear shows normocytic hypochromic RBCs with sickle cells, target cells and increased reticulocyte count.
  • Repeated urinalysis, urine culture to detect UTI and asymptomatic bacteriuria.
  • Renal function test (RFT) and liver function test (LFT).
  • Serum iron is high unless concomitant iron deficiency exists.
  • Tests for sickling.
    • Sickle test: 1 drop of fresh 2% reagent, such as sodium metabisulfite mixed on a slide with 1 drop of blood. The sickling of red cells is seen when examined after 1 hour.
    • Solubility test: It is a simple solubility test that uses 20 mL of blood mixed with 2 mL of sodium dithionite reagent. Clouding of solution indicates the presence of Hb S.
    Both above tests are screening tests. They do not differentiate between Hb SS and Hb AS.
  • Hb electrophoresis confirms Hb SS. Here there is no Hb A and Hb F is about 2–20%
  • High performance liquid chromatography (HPLC)5 has an advantage over Hb electrophoresis that it accurately 21identifies and measures abnormal hemoglobins. It is rapid and highly specific and sensitive method.
Prophylactic Blood Transfusions6
  • Its role is controversial. It is given every 6 weeks. It may decrease the incidence of crisis, but the obstetric outcome is not altered.
  • The risk of transfusion related diseases increase. The development of multiple other antibodies leads to future transfusion problematic. So any transfusion should be after proper checking of all minor RBC antigens and leucocyte poor.
  • Some authorities prefer blood transfusion only when need arises, i.e., crisis, severe anemia or in multiple pregnancy.
  • The purpose of prophylactic transfusion is to keep Hb around 10–11 g% and Hb S around 30–40%.
  • The patient is managed on the same lines as cardiac patient.
  • Continuous oxygen is given.
  • Good hydration is ensured if required by IV fluids.
  • Prolonged labor and acidosis is avoided by appropriate measures.
  • Continuous electronic fetal monitoring is advisable.
  • LSCS is done only for obstetric indications. Some patients may have bony deformities.
  • Regional (epidural) anesthesia is preferred to GA.
  • Proper antibiotic cover is must.
  • Breastfeeding is not contraindicated.
  • Antibiotics are continued.
  • Sterilization is advised even with one child due to short life span of the mother.
  • Oral pills are contraindicated due to thromboembolic risks. Progesterone only contraceptives can be given.
  • IUCD is contraindicated for risk of infection and bleeding.
  • Barrier contraceptives are preferred.
  • The drugs which increase the HbF level and thereby decrease the risk of sickling are used. These are hydroxyurea, butyrates, recombinant erythropoietin. The first two are antineoplastic drugs. Although no fetal anomalies are reported with their use during pregnancy, they are used with caution.
  • Bone marrow transplant during childhood is curative. But it is costly and risky. Intrauterine stem cell transplantation or gene therapy are under research.
  • Anemia is directly responsible for 15–20% of all maternal deaths and in another same % of deaths it is indirectly involved. Apart from this, maternal morbidity is considerable.
  • 1 pint of blood raises Hb by 0.8–1.2 g%.
  • 1 g of Hb can combine with 1.34 mL of O2.
  • 1 transferrin molecule binds 2 atoms of iron. Total iron bound to transferrin in the blood is 3–4 mg.
  • 1 mL of red cells contain 1.1 mg iron.
  • Antidote to iron are Desferioxamine and Deferiprone (L1). Desferioxamine is given SC or IV infusion, while Deferiprone (L1) has the advantage of oral route and low cost. Deferasirox is another antidote which can be given orally, but its safety during pregnancy and breastfeeding is not established.
  • Kelly-Paterson syndrome or Plummer-Vinson syndrome comprises a triad of dysphagia, iron deficiency anemia and esophageal webs. Patients will also have other symptoms of anemia.
  • Advantages of physiological anemia (hemodilution) include—(1) postpartum 22loss of RBCs is reduced, (2) blood viscosity is reduced and (3) increases gaseous exchange at placental level, (4) Overall increase in blood volume copes up with decreased peripheral resistance and increased cardiac output of pregnancy.
  • In hemoglobinopathies patients with sickling syndromes have more maternal morbidity and mortality than thalassemia patients.
  • History of worm infestation, malaria, dysentery, piles.
  • History suggesting malabsorption syndrome.
  • History suggesting hemolytic anemia—hemoglobinopathy.
  • History of bleeding from any site.
  • Personal history: Diet—vegetarian or nonveg, dietary habits, socioeconomical status.
  • Menstrual history: History of menorrhagia.
  • Obstetric history: High parity, pregnancies at short intervals, history of PPH in past pregnancy.
  • Pallor of skin and mucous membranes.
    • Tongue—glossitis can give false results.
    • Conjunctiva—conjunctivitis can give false results.
    • Nails—Koilonychia suggests chronic anemia.
    • Loss of color of palmar creases suggest severe anemia.
  • Edema legs—it may be due to anemia, or it may be physiological. Associated hypoproteinemia or PIH may be the cause.
  • Tachycardia
  • Hemic murmurs—ejection systolic murmurs.
  • Findings symptoms of multiple pregnancy—nutritional anemia is common in multiple pregnancy.
  1. NFHS-4—National Family Health Survey.>NFHS> Factsheet_NFHS-4.
  1. Thomas S, Srivastava A, Jeyaseelan L et al. NESTROFT as a screening test for the detection of thalassaemia and common hemoglobinopathies—an evaluation against a high performance liquid chromatographic method. Indian J Med Res. 1996;104:194–7.
  1. Bhavi SB, Jaju PB. Intravenous iron sucrose v/s oral ferrous fumarate for treatment of anemia in pregnancy. A randomized controlled trial. BMC Pregnancy Childbirth. 2017;17:137.
  1. Jose A, Mahey R, Sharma JB, et al. Comparison of ferric carboxymaltose and iron sucrose complex for treatment of iron deficiency anemia in pregnancy-randomised controlled tr ial. Pregnancy Childbirth. 2019;19(1):54.
  1. Khera R, Singh T, Khuana N, Gupta N, Dubey AP. HPLC in characterization of hemoglobin profile in thalassemia syndromes and hemoglobinopathies: a clinicohematological correlation. Indian Hematol Blood Transfus. 2015;31(1):110–5.
  1. Howard J. Sickle cell disease: when and how to transfuse. Hematology Am Soc Hematol Educ Program. 2016;2016(1):625–31.
1. What do you mean by physiological anemia during pregnancy? What are its advantages?
2. What are the complications of anemia in second trimester of pregnancy?
3. How will you treat severe anemia during pregnancy at any gestational age?
4. In what different ways blood is given during pregnancy?
5. What are the complications of blood transfusion?
6. Why I/V Inferno is not given nowadays? How will you treat anaphylactic reactions?
7. How will you treat moderate iron deficiency anemia at 16 weeks and at 36 weeks?
8. Which food articles contain good amount of iron?
9. How will you manage anemic patients in labor?
10. In which pregnant patient's anemia and PIH occur together?
11. What are the causes of normochromic normocytic anemia?23
12. What are the causes of hypochromic microcytic anemia?
13. What are the causes of megaloblastic anemia?
14. How will you diagnose hookworm infestation? How will you treat them?
15. What are the problems of folic acid deficiency during pregnancy?
16. Why pernicious anemia is not common during pregnancy?
17. What are different oral iron preparations? How are they different?
18. What is hemoglobinopathy? Which are commonly seen during pregnancy? How will you Rx them?
19. What is the relation of anemia and maternal mortality?
20. What is autologous blood transfusion?
21. What are the causes of acute anemia during pregnancy?
22. Which parenteral iron preparations are used now? How will you calculate the dose?