Disease of Infancy and Childhood2

Diseases of Infancy and Childhood 4/Oct/2022
NEONATAL RESPIRATORY
DISTRESS SYNDROME (NRDS)
By: Dr. Addisu A

Lecture for PC II
Objective
 By the end of the session, students will be able to

 define NRDS
 describe the morphologic changes of HMD
 elaborate the pathogenesis of HMD
 mention the clinical features of HMD
 have the basic cognitive capacity required to treat NRDS of prematurity
1
Outline
 Definition of NRDS
 Causes of NRDS
 Introduction to HMD
 Pathogenesis of HMD
 Morphology of HMD
 Clinical features of HMD
 Prevention and treatment of HMD
Key terms
 Hyaline material
 Preterm
2
Definition of
Neonatal Respiratory Distress Syndrome
(NRDS)
• any signs of breathing difficulties in the
neonate.
• occurs in up to 7 % of infants
Causes of NRDS
6
 Excessive sedation of the mother

 Fetal head injury during delivery
 Aspiration of blood or amniotic fluid
 Intrauterine hypoxia e.g. Nuchal cord
 RDS (hyaline membrane disease)

 Common cause of respiratory distress
3
Q&A
 Which one of the following could cause NRDS

A. Infection/ pneumonia
B. Pleural effusion
C. Diaphragmatic hernia
D. Pulmonary hypoplasia
E. Neuromuscular disorder (e.g. Congenital myotonic dystrophy)
Introduction to HMD
4
What are the histologic structures designated 1 – 6?
hyaline membrane disease (HMD)

/NRDS of prematurity/
10
 Is an acute lung disease of the newborn caused by

surfactant deficiency.
 RDS is basically a disease of premature infants.
 Occursin 60% infants born < 28 weeks of gestation,

 15% to 20% infants born between 32 and 36 weeks
 < 5% infants born > 37 weeks of gestation
5
Brainstorming
 Form buzz groups

 What is surface tension?
 What are the chemical bonds involved in formation of

these tension?
The physics of surface tension
• Surface tension is the elastic tendency of a fluid

surface which makes it acquire the least surface
area possible.
• Cohesive forces/ adhesive forces
• The molecules at the surface do not have other like
molecules on all sides of them and consequently they
cohere more strongly to those directly associated with
them on the surface.
6
13
 As a thin liquid film lines each

alveolus, there is air – water
interface.
 Water molecules are strongly
attracted to other water molecules
by hydrogen bonds.  ‘Surface
Tension’
Componentes of surfactant
14
 synthesized by type II pneumocytes

 90% lipid & 10% protein
 Phosphatdycholine – 70% (60% dipalmitoylphosphatidyl-choline

(lecithin))
 Protein
 Hydrophobic SP-B & SP-C → optimize rapid absorption & spreading of
phospholipids
 hydrophilic – SP-A & SP-D → innate host defense protein
 Surfactant produced by preterm is low in quantity & activity

because of difference in composition of lipid and protein
7
15
Function of surfactant
 Surfactants intersperses between the water molecules in the
fluid lining the alveoli, therefore, lowers the surface tension.
 Until the infant takes its first breath, the lung is filled with
liquid. With first breath surfactants rapidly coats the surface
of alveoli.
 Reducing surface tension → increases pulmonary compliance
[stretchability].
 Decreasing the pressure required to keep alveoli open (increase
the size of alveoli and avoiding alveolar collapse)
Surfactant synthesis is regulated by hormones

16
 Corticosteroids stimulate the formation of surfactant lipids

and associated proteins.
 Q & A (what if … . . ?)
 Labor vs cesarean section

 IUGR vs high blood levels of insulin in infant of diabetic mother
8
Pathogenesis
17
Pathogenesis…
18
9
Morphology
19
 The lungs in RDS infants are of normal

size but are heavy and relatively airless.
 Sink on water flotation test
 Gross = have a mottled purple color, and
 Microscopically = the tissue appears
solid, with poorly developed, generally
collapsed (atelectatic) alveoli.
Morphology…
20
 If the infant dies within the first

several hours of life, only necrotic
cellular debris is present in the
terminal bronchioles, alveolar ducts
and random alveoli.
 Later in the course, characteristic
eosinophilic hyaline membranes
line the respiratory bronchioles,
alveolar ducts, and random alveoli.
10
Morphology…
21
 These "membranes" contain necrotic epithelial cells admixed

with extravasated plasma proteins and neutrophilic
inflammatory reaction.
 If the infant dies after several days, evidence of reparative
changes, including proliferation of type II pneumocytes and
interstitial fibrosis, is seen.
Video for Clinical feature of HMD
11
Video for Clinical feature of HMD
Clinical Features
24
 Immature lung are in-able to synthesize sufficient surfactant

 Relatively greater inspiratory effort is required with each breath to
open the alveoli and
 Alveoli tend to collapse.
 New born respiratory muscles are weak, therefore infant rapidly

tires from breathing, and generalized atelectasis sets in.
 Clinical course and prognosis is dependent on the maturity and
birth weight of the infant and the promptness of institution of
therapy
12
problem-based activities/case studies/
 University of Alabama web site

 http://peir.path.uab.edu/wiki/IPLa
b#Lab_13:_Diseases_of_Infancy
Or
 Iplab HMD
Prevention
26
 Delaying labor until the fetal lung reaches maturity

 Inducing maturation of the lung in the fetus at risk
 Assess fetal lung maturity
 Analysis of amniotic fluid phospholipids

 Antenatal glucocorticoid therapy
 Prophylactic administration of exogenous surfactant after
delivery of premature baby
13
Design Treatment option based on the following

27
lead questions
 Make a group of 10 students

 What could be an immediate cause of death for preterm
with HMD?
 Oxygen
 Complication of prolonged administration are
 retrolental fibroplasia (also called retinopathy of prematurity) in the eyes, and
 bronchopulmonary dysplasia (BPD)
Design Treatment option based on the following

28
lead questions…
 Make a group of 10 students…

 What is the underlying problem?
 prophylactic surfactant treatments

 CPAP
14
NECROTIZING ENTEROCOLITIS
29
 most common in premature infants

 Incidence is inversly proportional to GA
 Most cases are associated with enteral feeding
 Postnatal insult → introduction of bacteria
 Large number of inflammatory mediators are linked with NEC
 PAF – promote enterocyte apoptosis; compromising tight junction →
increased mucosal permeability, break down of mucosal barrier →
inflammation → mucosal necrosis and further bacterial entry → sepsis and
shock
Clinical feature
30
 Bloody stool
 Abdominal distension
 Circulatory collpase
 Abdominal x-ray – gas within intestinal wall /pnematosis intestinalis/
15
Morphology
31
 Typically involves terminal ileum, cecum and right colon

 Distended
friable, congested
 Gangrenous → perforation → peritonitis
 Gross – submucosal bubbles

 Microscopic – mucosal or transmural coagulative necrosis, ulceration,
bacterial colonization
32
16
Prognosis and complication

33
 20-60% require resection of necrotic tissue

 Survivors often develop post NEC strictures from fibrosis caused by
healing process
 Perinatal mortality
SUDDEN INFANT DEATH SYNDROME

34
 “the sudden death of an infant under 1 year of age which remains

unexplained after a thorough case investigation, including performance
of a complete autopsy, examination of the death scene, and review of
the clinical history.” i.e. diagnosis of exclusion
 Aka crib death and cot death = as the infant usually dies while asleep
 third leading cause of death in US between the ages of 1 month and
1 year; mostly b/n 2-4 month
17
PATHOGENESIS
35
 Multifactorial condition
 A proposed “triple-risk” model of SIDS
1. vulnerable infant,
2. a critical developmentalperiod in homeostatic control, and
3. one or more exogenous stressors
 the most compelling hypothesis is that SIDS in vulnerable infant
reflects a delayed development of arousal and cardiorespiratory
control.
 particularly the arcuate nucleus may be due to a maldevelopment or
delay in maturation of this region due to genetic predisposion,
compromising the arousal response to noxious stimuli.
36
 Among the potential environmental causes; which are modifiable risk

factors
 prone sleeping position,
 sleeping on soft surfaces, and
 thermal stress
 Prevention
 “Back to Sleep”
 Factors Associated with Sudden Infant Death Syndrome (SIDS)  refer the table
on Robbins
18
FETAL HYDROPS
Accumulation of edema fluid in the fetus during intrauterine growth

• generalized edema of the fetus – hydrops fetalis
• localized degree of edema such as isolated
• pleural and peritoneal effusion or postnuchal fluid accumulation/cystic hygroma/
Major Causes of Fetal Hydrops

38
Cardiovascular Twin Gestation

Malformations Twin-twin transfusion
Tachyarrhythmia Infection (excluding
High-output failure parvovirus)
Chromosomal Cytomegalovirus
Turner syndrome Syphilis
Trisomy 21, Trisomy 18 Toxoplasmosis
Fetal Anemia Major Malformations
Homozygous α-thalassemia Tumors
Parvovirus B19 Metabolic Disorders
Immune hydrops Idiopathic = 20%
(Rh and ABO incompatibility)
19
Immune Hydrops
39
 results from an antibody-induced hemolytic disease in the newborn

caused by blood group incompatibility between mother (dd) and
fetus (DD or Dd)
 Commonly due to Rh and ABO blood group antigens of the fetus
inherited from the father.
 only the D antigen is a major cause of Rh incompatibility
40
 Fetal red cells may reach the maternal circulation during the last
trimester of pregnancy, when the cytotrophoblast is no longer present
as a barrier or during childbirth itself (fetomaternal bleeding).
 Maternal sensitization → production of IgM
 Ig M is replaced by Ig G later which can traverse the placenta
 Rh disease is very uncommon with the first pregnancy
 Rx = anti-D antibodies
 When?
20
41
Pathogenesis and complications

42
 immune hemolysis in utero uncompensated by hematopoiesis in

spleen and liver → progressive anemia → hypoxic injury to liver &
heart → ↓ plasma protein + intrauterine cardiac failure → anasarca
 Hemolysis → accumulation of unconjugated bilirubin →
↓
 Cross BBB → kernicterus
21
43
factors influencing the immune response to Rh-

44
positive fetal red cells
 Concurrent ABO
 dose of immunizing antigen (>1 mL of Rh-positive fetal red cells)
 isotype of the antibody (Ig M or Ig G)
22
ABO hemolytic disease

45
 ABO incompatibility occurs in 20% to 25% of pregnancies; however 1

in 10 of such infants develop hemolytic disease, and in general the
disease is much milder than Rh incompatibility(1 in 200 need Rx) .
 occurs
almost exclusively in infants of group A or B who are born to group O
mothers(MOM).
 For unknown reasons, certain group O women possess IgG, rather than
IgM antibodies directed against group A or B antigens (or both).
Therefore, the first born may be affected.
46
 Fortunately, even with transplacentally acquired antibodies, lysis of

the infant's red cells is minimal.
 Neonatal red cells poorly express A and B Ag
 Many cells also express A and B Ag → absorb some of the transferred Ab
23
Nonimmune Hydrops
47
 The major causes are those associated with

 cardiovascular defects,
 structural defects and functional abnormalities (i.e., arrhythmias)
 chromosomal anomalies → due to underlying structural cardiac anomalies
 Turner syndrome → abnormality of lymphatic drainage from the neck (cystic
hygromas)
 trisomies 21 and 18
 fetal anemia
 α-thalassemia
 Transplacental parvovirus B19 infection
 Twin-twin transfusion
48
 fetal anemia in both immune and nonimmune cause is tissue ischemia

with secondary myocardial dysfunction and circulatory failure.
Additionally, secondary liver failure may ensue, with loss of synthetic
function contributing to hypoalbuminemia, reduced plasma osmotic
pressure, and edema.
24
Morphology
49
 Hydrops associated with fetal anemia

 Gross
 Palefetus and placenta
 Hepatosplenomegaly due to HF and congestion
 Microscopic
 Bone marrow hyperplasia of erythroid precursors
 Large number of immature RBC in peripheral circulation
 Extramedullary hepatopoesis ( liver, spleen, LN, possibly the kidneys, lungs and
even heart)
50
TUMORS AND TUMOR-LIKE LESIONS

OF INFANCY AND CHILDHOOD
25
51
 Malignant neoplasms are the second most common cause of death in

children between the ages of 4 and 14 years; after accidents
 Benign tumors are more common than are cancers
 It is difficult to segregate, on morphologic grounds, true tumors from
tumor-like lesions in the infant and child.
 Heterotopia or choristoma
 Hamartoma
52
 Heterotopia or choristoma refers to microscopically normal cells or

tissues that are present in abnormal locations.
 E.g. a pancreatic tissue found in the wall of the stomach or small intestine
 Hamartoma refers to an excessive but focal overgrowth of cells and
tissues native to the organ in which it occurs.
 cellularelements are mature and identical to those found in the remainder
of the organ, but do not reproduce the normal architecture of the
surrounding tissue.
 demarcation between a hamartoma and a benign neoplasm is not clear
26
Benign Tumors
53
 Unlike adults hemangiomas, lymphangiomas, and sacrococcygeal teratomas occur

commonly in childhood.
Hemangiomas
 mostly located in the skin, particularly on the face and scalp, producing flat to
elevated, irregular, red-blue masses; the flat, larger lesions are referred to as port
wine stains.
 may enlarge as the child gets older, but in many instances they spontaneously regress
.
 rarely, they may be the manifestation of a hereditary disorder associated with
disease within internal organs, such as the von Hippel-Lindau and Sturge-Weber
syndromes
 Capillary hemangiomas in children are often more cellular than in adults, and hence
are deceptively worrisome.
54
Congenital capillary hemangioma at birth and at 2 years of age
27
Lymphangiomas
55
 represent the lymphatic counterpart of hemangiomas.

 characterized by cystic and cavernous spaces lined by endothelial
cells and surrounded by lymphoid aggregates; the spaces usually
contain pale fluid.
 They may occur on the skin but, more importantly, are also encountered
in the deeper regions of the neck, axilla, mediastinum, and
retroperitoneum.
 Though histologically benign, they tend to increase in size after birth
and may encroach on mediastinal structures or nerve trunks in axilla.
Sacrococcygeal teratomas
56
 are the most common germ cell tumors of childhood (>40%).

 ~ 10% of sacrococcygeal teratomas are associated with congenital
anomalies, primarily defects of the hindgut and cloacal region and other
midline defects (e.g., meningocele, spina bifida) not believed to result from
local effects of the tumor.
 ~ 75% of these tumors are histologically mature with a benign course, and
about 12% are malignant and lethal.
 The remainder is designated immature teratomas, and their malignant
potential correlates with the amount of immature tissue elements present.
 Most of the benign teratomas are encountered in younger infants (<4
months), whereas children with malignant lesions tend to be somewhat older.
28
57
Malignant Tumors
58
 Malignant tumors of infancy and childhood differ biologically and

histologically from those in adults.
 There is close relationship between abnormal development (teratogenesis)
and tumor induction (oncogenesis)
 Prevalence of constitutional genetic abnormalities or syndromes that
predispose to cancer
 Tendency of fetal and neonatal malignancies to spontaneously regress or
undergo “differentiation” into mature elements
 Improved survival or cure of many childhood tumors,
29
Common Malignant Neoplasms of Infancy and Childhood

59
0-4 Age yr 5-9 Age yr 10-14 Age yr

Leukemia Leukemia Hepatocellular carcinoma
Retinoblastoma Retinoblastoma Soft tissue sarcoma
Neuroblastoma Neuroblastoma Osteogenic sarcoma
Wilms' tumor Hepatocellular carcinoma Thyroid carcinoma
Hepatoblastoma Soft tissue sarcoma Hodgkin disease
Soft tissue sarcoma CNS tumors
(rhabdomyosarcoma) Ewing tumor
Teratomas Lymphoma
CNS tumors
60
 Histologically, many malignant pediatric neoplasms are unique.

 have a primitive (embryonal) rather than pleomorphic-anaplastic microscopic
appearance, and
 frequently they exhibit features of organogenesis specific to the site of
tumor origin
 Due to their primitive histologic appearance collectively referred to as
small, round, blue cell tumors. E.g. include
neuroblastoma, lymphoma, rhabdomyosarcoma, Ewing sarcoma
(peripheral neuroectodermal tumor), and some cases of Wilms' tumor.
30
Neuroblastoma
61
 The term "neuroblastic tumor" includes tumors of the sympathetic ganglia

and adrenal medulla that are derived from primordial neural crest cells
populating these sites.
 natural history of Neuroblastoma include
 spontaneous regression ( sometimes in presence of metastases) and
 spontaneous- or therapy induced maturation
 wide range of clinical behavior and prognosis
Epidemiology
62
 Neuroblastoma accounte for 7% to 10% of all pediatric neoplasms and

as many as 50% of malignancies diagnosed in infancy.
 Neuroblastoma is almost exclusively a disease of children.
 It is the third most common childhood cancer, after leukemia and brain
tumors, the second most common solid malignancy of childhood after
brain tumors, and is the most common solid extracranial tumor in children.
31
Embryogenesis
63
 Adrenal neuroblastomas are thought to develop from residual

microscopic neuroblastic nodules, which can be detected in fetuses, most
often between the 15th and 20th weeks of gestation, and regress by the
time of birth or shortly thereafter
 The subsequent malignant transformation of these cells may result, at
least in part, from a failure to respond fully to the normal signals that
stimulate morphologic differentiation .
 The origin of extraadrenal neuroblastomas is unknown, but presumably
reflects persistent rests of primitive ganglion cells in other locations as
well.
Etiology
64
 Most occur sporadically, but 1% to 2% are familial, with autosomal

dominant transmission, and in such cases the neoplasms may involve
both of the adrenals or multiple primary autonomic sites.
32
Morphology
65
 about 40% of neuroblastomas arise in the adrenal medulla.

 The remainder occur anywhere along the sympathetic chain, with the
most common locations being the paravertebral region of the
abdomen (25%) and posterior mediastinum (15%).
 range in size from minute nodules (the in situ lesions or silent lesions) to
large masses weighing more than 1 kg.
 Some neuroblastomas are sharply demarcated with a fibrous
pseudocapsule, but others are far more infiltrative and invade
surrounding structures, including the kidneys, renal vein, and vena cava,
and envelop the aorta.
66
33
67
 The most undifferentiated neuroblastomas are composed almost

entirely of neuroblasts, with very few Schwannian (or stromal) cells.
 Because of the lack of Schwannian cells, these tumors are called
"stroma-poor“
 Histologically, classic neuroblastomas are composed of small, primitive-
appearing cells with dark nuclei, scant cytoplasm, and poorly defined
cell borders growing in solid sheets.
 The background often demonstrates a faintly eosinophilic fibrillary

material (neuropil) that corresponds to neuritic processes of the
68
primitive neuroblasts.
 Typically, so-called Homer-Wright pseudo-rosettes can be found in
which the tumor cells are concentrically arranged about a central
space filled with neuropil (the absence of an actual central lumen
garners the designation “pseudo-”).
34
Ganglioneuroblastoma
69
 Ganglioneuroblastoma is called an "intermixed stroma-rich" or

"stroma-rich" tumor because of the increased proportion of
Schwannian cells
Ganglioneuroma
70
 Ganglioneuroma (Schwannian cell dominant) is predominantly

composed of Schwannian cells studded with maturing or fully mature
ganglion cells
35
71
Clinical Course
72
 generally present with large abdominal masses, fever, and possibly

weight loss.
 Metastases: Bones, Orbital region, Liver, Lung, Lymph nodes
 Subcutaneous nodules – with deep blue discoloration to the skin
(“blueberry muffin baby”)
36
Clinical Course
73
 About 90% of neuroblastomas, regardless of location, produce

catecholamines
 elevated blood levels of catecholamines and elevated urine levels of the
metabolites vanillylmandelic
acid [VMA] and homovanillic acid [HVA]
 HTN is much less frequent than pheochormocytoma
74
Less common presentation

 Superior cervical ganglion tumor →Horner syndrome
 Parspinal NB→ spinal cord and nerve root compression
 Paraneoplastic syndrome of autoimmune origin → ataxia or
opsomyoclonus
 Catecholamine producing tumors = 90% of neuroblastomas
 Swelling
 Palpitation
 Hypertension – less common
 Vasoxctive intestinal peptide releasing tumors
→ Secretary Diarrhea
37
Diagnosis
75
 elevated blood levels of catecholamines and elevated urine

levels of catecholamine metabolites such as vanillylmandelic
acid [VMA] and homovanillic acid [HVA]).
 Biopsy / BM – Neuroblasts
 Radiographs- Multiple masses with
Calcification
Prognosis
76
 Many factors influence prognosis, but the most important are the stage
of the tumor and the age of the patient
 Tumors of all stages diagnosed in the first 18 months of life, as well as low-
stage tumors in older children, have a favorable prognosis, while high-stage
tumors diagnosed in children younger than 18 months of age have the
poorest outcome.
38
Prognostic
77
Features
Retinoblastoma
78
 the most common primary intraocular malignancy of children

 tend to be nodular masses, usually in the posterior retina
 cell of origin is neuronal
 ~ 40% due to germline mutation →therefore heritable
 Bilateral multiple tumors are common
 increased risk for the development of osteosarcoma and other soft
tissue tumors.
 are ~ 60% sporadic somatic mutations
 All are unilateral and unifocal
39
79
 The median age at presentation is 2 years
 Tumor cells may disseminate beyond the eye through the optic nerve or
subarachnoid space.
 The most common sites of distant metastases are the CNS, skull, distal
bones, and lymph nodes.
Nephroblastoma / Wilms tumor

80
 Wilms tumor is the commonest renal cancer in children accounting for

90% of renal tumors.
Epidemiology
 Age 2-5 yrs
 Incidence ≈8/million children < 15 yrs
 Comprises≈ 6% of pediatric cancers
 Bilateral ≈ 7%
40
81
Associated with
 WAGR ( Wilms tumor,GUT anomalies, Aniridia, Mental retardation) -
one in three will develop Wilms tumor

 Denys-Drash syndrome (DDS) – 90% develop Wilms tumor
 Hemi hypertrophy
 Aniridia
 GUT anomalies – Cryptorchidism, hypospadia, horseshoe kidney
Morphology
82
 typically is a large, solitary, well-

circumscribed mass, although 10% are either
bilateral or multicentric at the time of
diagnosis.
41
83
Embryonal tumor of the kidney with histologic

categories.
 Favorable
 Blastemal
 Epithelial Elements good prognosis

 Stromal
 Unfavorable – anaplastic
 correlates with the presence of acquired TP53 mutations
Clinical manifestations
84
 Initially asymptomatic abdominal mass

 Malaise, Anorexia
 Abdominal pain
 Gross or microscopic hematuria
 Hypertension
42
85
43

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Diseases of Infancy and Childhood 4/Oct/2022

By: Dr. Addisu A

 By the end of the session, students will be able to

 elaborate the pathogenesis of HMD

 mention the clinical features of HMD

 have the basic cognitive capacity required to treat NRDS of prematurity

 Excessive sedation of the mother

 Aspiration of blood or amniotic fluid

 Intrauterine hypoxia e.g. Nuchal cord

 RDS (hyaline membrane disease)

 Which one of the following could cause NRDS

What are the histologic structures designated 1 – 6?

hyaline membrane disease (HMD)

 Is an acute lung disease of the newborn caused by

 Occursin 60% infants born < 28 weeks of gestation,

 < 5% infants born > 37 weeks of gestation

 Form buzz groups

 What are the chemical bonds involved in formation of

The physics of surface tension

• Surface tension is the elastic tendency of a fluid

 As a thin liquid film lines each

 synthesized by type II pneumocytes

 Phosphatdycholine – 70% (60% dipalmitoylphosphatidyl-choline

 Surfactant produced by preterm is low in quantity & activity

Surfactant synthesis is regulated by hormones

 Corticosteroids stimulate the formation of surfactant lipids

 Labor vs cesarean section

 The lungs in RDS infants are of normal

 If the infant dies within the first

 These "membranes" contain necrotic epithelial cells admixed

Video for Clinical feature of HMD

Video for Clinical feature of HMD

 Immature lung are in-able to synthesize sufficient surfactant

 New born respiratory muscles are weak, therefore infant rapidly

problem-based activities/case studies/

 University of Alabama web site

 Delaying labor until the fetal lung reaches maturity

 Assess fetal lung maturity

 Analysis of amniotic fluid phospholipids

Design Treatment option based on the following

 Make a group of 10 students

Design Treatment option based on the following

 Make a group of 10 students…

 prophylactic surfactant treatments

 most common in premature infants

 Typically involves terminal ileum, cecum and right colon

 Gross – submucosal bubbles

Prognosis and complication

 20-60% require resection of necrotic tissue

SUDDEN INFANT DEATH SYNDROME

 “the sudden death of an infant under 1 year of age which remains

 Among the potential environmental causes; which are modifiable risk

Accumulation of edema fluid in the fetus during intrauterine growth

Major Causes of Fetal Hydrops

Cardiovascular Twin Gestation

 results from an antibody-induced hemolytic disease in the newborn

Pathogenesis and complications

 immune hemolysis in utero uncompensated by hematopoiesis in

factors influencing the immune response to Rh-

ABO hemolytic disease

 ABO incompatibility occurs in 20% to 25% of pregnancies; however 1

 Fortunately, even with transplacentally acquired antibodies, lysis of

 The major causes are those associated with