PAL COLLEGE OF NURSING AND MEDICAL SCIENCES, HALDWANI

LESSON PLAN

ON

CONGENITAL ANOMALIES

SUBMITED TO SUBMIITD BY

Dr. PRATITI HALDAR MS. ANITA RAJ

ASSISTANT PROFESSOR M. SC. II YEAR

PCNMS PCNMS

SUBMITTED ON- 30/11/2022

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INTRODUCTION

NAME OF STUDENT:- Anita raj

TITLE OF THE COURE:- M.sc nursing II year

CLASS:- II YEAR

NUMBER OF THE STUDENTS:- 02

DATE:- 30/11/2022

SUBJECT:- Child health nursing

TOPIC:- Congenital abnormality

VENUE:- Specialty class room

DURATION:- 1hrs.

AV AIDS:- White board, PPT, chart

NAME OF EVALUATOR:- Mrs. Pratiti Haldar

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GENERAL OBJECTIVES
At the end of the class students will be able to understand about congenital abnormalities.
Specific objectives-
 To introduce about congenital anomalies.
 To define congenital anomalies.
 To enlist the classification of congenital anomalies.
 To define anencephaly.
 To define Encephalocele, Iniencephaly and spina bifida.
 To explain types of spinal bifida.
 To explain about types of spina bifida.
 To discuss Microcephaly.
 To discuss regarding craniorachischisis.
 To discuss regarding diagnostic test.
 To introduce Encephalocele.
 To discuss regarding management of Encephalocele.
 To discuss regarding congenital heart diseases.
 To discuss the causes.
 To enlist sign and symptoms.
 To discuss diagnosis of TOF.
 To explain about the management of TOF?
 To introduce tetralogy of fallot.
 To explain about pathophysiology of tetralogy of fallot.
 To explain treatment of tetralogy of fallot.
 To introduce tricuspid valve atresia.
 To explain about pathophysiology.
 To enlist sign and symptoms and diagnostic test.
 To discuss the management.
 To introduce about talipes.
 To enlist etiology of talipes.
 To explain treatment.
 To introduce gastroschisis.
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 To enlist causes and sign and symptoms and diagnostic test gastrochisis.
 To explain treatment of gastroschisis.
 To introduce about cleft lip and cleft foot.
 To enlist causes and sign and symptoms.
 To discuss the treatment of cleft lip and palate.
 To introduce renal agenesis/ hypoplasia.
 To explain the types.
 To enlist the causes.
 To enlist sign and symptoms.
 To enlist diagnostic test.
 To discuss treatment.
 To introduce hypospadias.
 To enlist causes and risk factors.
 To discuss sign and symptoms.
 To enlist diagnostic test.
 To discuss about treatment.
 To explain about trisomy 21.
 To enlist causes.
 To enlist sign and symptoms.
 To explain about preventions of chromosomal abnormalies.
 To discuss about nursing management.

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SPECIFIC AV METHOD EVALUTIO
OBJECTIVES CONTENT TIME AIDS OF
TEACHING
To introduce Introduction- Congenital anomalies can be defined as structural or functional 1min. Ppt What do you
about congenital anomalies that occur during intrauterine life. L
understand b
anomalies. It also called birth defects, congenital disorders, or congenital malformations, E
these conditions develop in prenatal period and may be identified before or at C congenital
birth, or later in life.
T anomalies?
Meaning:-
 It includes all biochemical, structural and functional disorders present at the U
To define birth. 1min. R
congenital  Congenital malformation: It include only the structural defects present at the E
anomalies. birth. R
Incidence rate: About 30 to 70/1000 live birth. In India - 2.5 to 4 % Most
common type of birth defect-CNS abnormalities (22%). C
An estimated 6% of babies worldwide are born with a congenital U
abnormality, resulting in thousands of associated deaths.
1min. Chart M
To discuss the
classification of  Classification of congenital anomalies What are the
Central nervous system:- D classification
congenital
i) Anencephaly- It is also called as “open skull,” anencephaly happens 2min. Ppt I
anomalies.
when the upper part of the neural tube doesn’t close completely during S What do you
To define the baby’s development. C understand b
anencephaly. Meaning:- Anencephaly is a type of birth defect. It occurs when the baby’s anencephaly?
U
brain, skull and scalp do not develop in the womb.
Portions of the baby’s brain and skull are missing. The brain tissue that does S
What do you
form is usually exposed because there isn’t enough skin and bone to cover it. S understand b
Incidence – I Encephaloce
About one out of every 5,000 to 10,000 babies is born with anencephaly, and O Iniencephaly
the condition affects girls more often than boys. N and spina
To define bifida?
Encephalocele, ii) Encephalocele 2min. Ppt
Iniencephaly and Encephalocele is a neural tube defect characterized by sac-like protrusions of
the brain and the membranes that cover it through openings in the skull.

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spina bifida. L
iii) Iniencephaly
Iniencephaly is a rare and complex neural tube defect (NTD) involving the E
occiput and inion, resulting in extreme retroflexion of the head, with C
combined with occipital encephalocele or rachischisis of the cervical or
thoracic spine. T
Causes and risk factors U
 Genetic Factors: Chromosomal abnormalities-eg. Down’s syndrome:
R
 Single gene disorders
- Autosomal inheritance E
- Dominant traits-0ne affected parent
R
- Recessive traits-Both parents
 X- linked or sex linked inheritance 
- Dominant traits-daughter affected. C
- Recessive traits-son affected
 Polygenic or multifactorial inheritance. U
 Environmental factor: M
 Intra uterine infections – STORCH (Syphilis, Toxoplasmosis,
D
Rubella, cytomegalaovirus and Herpes Virus)
 Maternal history: I
- Drugs intake during pregnancy- Steroids, Anticonvulsants,
S
Cocaine, Lithium, etc.,
- X- Ray exposure during pregnancy C
- Maternal diseases - DM, CF, endocrine abnormalities, iodine
U
deficiency, folic acid deficiency, malnutrition.
- Abnormal intrauterine environment - bicornuate uterus, septed S
uterus, polyhydramnios, etc. 1min Ppt
To explain types S
What are the
of spinal bifida. iv) Spina Bifida I types of spin
Spina bifida (Latin: "split spine") is a developmental congenital disorder Ppt
O bifida?
caused by the incomplete closing of the embryonic neural tube.
If the opening is large enough, this allows a portion of the spinal cord to N
protrude through the opening in the bones.

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 There may or may not be a fluid-filled sac surrounding the spinal cord. L
Incidence- 1-2 cases per 1000 births, This condition is more likely to appear 1min. E
in females.
Types C
 Spina bifida Occulta- Occulta is Latin for "hidden". This is the mildest What are the
T
To explain about form of spina bifida.
U types of spin
In occulta, the outer part of some of the vertebrae is not completely closed.
types of spina The splits in the vertebrae are so small that the spinal cord does not protrude. bifida.
R
bifida. The incidence of spina bifida Occulta is approximately 10% of the 1min.
population, and most people are diagnosed incidentally from spinal X- rays E
 Spina bifida cystic R
- Spina bifida cystica with meningocele- The least common form of
spina bifida is a posterior meningocele (or meningeal cyst). In this form,
the vertebrae develop normally, but the meninges are forced into the C
gaps between the vertebrae.
- Spina bifida cystica with myelomeningocele- (The most common U
location of the malformations is the lumbar and sacral areas). This type M
of spina bifida often results in the most severe complications.
- The unfused portion of the spinal column allows the spinal cord to
protrude through an opening. D
- The meningeal membranes that cover the spinal cord form a sac
enclosing the spinal elements. 2min. I
- The exposure of these nerves and tissues make the baby more prone to S
life-threatening infections such as meningitis. What do you
C
understand b
v) Microcephaly U Microcephaly
To discuss Microcephaly is a condition in which a baby’s head is smaller than average
Microcephaly. for an infant’s size and age. The baby is either born with a smaller head S
(congenital), or the condition develops as the baby gets older (acquired). S
Microcephaly is rare, occurring in 2-12 babies per 10,000 births.
I
What do you
To discuss vi) Craniorachischisis- Craniorachischisis is a genetic disease, O understand b
regarding Craniorachischisis is a very serious neural tube defect characterized by the the term

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craniorachischisis. combination of anencephaly (absence of the brain and cranial vault, without Ppt N craniorachisc
skin covering) with a contiguous bony defect of the cervical spine (also sis
without meninges covering the neural tissue – rachischisis).
To discuss Diagnostic test:- L
What are
regarding Prenatal diagnosis- E diagnostic
diagnostic test.  Maternal and family history 5min. C test?
 Physical examination- Early detection T
 Amniocentesis at 14-16 weeks- Chromosomal abnormalities and U
inborn errors of metabolism R
 Chorionic villi sampling.
E
 Maternal serum alpha-feto protein & gonadotrophin- Neural tube
defect & trisomy  R
 USG.
 Amniography. C
 Fetoscopy U
 Protein assay, M
 DNA diagnosis
 Radiography D
 Antenatal screening- Maternal disease, metabolic & endocrine I
functions. S
Postnatal diagnosis C
 Maternal and family history U
 Physical examination- Early detection
Ppt S
 Biochemical assay
S
 Cytogenic study
I
 Blood test
 Hormonal assay O
1min. N
 Radiography
What is
To introduce Treatment:- There is no cure for these condition, only symptomatic
Encephaloce
encephalocele. management can be done.
vii) Encephalocele ?
Encephalocele is a neural tube defect characterized by sac-like protrusions of
What is the

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To discuss the brain and the membranes that cover it through openings in the skull. management
regarding Management:- By surgical management it will corrected of
management of  Craniotomy: - Surgery is done to put the protruding contents of an Encephaloce
encephalocele. encephalocele back into the skull. The neurosurgeon will cut and ?
remove a portion of the skull, allowing access to the brain. L
 Next, the neurosurgeon will relocate any herniated portion of the E
To discuss brain, meninges and fluid back into the skull and will remove the C
regarding surrounding sac. T
congenital heart Afterward, the dura mater is closed and the skull is repaired either by Ppt
replacing the piece of the skull that was initially removed or using an U What are the
diseases.
artificial replacement. R congenital
To discuss the E heart
causes. Congenital heart diseases 2min. R disorders?
i) Transposition of great arteries
Transposition of the great arteries (TGA) is a serious, rare heart problem in C What are the
which the two main arteries leaving the heart are reversed (transposed). The causes of
U
condition is present at birth (congenital heart defect). TOF?
Causes M
 Usually, the artery that carries blood from the heart to the lungs Ppt
(pulmonary artery) connects to the heart's lower right chamber (right D
3min.
ventricle). I
To explain  Oxygen-rich blood is then pumped from the lungs to the heart's upper S
left chamber (left atrium). C
symptoms of  The body's main artery (aorta) typically connects to the left ventricle. It U
TOF. carries oxygen-rich blood out of the heart to the rest of the body. S
 Drinking alcohol or taking certain medications during pregnancy
S
 Smoking during pregnancy
 Poorly controlled diabetes in the mother during pregnancy I
O
To enlist sign and
Symptoms N
symptoms. What are the
 Blue color of the skin (cyanosis)
 Shortness of breath symptoms of
 Weak pulse

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  Lack of appetite TOF?
To discuss  Poor weight gain
Diagnosis
diagnosis of TOF.  An echocardiogram can show the position of the aorta and the 1min.
pulmonary artery. The test can also identify other associated L What are the
congenital heart defects, such as a ventricular septal defect, atrial diagnoses of
E
septal defect or patent ductus arteriosus. TOF?
C
 Chest X-ray- it does allow the provider to see the baby's heart size T
and determine if blood flow is collecting in the lungs. 2min.
 Electrocardiogram (ECG or EKG)- To records the electrical U
activity of the heart. An ECG can show if the heart is beating too fast, R
To explain about too slow or not at all. E
the management Medication R
of TOF.  Alprostadil (Caverject, Edex, others)- may given to increase blood
What is the
flow and improve mixing of oxygen-poor and oxygen-rich blood. C
Surgical management: U management
 Atrial septostomy- The procedure, also called balloon atrial
M of TOF?
septostomy, widens a natural connection between the heart's upper
chambers (atria). It helps mix oxygen-rich and oxygen-poor blood,
increasing oxygen delivery to the baby's body. D
 Arterial switch operation- The pulmonary artery is connected to the I
right ventricle, and the aorta is connected to the left ventricle. The S
heart arteries also are reattached to the aorta. C
 Rastelli procedure- The surgeon closes the whole (septal defect) in U
the heart using a synthetic patch and redirects blood flow from the left S
ventricle to the aorta, allowing the oxygen-rich blood to go to the
To introduce S
body. A connection is then made with an artificial valve from the right
ventricle to the artery connected to the lungs (pulmonary artery). I
tetralogy of fallot. O
Tetralogy of fallot:- It is the most complex congenital heart defect with N What is
decreased pulmonary blood flow.
tetralogy of
Tetralogy of fallot is a rare condition caused by a combination of four heart
defects that are present at birth (congenital). fallot?

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 These are:
 Ventricular septal defect (VSD) − a hole between the right and left
pumping chambers of the heart
 Overriding aorta − the aortic valve is enlarged and appears to arise L
from both the left and right ventricles instead of the left ventricle as in E
normal hearts C
 Pulmonary stenosis − narrowing of the pulmonary valve and outflow T
To explain about tract or area below the valve that creates an obstruction (blockage) of U
pathophysiology blood flow from the right ventricle to the pulmonary artery
R
 Right ventricular hypertrophy − thickening of the muscular walls of
of tetralogy of the right ventricle, which occurs because the right ventricle is E What is the
pumping at high pressure 2min. R pathophysiol
fallot.
Pathophysiology:
The blood normally returns from the systemic circulation into the right atrium C y of tetralogy
U of fallot?
Right ventricles M
The outflow of blood from the right ventricles to lungs is resisted due to
pulmonary stenosis D
I
Right ventricular hypertrophy S
Pressure in right ventricle increases due to pulmonary stenosis,blood start C
shunting from right to left U
S
Through venticular septal defect
S
Unoxygenated blood mixes with oxygenated blood I
O
Lack of blood supply to lungs due to pulmonary stenosis N
To explain
Increase in amount of unoxygenated blood reaches Systemic circulation
treatment of Through overriding of aorta
What is the
tetralogy of fallot. Cyanosis treatment of
Medical management tetralogy of

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 • Tab. Propanolol 1mg/kg ,4 times fallot?
• Prostaglandin E1 therapy IV 0.05-0.020
• Morphine 0.1-0.2 mg/kg ,once
• Inj. Sodium bicarbonate IV ,1-2mEq/body weight for correction of
acidosis L
• Place the infant in knee chest position. E
Infants will usually require surgical intervention in the neonatal period.  C
Surgical management
T
1.Pallative Surgery
The surgeries are done if the infant is too young for a full repair. U
a) Blalock – Taussing shunt- Artificial ductus is created by connecting R
right or left Subclavian artery to the pulmonary artery on the same E
side. R
b) Pott’s procedure- The upper descending aorta is anastomosed with
left pulmonary artery C
c) Waterston shunt- It involves side to side anastomosis of ascending
U
aorta with right pulmonary artery.
d) Brock’s procedure- Pulmonary valvotomy is done to correct M
pulmonary stenosis. The surgery increases pulmonary blood flow but
does not correct VSD. D
2. Corrective Surgery I
• The hole in the ventricular septum is closed with a patch and the S
obstruction to right ventricular outflow, pulmonary stenosis, C
is opened. U
• These corrections allow blood flow to the lungs for oxygenation
before being pumped out into the body. 1min. Ppt S
To introduce Complications S
• Infective endocarditis I
tricuspid valve What is
• Dysrhythmias O
tricuspid valv
atresia. • Renal Failure N atresia?
• Heart failure

Tricuspid valve atresia

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 - Atresia means closed or absent. 2min. Ppt
To explain about - Tricuspid Atresia results in a number of problems:
- The tricuspid valve is closed or absent.
pathophysiology. What is the
- The right ventricle is small.
L pathophysiol
- The pulmonary artery is narrow.
y of
- The pulmonary valve may be blocked. E
pathophysiol
Congenital absence or agenesis of the tricuspid valve, with no direct C y?
communication between the right atrium and right ventricle. T
Pathophysiology U
Atresia of tricuspid valve
R
No communication between RA and RV E
R
RV is underdeveloped, Systemic venous blood received by RA
C
Enters LA through patent foramen ovale or Atrial Septum Defect. U
1min. Ppt M
Mixing of systemic and pulmonary blood

Enters Left Ventricle D

To enlist sign and
I
symptoms and Blood enters RV through VSD From RV blood enters S
Pulmonary trunk C
diagnostic test.
Blood enters pulmonary trunk via PDA U
S
Increased pulmonary blood flow LA and LV hypertrophy
S
Congenital Heart Failure I
Sign and symptoms O
• Progressive  cyanosis N
• Hypoxic spell
• Tachypnea  over the first 2 weeks of life
• Dyspnea

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 • Acidosis
• Left ventricular hypertrophy   3min. Ppt
• Clubbing
Diagnostic tests L
To discuss the 1. History collection E
2. Physical Examination What is the
C
management.  Aterial blood gas
management
T of tricuspid
 CBC U
 MRI
valve atresia?
R
 CT
 Electrocardiography E
 X-ray R
 Echocardiography
 Cardiac catheterization C
Medical management U
• Intravenous infusion of Prostaglandin 0.03-0.1 mcg/kg to open the M
ductus arteriosus
• Anticongestive therapy with digoxin 7.5-11.3mcg/kg/day ,IV
D
Surgical management
a) Palliative Surgery I
1min. Ppt S
 Atrial septostomy- A balloon is used to create or enlarge the opening
To introduce between the heart's upper chambers to allow more blood to flow from C
about talipes. the right atrium to the left atrium. 1min. Ppt U
 Blalock-Taussig (BT) shunt- A small tube that connects the arterial S What is
To enlist etiology circulation to the pulmonary circulation in order to get more blood to S talipes?
the lungs. I
of talipes.
 Glenn operation- When a child is between 3 and 6 months old. 2min. Ppt What are the
O
Doctors remove the first shunt, then connect one of the large veins etiologies of
that normally returns blood to the heart (the superior vena cava) to the N talipes?
To explain
pulmonary artery.
treatment.  Fontan procedure- Creation of communication between right atrium What is the
and pulmonary artery or the right ventricle by direct anastomosis. treatment of
talipes?

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 Musculoskeletal abnormalities
i) Talipes- A congenital deformity in which the foot is twisted out of
shape or position. It is also called clubfoot.
Etiology L
To introduce  Unknown E
 Teratogenic agents C
gastroschisis. What is
 Oligohydramnios T gastroschisis
Treatment U
Permanent immobilization of the foot in corrected position using elastic R
bandages, plates, splints at first,
To enlist causes E
Ponseti technique 
and sign and R What are the
symptoms and The clubfoot and above the knee casting of the clubfoot molded by the
surgeon weekly, (may involve cutting the Achilles tendon-tenotomy) causes, sign
diagnostic test C and symptom
gastrochisis. Post-op Care  U and diagnost
 Keep cast uncovered to allow drying. test?
M
 Keep leg elevated on pillows.
 Perform neurovascular checks
2min. Ppt D
 Circle with a pen any area of bleeding on the cast.
I
 Observe for skin irritation.
Denis Browne splint After 3 weeks, the infant will wear splints such as S
Denis Browne splint C
2min. Ppt U
To explain Gastrointestinal abnormalities S
treatment of  Gastroschisis S
Gastroschisis is a birth defect where baby is born with their organs outside of What are the
gastroschisis. I
their body due to their abdominal wall not forming completely in the treatments of
womb. Intestines (stomach, large or small intestines) exit their body from a 2 O
gastroschisis
to 5centimeter hole beside their belly button during fetal development.  N
Causes - Unknown
Sign and symptoms
 Stomach, large or small intestines located outside of baby’s body.
 Swollen intestines.

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  Twisted intestines.
 Low body temperature (hypothermia).
Diagnostic test:-
 Ultrasound: An imaging test using sound waves to see details of soft 3min. Ppt L
tissues inside body. E
 Blood screening: A blood test that measures substances in blood,
What do you
To introduce C
including alpha-fetoprotein, which, if tested at higher than normal understand b
about cleft lip and T
levels between 18 and 22 weeks, could be a sign of gastroschisis. cleft lip/ clef
cleft foot. U
 Magnetic resonance imaging (MRI): An imaging test to take a
palate?
R
detailed picture of the inside of body and the baby.
To enlist causes Treatment E
R What are the
and sign and Surgery management- treatment of
symptoms. Surgery is necessary to place baby’s organs back inside their body. Surgery cleft lip and
also repairs the hole near belly button to prevent their organs from returning C palate?
back outside of their body. U
there are two types of surgery to relocate your baby’s organs and repair their M
abdominal wall:
 Primary repair: If possible, baby will receive surgery immediately
2min. Ppt
D
after they are born to move the organs back into their body and repair
the hole in their abdomen. I
 Staged repair: If the gastroschisis is more complicated, baby’s surgeon S
will perform surgery slowly in stages. A staged repair could be most 3min. Ppt C
effective if baby isn’t healthy enough for surgery, or if their abdomen U
isn’t big enough to hold all of their organs. S
S
Cleft lip/ cleft foot
Cleft lip and cleft palate are openings or splits in the upper lip, the roof of the I
mouth (palate) or both. Cleft lip and cleft palate result when facial structures O
that are developing in an unborn baby don't close completely. N
Cleft lip and cleft palate are among the most common birth defects. 
Risk factors What is the
To discuss the  Family history- Parents with a family history of cleft lip or cleft palate treatment of
treatment of cleft face a higher risk of having a baby with a cleft. cleft lip/ clef

16
lip and palate.  Exposure to certain substances during pregnancy. palate?
 Diabetes
 Certain drug abuse
Sign and symptoms
 A split in the lip and roof of the mouth (palate) that affects one or both L
sides of the face E
 A split in the lip that appears as only a small notch in the lip or extends
C
from the lip through the upper gum and palate into the bottom of the
T
nose 2min. Ppt
 Difficulty with feedings U
 Difficulty swallowing, with potential for liquids or foods to come out R
the nose E
 Nasal speaking voice R
 Chronic ear infections

Diagnostic test C
To introduce renal U
 USG
agenesis/ M What is renal
 Amniocentesis
hypoplasia. agenesis?
Treatment / surgery
Surgeries typically are performed in this order: D
To explain the  Cleft lip repair — within the first 3 to 6 months of age I
 Cleft palate repair — by the age of 12 months, or earlier if possible What are the
types. S types of rena
 Follow-up surgeries — between age 2 and late teen years
Surgical procedure may include:- C agenesis?
 Cleft lip repair. To close the separation in the lip, the surgeon makes U
incisions on both sides of the cleft and creates flaps of tissue. The flaps S
are then stitched together, including the lip muscles. The repair should S
3min. Ppt
create a more normal lip appearance, structure and function. Initial I What are the
To enlist the nasal repair, if needed, is usually done at the same time. O causes?
causes.  Cleft palate repair. Various procedures may be used to close the
N
separation and rebuild the roof of the mouth (hard and soft palate),
depending on your child's situation. The surgeon makes incisions on
both sides of the cleft and repositions the tissue and muscles. The repair
is then stitched closed.

17
  Surgery to reconstruct appearance. Additional surgeries may be
needed to improve the appearance of the mouth, lip and nose.
Genitourinary system abnormalities
 Renal agenesis/ hypoplasia 3min. Ppt L
Renal agenesis is a complete absence of one (unilateral) or both (bilateral)
E What are the
kidneys, whereas in renal aplasia the kidney has failed to develop beyond it’s
most primitive form. C symptoms?
Incidence- one in 1,000neborns T
To enlist sign and
Types U
symptoms. Bilateral- Bilateral renal agenesis is a condition in which both kidneys of a R
fetus fail to develop during gestation. It is incompatible with life. It is one E
causative agent of Potter sequence. R
Unilateral- This is much more common, but is not usually of any major
health consequence, as long as the single kidney is healthy. However, this C
kidney tends to be hypertrophied, ectopic and prone to infection and damage. 1min. Ppt What is the
U investigation
Causes-
 Unknown M
To enlist
 Genetic history
diagnostic test. D
 Maternal factors
 Environmental / lifestyle factors I
What are the
 Cat-Eye syndrome- where there’s a fissure in the eye, no anal opening, S treatments?
and renal agenesis C
To discuss  Rokitansky sequence- where the vagina and uterus don’t form completely U
treatment.  Fraser syndrome- where baby is born with sealed eyelids and partially S
formed sexual organs
S
 Melnick-Fraser syndrome- which causes hearing loss and kidney
deformities. I
 Mullerian duct, renal, and cervical vertebral defects, which causes O
irregular vertebrae and missing vagina and kidneys 1min. Ppt N
Sign and symptoms
 High blood pressure
 Poorly working kidney

18
  Urine with protein or blood
 Swelling in the face, hands, or legs What is
2min. Ppt
babies with bilateral renal agencies having the sign of- hypospadias?
To introduce  Widely separated eyes with skin folds over the eyelids
hypospadias.  Ears that are set low
 A nose that is pressed flat and broad
L What are the
 A small chin
 Defects of the arms and legs E causes?
. C
To enlist causes
Diagnostic testes T
and risk factors..  Physical examination U
 Prenatal USG R
 MRI E
 Genetic testing R
Management
short-term treatment 2min. Ppt
C
 Bilateral renal agenesis is fatal.
U
 If one kidney is present, the child will develop normally. The remaining
kidney, if properly functioning, can very effectively remove the wastes M
from the blood and keep the body entirely healthy. 1min. Ppt What are the
 Once detected, families where renal agenesis has occurred will be D symptoms?
To discuss sign offered genetic counseling because of the possibility of recurrence in I
and symptoms. future pregnancies. S
Long-term treatment C
 Protect the remaining kidney from infection or injury. U
 Periodic examinations of the kidney and prompt treatment of any urinary S
To enlist tract infection is required.
S
 Counseling to avoid contact sports where the kidney could be injured.
diagnostic test? I
What are the
Hypospadiasis O
treatments?
Hypospadiasis is a birth defect (congenital condition) in which the opening of N
To discuss about the urethra is on the underside of the penis instead of at the tip. The urethra is
the tube through which urine drains from your bladder and exits your body.

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treatment? 2min. Ppt
Causes
 Unknown
 Genetic L What is
 Environmental E trisomy 21?
Risk factor C
 Family history- This condition is more common in infants with a family T
To explain about history of hypospadias. U
 Genetics- Certain gene variations may play a role in disruption of the
trisomy 21. R What are the
hormones that stimulate formation of the male genitals.
3min. Ppt E causes?
 Maternal age over 35- Some research suggests that there may be an
increased risk of hypospadias in infant males born to women older than R
35 years. What are the
To enlist causes?  Exposure to certain substances during pregnancy. There is some C sign and
speculation about an association between hypospadias and a mother's U symptoms?
exposure to certain hormones or certain medication. M
Symptoms
To enlist sign and  Opening of the urethra at a location other than the tip of the penis 1min. Ppt
D
 Downward curve of the penis (chordee)
symptoms. I
 Hooded appearance of the penis because only the top half of the penis is
covered by foreskin S
 Abnormal spraying during urination C
Diagnosis U
2min. Ppt
 History collection S
 Physical examination S
 Urine examination I What are the
Treatment diagnostic
2min. Ppt O
Surgery is usually done between the ages of 6 and 12 months. tests?
The operation mostly involves 4 steps: N
 Straightening the shaft
To explain
 Making the urinary channel
diagnostic test.  Positioning the meatus in the head of the penis
 Circumcising or reconstructing the foreskin

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  Chromosomal abnormality:-
Trisomy 21- It is a genetic condition that causes delays in physical and
intellectual development.
• There is extra genetic material from chromosome 21, so individuals L
with down syndromes in total instead of 46 chromosomes. E
It means there’s an extra copy of chromosome 2 in every cell. This is the 2min. Ppt
C
most common form of Down syndrome.
Causes and risk factors T
• Genetic U
• Advance maternal age R
• Previous pregnancy with down syndrome. E
• Teratogenic drugs R
Sign and symptoms
- flat facial features What are the
C preventions f
- Small head and ears
U chromosoma
- Short neck
M abnormalities
- Bulging tongue
- Eyes that slant upward
To explain about - Atypically shaped ears D
- Poor muscle tone I
the prevention of S
Mental and social developmental delay may lead to-
chromosomal - Impulsive behavior C
abnormalities? - Poor judgment U
- Short attention span S
- Slow learning capabilities S
Diagnosis- I
First trimester- 3min. Ppt
O
- Ultrasound
N
- Blood test
Second trimester-
- Ultrasound

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 - QMS (quadruple marker screen)- it can help identify down syndrome
and other defects in the brain and spinal cord . this test is done
between 15 and 20 weeks of pregnancy. What are the
- Amniocentesis. nursing
- Chronic villus sampling(cvs) diagnoses?
- Cordocenthesis, umbilical blood sampling.
complication includes-
To explain - Hearing loss
nursing
- Poor vision
management.
- Cataracts
- Hip dislocation
- Leukemia
- Sleep apnea
- Dementia
- Hypothyroidism
- Obesity
- Alzheimer’s disease later in life
Prevention of congenital anomalies-
 Genetic counseling-It is a problem solving approach or
communication process in relation to genetic disorders or congenital
anomalies in the family.
 Avoid late marriage and pregnancy
 Discourage consanguineous marriages
 Protection of individuals & whole communities against mutagens (X-
ray, drugs ,alcohol)
 Promotion of health of girl child and pre pregnant health status of the
females by prevention of malnutrition, anemia, folic acid deficiency, 3min. Ppt
iodine deficiency, etc.
 Elimination of active and passive smoking of tobacco by mothers.
 Immunization by anti-D immunoglobin to the Rh-negative mothers
after abortion.
 Avoidance of drug intake without consulting physician in the first

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 trimester of pregnancy. 
 Prevention of intrauterine infections and promotion of sexual hygiene.
 Promotion of therapeutic abortion after prenatal diagnosis.
 Efficient antenatal care.  
 Increasing public awareness about the risk factors and etiological
factors of congenital anomalies and their preventive measures.
 Discouraging reproduction after birth of a baby with congenital
anomalies.
Nursing management:-
1. Altered nutrition less than body requirements related to difficulty
in eating.
Goal- To provide adequate nutritional intake.
Intervention:- Administer diet appropriate for age (specify).
 Modify feeding techniques to adjust to defect.
 Hold the child in upright position.
 Use special feeding appliances.
 Bubble frequently.
 Assist mother with breast-feeding if this is mother’s preference.
Expected outcome- Infant consumes an adequate amount of nutrients 
2. High risk for altered parenting related to infant with a highly
visible physical defect.
Goal- facilitate family’s acceptance of infant.
Intervention-Allow expression of feelings.
 Convey attitude of acceptance of infant and family.
 Indicate by behavior that child is a valuable human being.
 Describe results of surgical correction of defect (use photographs
of satisfactory results).
L
 Arrange meeting with other parents who have experiences of
E
similar situations and coped successfully.
C
Expected outcome- Family exhibits an attitude of acceptance of infant.
T
3. High risk for trauma related to surgical procedure, dysfunctional
U
swallowing.
R

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 Goal- Prevent trauma to suture line. E
Intervention- Maintain lip protective device. R
 Use non-traumatic feeding techniques.
 Restrain arms to prevent access to operative site. (use jacket C
restraints on older infant). U
 Cleans suture line gently after feeding and as necessary in manner M
ordered by surgeon.
 Teach cleansing and restraining procedures, especially when infant D
will be discharged before suture removal. I
Expected outcome- Operation site remains un-damaged S
4. Altered nutrition; less than body requirements related to physical C
defect, surgical procedure. U
Goal- provide adequate nutrition intake. S
Intervention- S
I
 Administer diet appropriate for age.
O
 Involve family in determining best feeding methods.
N
 Modify feeding techniques to adjust to defect:-
 Feed in sitting position.
 Use special appliances.
 Encourage frequent bubbling.
 Assist with breast-feeding if method of choice.
 Teach feeding and suctioning techniques to family.
 Monitor IV fluids (if prescribed).
Expected outcome- Maintain adequate amount of nutrients 
Summary- At the end of the class students will be able to understand about the topic congenital anomalies.
Conclusion- Congenital anomalies are a major cause of stillbirths and infant mortality. Evaluation of cardiovascular system to rule out
congenital heart disease in high-risk mothers' babies is the important factor to be considered.
Research article:- Congenital malformations at birth in Central India: A rural medical college hospital based data
Author- Amar Taksande, Krishna Vilhekar, Pushpa Chaturvedi, and Manish Jain
Objective:
To study the incidence of congenital anomalies and the associated risk factors in Department of Pediatrics at Mahatma Gandhi
Institute of Medical Sciences, Sevagram, Wardha, a rural medical college hospital in central Maharashtra.
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Materials and methods:
All the intramural deliveries between 1 January 2005 and 31 July 2007 comprised 9386 births and their 9324 mothers (62 mothers
gave birth to twin babies). The newborns were examined and assessed systematically for the presence of congenital anomalies, system
wise distribution of anomalies and risk factors attributable.
Results:
Out of the total 9386 deliveries, 9194 were live births and 192 were stillbirths. The total number of babies with congenital
malformations was 179 (1.91%). Out of the 9262 singleton births, 177 (1.05%) were malformed, whereas 2 of the 62 pairs of twins
had birth defects. Nine of the 179 malformed babies (5.02%) were still born. Prematurity, increased maternal age, increasing birth
order and low birth weight were found to have a higher risk of congenital anomalies. Cardiovascular malformations were most
common in live births, followed by musculoskeletal and genitourinary anomalies.
Conclusion:
Congenital anomalies are a major cause of stillbirths and infant mortality. Evaluation of cardiovascular system to rule out congenital
heart disease in high-risk mothers’ babies is the important factor to be considered.

Bibliography
 Gupta Piyush. essential pediatric nursing:2 ed. New Delhi: CBS publisher;2010. p.no. 354-62
nd

 Wong's. Essential of Pediatric Nursing: 1st ed. Elsevier publication.P .no- 166-169
 Gump WC. Endoscopic Endonasal Repair of Congenital Defects of the Anterior Skull Base: Developmental Considerations
and Surgical Outcomes. J Neurol Surg B Skull Base. 2015 Aug;76(4):291-5.
 Taksande A, Vilhekar K, Chaturvedi P, Jain M. Congenital malformations at birth in Central India: A rural medical college
hospital based data. Indian J Hum Genet. 2010 Sep;16(3):159-63. doi: 10.4103/0971-6866.73412. PMID: 21206705; PMCID:
PMC3009428.

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