Congenital heart disease is one or more problems with the heart's structure that exist since birth. Congenital means that you're born with the defect. Congenital heart disease, also called congenital heart defect, can change the way blood flows through your heart. IF YOU LIKE GIVE YOUR LIKES AND FOLLOW THIS LINK
Congenital heart disease is one or more problems with the heart's structure that exist since birth. Congenital means that you're born with the defect. Congenital heart disease, also called congenital heart defect, can change the way blood flows through your heart. IF YOU LIKE GIVE YOUR LIKES AND FOLLOW THIS LINK
ACYANOTIC DISEASE- Non cyanotic heart diseasesNelsonNgulube
ETIOLOGY AND EPIDEMIOLOGY
Congenital heart disease occurs in 8 per 1,000 births. The spectrum of lesions ranges from asymptomatic to fatal. Although most cases of congenital heart disease are multifactorial, some lesions are associated with chromosomal disorders, single gene defects, teratogens, or maternal metabolic disease (see Table139-2).
Congenital heart defects can be divided into three pathophysiological groups (Table 143.1).
1. Left-to-right shunts
2. Right-to-left shunts
3. Obstructive, stenotic lesions
Acyanotic congenital heart disease includes left-to-right shunts resulting in an increase in pulmonary blood flow (patent ductus arteriosus [PDA], ventricular septal defect [VSD], atrial septal defect [ASD]) and obstructive lesions (aortic stenosis, pulmonary stenosis, coarctation of the aorta), which usually have normal pulmonary blood flow.
VENTRICULAR SEPTAL DEFECTEtiology and Epidemiology
The ventricular septum is a complex structure that can be divided
into four components. The largest component is the muscular
septum. The inlet or posterior septum comprises endocardial
cushion tissue. The subarterial or supracristal septum com
prises conotruncal tissue. The membranous septum is below
the aortic valve and is relatively small. VSDs occur when any of these components fail to develop normally (Fig. 143.1). VSD,
the most common congenital heart defect, accounts for 25% of all congenital heart disease. Perimembranous VSD
Approach to Short Stature
Dr Raheel Ahmed
FCPS in Paediatric Medicine
Children Hospital, Chanka Medical College, Larkana
Topics
Definition.
Etiology
Measurements.
Examination.
Investigations.
Management.
Take home message.
Who is short child?
Short stature is defined as height that is two standard deviations below the mean height for age and sex (less than the third percentile).
OR
more than two standard deviations below the mid-parental height.
Etiology
Proportionate Short Stature
1) Normal Variants:
i) Familial
ii) Constitutional Growth Delay
2) Prenatal Causes:
i) Intra-uterine Growth Restriction-
Placental causes, Infections, Teratogens
ii) Intra-uterine Infections
iii) Genetic Disorders (Chromosomal
& Metabolic Disorders)
Postnatal Causes:
i) Undernutrition
ii) Chronic Systemic Illness
- Cardiopulmonary: CHD, Chronic Asthma,
Cystic Fibrosis
- Renal: RTA, CRF, Steroid dependent
Nephrotic Syndrome
- GI and Hepatic: Malabsorption, IBD, chronic
liver disease
- Chronic Severe Infections
- Hematological : Thalassemia, Sickle cell
anemia
iii) Psychosocial Short Stature
(emotional deprivation)
iv) Endocrine Causes:
- Growth Hormone Deficiency/ insensitivity
- Hypothyroidism
- hypopituitrism
- Diabetes Mellitus
- Cushing Syndrome
- Pseudohypoparathyroidism
- Precocious/ delayed puberty
Disproportionate Short Stature
1) With Short Limbs:
Achondroplasia,
Hypochondroplasia,
Chondrodysplasia punctata,
Chondroectodermal Dysplasia,
Diastrophic dysplasia,
Metaphyseal Chondrodysplasia
Osteogenesis Imperfecta,
Refractory Rickets
2) With Short Trunk:
Spondyloepiphyseal dysplasia,
Mucolipidosis
Mucopolysaccharidosis
Mid Parental Height
TCR
Calculated by MPH +-10
How to measure upper and lowersegments?
You should measure the upper segment( US ) then by using the total height you will obtain LS.
Upper segment is the sitting height.
Disproportionate short statue with short LS:-
Achondroplesia
Osteogenesis imperfecta.
Refractory rickets.
Disproportionate short stature with short US:-
Spondyloepiphysial dysplasia.
Mucopolysaccharidosis.
Growth velocity
0-1 year : 25cm/year
1-2 year: 12cm/year
2-3 year: 8cm/year
3-4 year: 7cm/year
4-9 year : 5-6 cm/year
As a rule any growth rate <4.5cm/year between 2-12 year is pathological.
Dysentery
Dr. Raheel Ahmed
FCPS Pediatric Medicine
Children Hospital, Chandka Medical College, Larkana
On a global scale, of the estimated 165 million Shigella diarrhoeal episodes estimated to occur each year, 99% occur in developing countries, mainly in children.
1999, reported Shigella to be responsible for 1.1 million deaths per year, 61% of which in children less than 5 years of age
In 2013, estimates suggesting between 28,000 and 48,000 deaths annually amongst children under 5 years due to Shigellosis
Dysentry occurs predominantly in developing countries due to overcrowding and poor sanitation.
Infants,
non-breast fed children,
children recovering from measles,
malnourished children, and
adults older than 50 years
have a more severe illness and a greater risk of death.
Bascillary Dysentery
Shigella is a Gram-negative, non-motile bacillus belonging to the Enterobacteriaceae family.
There are four species of Shigellae:
S. dysenteriae, S. flexneri, S. boydii and S. sonnei
(designated as serogroups A, B, C and D respectively).
S. boydii and S. sonnei usually cause a relatively mild illness (watery or bloody diarrhoea only),
S. flexneri and S. dysenteriae are chiefly responsible for endemic and epidemic shigellosis (respectively) in developing countries, with high transmission rates and significant case fatality rates.
Transmission occurs via the faecal-oral route, person-to-person contact, household flies, infected water, and inanimate objects.
Shigella species can survive in gastric acid, and infection can occur following exposure to as few as 10-100 organisms.
Once infected, all Shigella species multiply invading the colonic epithelium where pro-inflammatory cytokines are released, and the subsequent inflammatory reaction destroys the epithelial cells lining the gut mucosa, allowing for further direct invasion by Shigella.
The resultant infectious diarrhoea is associated with loss of water and electrolytes and a clinical picture of abdominal cramping, fever, and bloody/mucoid stools.
History
Examination
Investigation
Case Definitions
Suspected case: a case with gastroenteritis, bloody mucoid diarrhea, abdominal cramps, fever and rectal pain.
Probable case: A clinical compatible case thatis epidermiologically linked i.e. Is a contact toa confirmed case or a member of risk group defined by public health authorities during an outbreak.
Confirmed case: a case that meets the confirmed laboratory criteria for diagnosis i.e. ISOLATION of Shigella species from a clinical specimen.
Period of Communicability: shed in feces 4 weeks after infection then as long as organisms present in faeces.
More Related Content
Similar to Approach to Pediatric Cardiovascular diseases.pptx
ACYANOTIC DISEASE- Non cyanotic heart diseasesNelsonNgulube
ETIOLOGY AND EPIDEMIOLOGY
Congenital heart disease occurs in 8 per 1,000 births. The spectrum of lesions ranges from asymptomatic to fatal. Although most cases of congenital heart disease are multifactorial, some lesions are associated with chromosomal disorders, single gene defects, teratogens, or maternal metabolic disease (see Table139-2).
Congenital heart defects can be divided into three pathophysiological groups (Table 143.1).
1. Left-to-right shunts
2. Right-to-left shunts
3. Obstructive, stenotic lesions
Acyanotic congenital heart disease includes left-to-right shunts resulting in an increase in pulmonary blood flow (patent ductus arteriosus [PDA], ventricular septal defect [VSD], atrial septal defect [ASD]) and obstructive lesions (aortic stenosis, pulmonary stenosis, coarctation of the aorta), which usually have normal pulmonary blood flow.
VENTRICULAR SEPTAL DEFECTEtiology and Epidemiology
The ventricular septum is a complex structure that can be divided
into four components. The largest component is the muscular
septum. The inlet or posterior septum comprises endocardial
cushion tissue. The subarterial or supracristal septum com
prises conotruncal tissue. The membranous septum is below
the aortic valve and is relatively small. VSDs occur when any of these components fail to develop normally (Fig. 143.1). VSD,
the most common congenital heart defect, accounts for 25% of all congenital heart disease. Perimembranous VSD
Approach to Short Stature
Dr Raheel Ahmed
FCPS in Paediatric Medicine
Children Hospital, Chanka Medical College, Larkana
Topics
Definition.
Etiology
Measurements.
Examination.
Investigations.
Management.
Take home message.
Who is short child?
Short stature is defined as height that is two standard deviations below the mean height for age and sex (less than the third percentile).
OR
more than two standard deviations below the mid-parental height.
Etiology
Proportionate Short Stature
1) Normal Variants:
i) Familial
ii) Constitutional Growth Delay
2) Prenatal Causes:
i) Intra-uterine Growth Restriction-
Placental causes, Infections, Teratogens
ii) Intra-uterine Infections
iii) Genetic Disorders (Chromosomal
& Metabolic Disorders)
Postnatal Causes:
i) Undernutrition
ii) Chronic Systemic Illness
- Cardiopulmonary: CHD, Chronic Asthma,
Cystic Fibrosis
- Renal: RTA, CRF, Steroid dependent
Nephrotic Syndrome
- GI and Hepatic: Malabsorption, IBD, chronic
liver disease
- Chronic Severe Infections
- Hematological : Thalassemia, Sickle cell
anemia
iii) Psychosocial Short Stature
(emotional deprivation)
iv) Endocrine Causes:
- Growth Hormone Deficiency/ insensitivity
- Hypothyroidism
- hypopituitrism
- Diabetes Mellitus
- Cushing Syndrome
- Pseudohypoparathyroidism
- Precocious/ delayed puberty
Disproportionate Short Stature
1) With Short Limbs:
Achondroplasia,
Hypochondroplasia,
Chondrodysplasia punctata,
Chondroectodermal Dysplasia,
Diastrophic dysplasia,
Metaphyseal Chondrodysplasia
Osteogenesis Imperfecta,
Refractory Rickets
2) With Short Trunk:
Spondyloepiphyseal dysplasia,
Mucolipidosis
Mucopolysaccharidosis
Mid Parental Height
TCR
Calculated by MPH +-10
How to measure upper and lowersegments?
You should measure the upper segment( US ) then by using the total height you will obtain LS.
Upper segment is the sitting height.
Disproportionate short statue with short LS:-
Achondroplesia
Osteogenesis imperfecta.
Refractory rickets.
Disproportionate short stature with short US:-
Spondyloepiphysial dysplasia.
Mucopolysaccharidosis.
Growth velocity
0-1 year : 25cm/year
1-2 year: 12cm/year
2-3 year: 8cm/year
3-4 year: 7cm/year
4-9 year : 5-6 cm/year
As a rule any growth rate <4.5cm/year between 2-12 year is pathological.
Dysentery
Dr. Raheel Ahmed
FCPS Pediatric Medicine
Children Hospital, Chandka Medical College, Larkana
On a global scale, of the estimated 165 million Shigella diarrhoeal episodes estimated to occur each year, 99% occur in developing countries, mainly in children.
1999, reported Shigella to be responsible for 1.1 million deaths per year, 61% of which in children less than 5 years of age
In 2013, estimates suggesting between 28,000 and 48,000 deaths annually amongst children under 5 years due to Shigellosis
Dysentry occurs predominantly in developing countries due to overcrowding and poor sanitation.
Infants,
non-breast fed children,
children recovering from measles,
malnourished children, and
adults older than 50 years
have a more severe illness and a greater risk of death.
Bascillary Dysentery
Shigella is a Gram-negative, non-motile bacillus belonging to the Enterobacteriaceae family.
There are four species of Shigellae:
S. dysenteriae, S. flexneri, S. boydii and S. sonnei
(designated as serogroups A, B, C and D respectively).
S. boydii and S. sonnei usually cause a relatively mild illness (watery or bloody diarrhoea only),
S. flexneri and S. dysenteriae are chiefly responsible for endemic and epidemic shigellosis (respectively) in developing countries, with high transmission rates and significant case fatality rates.
Transmission occurs via the faecal-oral route, person-to-person contact, household flies, infected water, and inanimate objects.
Shigella species can survive in gastric acid, and infection can occur following exposure to as few as 10-100 organisms.
Once infected, all Shigella species multiply invading the colonic epithelium where pro-inflammatory cytokines are released, and the subsequent inflammatory reaction destroys the epithelial cells lining the gut mucosa, allowing for further direct invasion by Shigella.
The resultant infectious diarrhoea is associated with loss of water and electrolytes and a clinical picture of abdominal cramping, fever, and bloody/mucoid stools.
History
Examination
Investigation
Case Definitions
Suspected case: a case with gastroenteritis, bloody mucoid diarrhea, abdominal cramps, fever and rectal pain.
Probable case: A clinical compatible case thatis epidermiologically linked i.e. Is a contact toa confirmed case or a member of risk group defined by public health authorities during an outbreak.
Confirmed case: a case that meets the confirmed laboratory criteria for diagnosis i.e. ISOLATION of Shigella species from a clinical specimen.
Period of Communicability: shed in feces 4 weeks after infection then as long as organisms present in faeces.
COMMON Pediatrics' SURGICAL EMERGENCIES
Presented By: Dr. Raheel Ahmed
FCPS – Pediatrics Medicine
Children hospital, Chandka Medical College, Larkana
Topics we will be discussing today are:
Tracheoesophageal Fistula.
Duodenal Atresia.
Meckel’s Diverticulum.
Hirschprung’s Disease.
Appendicitis.
Biliary Atresia.
Adenoids
Definition
The adenoids are enlarged and hypertrophied nasopharyngeal tonsils, sufficient to produce symptoms
It is disease of infancy and childhood.
Adenoids are subjected to physiological enlargement in childhood hence nasopharyngeal tonsils are commonly called Adenoids.
Nasopharyngeal Tonsil
Single pyramidal mass of sub-epithelial lymphoid tissue, present in nasopharynx at the junction of its roof and posterior wall.
The pharyngeal tonsil is composed of vertical ridges of lymphoid tissues separated by deep cleft and covered by Pseudostraitified ciliated columinar epithelium.
The free surface has 6 folds
It has no capsule
These lymphoid tissues consits of T and B lymphocytes.
It forms roof of waledeyer’s ring.
Can't normally see them because they are above and behind the uvula.
Arterial Supply
Ascending branch of facial artery
Ascending pharyngeal branch of external carotid
Pharyngeal branch of third part of maxillary artery.
Ascending cervical branch of inferior thyroid artery of thyrocervial trunk
Development
Adenoids begin forming in 3rd month of fetal development
Glandular primordia on posterior pharynx are infiltrated by lymphocytes.
Covered by pseudostratified ciliated epithelium
Fully formed by 7 month
Growth
They are not visible on X-ray in infants under age of one month.
50% of cases, it is visible at 6 month.
At the age of 2 years undergo hypertrophy and hyperplasia.
Can become nearly the size of a Table Tennis ball
Hypertrophy continues up to puberty (12 years)
Then, undergoes atrophy after puberty
Finally disappears in adults
Why does adenoid physiologically enlarge?
Poorly develop at birth.
Grows rapidly during childhood.
Generalized lymphoid hyperplasia occurs in children
Among the first aggregative lymphoid tissues in respiratory tract.
Physiology
Part of secondary immune system
No afferent lymphatics
Exposed to inspired antigens passed through the epithelial layer
Membrane cells and antigen presenting cells are involved in transport of antigen from the surface to the lymphoid follicle
Antigen is presented to T-helper cells
T-helper cells induce B cells in germinal center to produce antibody
Secretory IgA is primary antibody produced
Involved in local immunity
Etiology
Age : 3 -12 years
Season: winter
Food: Cold, sour, oily food
General lymphoid hyperplasia
Infection in tonsils alone or associated with
Rhinitis, Sinusitis, Tonsillitis
(esp. chronic maxillary sinusitis)
Recurrent attacks of rhinitis, sinusitis or tonsillitis may causes chronic adenoid infection
Allergy of respiratory tract.
Clinical features
Symptoms occur most commonly between ages of
3-7 years.
Depending on size of adenoid mass and space
3 types
Nasal symptoms
Aural symptoms
General symptoms
Nasal symptoms
Bilateral Nasal obstruction
Mouth breathing
interfere
Continents
Definitions
EPI
Current EPI Schedule
Different EPI Vaccines
Cold Chain
Non-EPI vaccines
Immunization
It is process where by a person is made immune or resistant to an infection, typically by administration of vaccine
It is proven tool for controlling and elimination life-threatening infectious.
Types of immunity
Innate or natural Immunity
Immunity with birth
Acquired Immunity
Develops during life time
Acquired naturally or artificially
Vaccine
A vaccine is a non- pathogenic antigen that mimics a particular pathogen in order to elicit an immune response as if that actual pathogen were in the body
Types
Live, attenuated Vaccine
Inactive Vaccine
Whole cell vaccine
Protein based: Toxoid, subunit
Polysaccharide based: Conjugate, pure
EPI: Extended Program of Immunization
EPI was established in 1974.
Built on success of the global smallpox eradication
It ensures that all children in worldwide benefited from life saving vaccines.
AIM
It focuses on following items
Standard Immunization Schedule
Supplemental immunization activities
Disease survillance
Mopping up
Promoting safe injection techniques
Improving the stocking and availability of vaccines
Protecting vaccines’ potency through cold chain management
To prepare for introduction of new vaccines
Objectives
To increase coverage of immunization for eligible children
To reduce incidence of immunizable diseases among children below five years of age
Eradication of polio, measles, neonatal tetanus, diphtheria
Reduce incidence of hepatitis B, whooping cough, bacterial meningitis
Prevention of severe forms of TB
Management of Preterm And Low Birth Weight
Dr. Raheel Ahmed FCPS Pediatrics
Children Hospital, Chandka Medical College Larkana
Definitions
Prevalent
Etiology
Assessment of gestational age
Problems of prematurity
Management
Antenatal (Prevention)
Natal (Delivery room care)
Post natal (after birth care)
Prognosis
Discharge criteria
Definitions
Term?
Preterm?
Immature?
LBW? VLBW?ELBW? ILBW?
SGA?
IUGR?
Gestational Age
Full-term
infant born after 37 completed menstrual weeks of pregnancy
Preterm (or premature) infant
infant born before 37 completed weeks of gestation
Late preterm infant (a recently identified category)
infant born between 34 and 36 weeks gestation
Moderately preterm infant
infant born between 32 and 34 completed weeks of gestation
Very preterm infant/ Early preterm
infant born before 32 completed weeks of gestation
Immature < 28 weeks
ELGAN: Extremely Low Gestational Age Newborn < 26 weeks
Weight
Low birth weight (LBW)
infant who weighs less than 2,500 grams at delivery
Very low birth weight (VLBW)
infant who weighs less than 1,500 grams at delivery
Extremely low birth weight (ELBW)
infant who weighs less than 1,000 grams at delivery
Incredible Low birth weight
infant who weighs less than 750 grams at delivery
APPROACH TO AKI IN CHILDREN
ACUTE KIDNEY INJURY
It is defined as abrupt loss of kidney function leading to rapid decline in GFR , accumulation of waste products BUN and creatinine and dysregulation of extracellular volume and electrolyte homeostasis.
AKI can ranges from small increase in creatinine to complete anuric renal failure .
INCIDENCE
2-5 % of all hospitalization.
>25% in critically ill children .
CLASSIFICATION OF AKI
CAUSES
CLINICAL MANIFESTATION
DIAGNOSTIC TEST
HISTORY AND PHYSICAL
EXAMINATION
IDENTIFICATION OF PRECIPTATING CAUSE
COMPLICATION
MANAGEMENT
MANAGEMENT
There is no definitive therapy for AKI, supportive care is mainstay of management regardless of aetiology.
Goal of treatment is :
Minimize degree of insult.
Reduce extrarenal complication.
Restoration of AKI.
Optimize the systemic and renal hemodynamic(fluid resuscitation or use of vasopressor).
Avoid the nephrotoxic drugs (e.g aminoglycoside, NSAIDs, ACE inhibitor, ARB blocker, acyclovir) or adjust the dose .
Catheterize the patient in case of obstruction like PUV, UPJ obstruction
POST-RENAL AKI
Prompt relieve of urinary tract obstruction.
Relief of obstruction is usually followed by an appropriate diuresis and may require continue administration of iv fluids and electrolyte.
RENAL REPLACEMENT THERAPY
The purpose of RRT is to prevent morbidity.
It may be necessary for days or upto 12 weeks.
Mostly require dialysis support for 1-3 weeks.
Indication Of RRT :
A= ACIDOSIS, ANURIA
E= ELECTROLYTE DISTURBANCE (hypokalemia)
I= INTOXICATION
O= OVERLOAD(hypertension, pulmonary edema)
U= UREMIA
PROGNOSIS
Pre-renal and post-renal have better prognosis.
In case of post-infectious glomerulonephritis is 1%
In case of multi organ failure >50%.
Kidney may recover even after dialysis .
10% cases requiring dialysis develop CKD.
CARRY HOME MESSAGE
Diagnose early- biomarkers have great potential.
Look for aetiology.
Prevent rather than treat.
No role of low dose dopamine prevention and treatment .
Initiate RRT when indicated.
CP
Non-specific term that include disorders characterized by early onset and impaired movement and posture.
Non-progressive and may include perceptual problems, language deficits, and intellectual involvement.
Incidence
Most common physical disability of childhood.
Incidence has increased since the 60’s, maybe due to improved survival of VLBW infants.
Etiology
Variety of perinatal, prenatal, and postnatal factors contribute, either singly or multifactorily to CP.
Commonly thought to be due to birth asphyxia; now known to be due to existing prenatal brain abnormalities.
Premature delivery is the single most important determinant of CP.
In 24% of cases, no cause is found.
Approach and Management of Malabsorption Syndromes in children.pptxRaheelAhmed210939
Approach and Management of Malabsorption Syndromes in children
Dr. Raheel Ahmed MBBS, FCPS
Children Hospital, Chandka Medical College, Larkana
Etiology
Common causes
Coeliac Disease
Cystic Fibrosis
Post gastroenteritis syndrome
Bacterial overgrowth
Tuberculosis
HIV (immunodeficiency)
Giardiasis
Rare Causes
IBD;
Crohn’s disease (CD); Ulcerative colitis (UC)
Short Bowel Syndrome
CLD with cholestasis
Immunodeficiency syndromes
Intestinal lymphangiectasia
Abetalipoproteinemia
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Dr Marta Lomazzi, Executive Manager, World Federation of Public Health Associations
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CHAPTER 1 SEMESTER V - ROLE OF PEADIATRIC NURSE.pdfSachin Sharma
Pediatric nurses play a vital role in the health and well-being of children. Their responsibilities are wide-ranging, and their objectives can be categorized into several key areas:
1. Direct Patient Care:
Objective: Provide comprehensive and compassionate care to infants, children, and adolescents in various healthcare settings (hospitals, clinics, etc.).
This includes tasks like:
Monitoring vital signs and physical condition.
Administering medications and treatments.
Performing procedures as directed by doctors.
Assisting with daily living activities (bathing, feeding).
Providing emotional support and pain management.
2. Health Promotion and Education:
Objective: Promote healthy behaviors and educate children, families, and communities about preventive healthcare.
This includes tasks like:
Administering vaccinations.
Providing education on nutrition, hygiene, and development.
Offering breastfeeding and childbirth support.
Counseling families on safety and injury prevention.
3. Collaboration and Advocacy:
Objective: Collaborate effectively with doctors, social workers, therapists, and other healthcare professionals to ensure coordinated care for children.
Objective: Advocate for the rights and best interests of their patients, especially when children cannot speak for themselves.
This includes tasks like:
Communicating effectively with healthcare teams.
Identifying and addressing potential risks to child welfare.
Educating families about their child's condition and treatment options.
4. Professional Development and Research:
Objective: Stay up-to-date on the latest advancements in pediatric healthcare through continuing education and research.
Objective: Contribute to improving the quality of care for children by participating in research initiatives.
This includes tasks like:
Attending workshops and conferences on pediatric nursing.
Participating in clinical trials related to child health.
Implementing evidence-based practices into their daily routines.
By fulfilling these objectives, pediatric nurses play a crucial role in ensuring the optimal health and well-being of children throughout all stages of their development.
5. History
Maternal history of medication, drugs,
alcohol abuse, excessive smoking.
Prenatal history: infection
Family history of CHD, hereditary,
chromosomal
6. Symptoms
Difficult Feeding
Sweating during
feeding
Poor growth
Poor weight gain
Difficult
Breathing
Chest indrawing
Fast breathing
Frequent
respiratory
infections
Syncope
Exercise intolerence
Easy fatigability
Seizure
Focal neurological
lesion
8. Physical Examination
• Appearance : Pale, Dusky, Polycythemic, Syndromic
• Presence of Cyanosis, Clubbing,Edema
• Tachypnea, Respiratory distress
• Weight, Height for physical development
• Skeletal abnormalities: Polydactyly, others
• Pulse : Tachycardia, Arrhythmia, Volume, Palpability
• BP : All 4 limb BP in complex CHD
• JVP : - Elevated in Tricuspid Atresia, Eisenmenger
physiology
- Normal in TOF
• Abd: - Sidedness of liver/spleen + palpation of Apical
Impulse
to rule out Dextrocardia
- Hepatomegaly
9. Blood pressure
Methods sphingnonaometer (different cuffs)
-Palpation method
-Doppler method
Wide pulse pressure
-Aortic insufficiency
-A-V communication
-PDA
Low blood pressure(H.F, pericardial tamponade, cardiomyopathy).
Difference in BP between upper and lower extremities
Co-ao.
10. What is cyanosis?
Cyanosis is a bluish discoloration of skin
and mucus membrane that results when
the absolute level of reduced hemoglobin
in the capillary bed exceeds 3 g/dL.
11. Cyanosis: is it a cardiac cause or
lung cause
Hyperoxia test
◦ Neonates with cyanotic congenital heart
disease usually do not have significantly
raised arterial Pao2 during administration
of 100% oxygen.
13. Auscultation
a-First heart sound (A-V valves closure)
“Best heard at the Lt. lower sternal border or apex”
b-Second heart sound (semilunar valve closure)
“Best heard on the 1st and 2nd I.C.S” , normally there
is normal splitting of the 2nd heart sound ,
-Single Aortic atresia,Pulmonary Artesia
-Fixed splitting ASD,PS,Rt.B.B.B
c-Murmurs Systolic
Diastolic
Continous
14.
15. innocent or functional
murmurs
most common
heard in up to 30% of patients
◦ Asymptomatic
◦ Soft blowing
◦ Systolic
◦ Left sternal edge
Also
◦ Normal heart sound
◦ No thrill
◦ No radiation
Heard during
◦ Febrile illness or anemia
◦ Inc cardiac output
16. If we suspect C.H.D
Investigation
CBC---- polycythemia, anemia….etc
CXR----heart size and shape
ECG---HR,axis ,rythm
LVH,RVH,BVH,BBB.
Echocardiography
MRI
Cardiac catheterization
17. Prevalence
Congenital 8/1000
The incidence is higher in
◦ stillborns (3-4%),
◦ spontaneous abortuses
(10-25%),
◦ premature infants
Acyanotic: 68%
Cyanotic: 22%
Congenital Heart Disease
18. Etiology
Multifactorial inheritance pattern “mostly”
Chromosomal abnormality (5-10%).
-Trisomy 21 (50%) > A-V canal,VSD,ASD, others.
-Trisomy 18 (80%)> VSD,ASD,others.
-Trisomy 13 (40%)> VSD,ASD,PDA,others.
-Turner syndrome (xo)>Bicuspid aortic valve and co-ao
-others.
Maternal infections >Rubella:PDA,PS
Maternal diseases> PKU-VSD,ASD
DM:left septal hypertrophy
Drugs>fetal hydntoin syndrome- VSD
Valproate effect-co ao left heart hypoplasia
Fetal alcohol syndrome> VSD,ASD,CO-AO.
Advance maternal age.
Majority of cases of the congenital heart diseases are unknown
23. Ventricular Septal Defect
Subtype
◦ Small (<0.5cm2)
◦ Moderate (0.5-1 cm2)
◦ Large (>1cm2)
◦ Perimembraneous
◦ Muscular
◦ Supracristal (superior to
crista supraventricularis)
80%
24. Ventricular Septal Defect
Small VSD (<0.5cm2)
◦ Asymptomatic
◦ A loud, harsh, or blowing
holosystolic murmur at LSE
Large VSD(>1cm2)
◦ dyspnea, feeding
difficulties, poor growth,
profuse perspiration,
recurrent pulmonary
infections, and cardiac
failure in early infancy.
◦ Apical thrust, systolic thrill
at LSE
◦ Pansystolic murmur(less
25. Ventricular Septal Defect
Large VSD: The presence of right ventricular hypertrophy, olegeimic lung fields
(pulmonary hypertension or an associated pulmonic stenosis), gross
cardiomegaly with prominence of both ventricles, the left atrium.
Small VSDs, the chest radiograph is usually normal
26. Ventricular Septal defects:
management
30–50% of small defects close spontaneously, most
frequently during the 1st 2 yr of life. Vast majority will
close up to 4yaers.
Small muscular VSDs are more likely to close (up to
80%) than membranous VSDs are (up to 35%).
Medical management: treat heart failure if present.
Surgical repair prior to development of an irreversible
increase in pulmonary vascular resistance (usually prior
to the patient's second birthday), chronic volume
overload and heart failure.
27. Indications of surgery
Failure to controle CCF
Failure to thrive
Supracristal VSD
Associated Pulmonary stenosis
Development of AR
6-12 month child with rising P.HTN
>2years child PBF twice of Systemic
BF
28. Atrial Septal Defects
Subtypes
◦ Sinus venosus (high)
◦ Ostium secundum (mid
portion) most common
◦ Ostium primum (low )
29. Atrial Septal Defects: secundum
Most common form of ASD
In large defects, a
considerable shunt of
oxygenated blood flows from
the left to the right atrium.
Mostly asymptomatic
The 2nd heart sound is
characteristically widely split
and fixed.
Soft systolic murmur at
upper LSE
Secundum
30. Atrial Septal Defects:primum
Situated in the lower portion of the
atrial septum
overlies the mitral and tricuspid
valves.
In most instances, a cleft in the
anterior leaflet of the mitral valve
is also noted.
Combination of a left-to-right shunt
across the atrial defect and mitral
insufficiency
Apical pansystolic murmur(AVr)
The 2nd heart sound is split and
fixed
31. Atrial Septal Defect
X-ray
Enlargement of the
right ventricle
Enlargement of
atrium
Large pulmonary
artery
increased pulmonary
vascularity
ECG :supeior axis in
primum, RVH, partial
RBBB
32. Atrial Septal Defects
Secundum ASDs are well tolerated during
childhood.
Antibiotic prophylaxis for isolated secundum ASDs
is not recommended.(except if MR present)
Surgery or transcatheter device closure is advised
for all symptomatic patients and also for
asymptomatic patients with a shunt ratio of at least
2:1. or those with RVH
Intervention : after 1 year before school entery.
Ostium primum defects are approached surgically
33. Prognosis
Small to moderate-sized ASDs detected in
term infants may grow smaller or close
spontaneously
Pulmonary hypertension, atrial dysrhythmias,
tricuspid or mitral insufficiency, and heart
failure are late manifestations
The results after surgical or device closure in
children with moderate-size to large shunts
are excellent
34. Patent Ductus Arteriosus
Connects pulmonary
artery and descending
aorta.
Normally closed shortly
after birth.
Common in VLBW with
pulmonary diseases and
in congenital rubella.
F:M 2:1
Spontaneously close in
premature
PDA persisting in term
beyond 1st few weeks will
rarely close
spontaneously
35. Patent Ductus Arteriosus
Small defect:
◦ no symptoms.
◦ Pulses are normal
Large defect:
◦ Breathlessness while
feeding
◦ Slow growth
◦ Repeated Lower RTI
◦ Wide pulse pressure
◦ Enlarged heart
◦ Apical heaving
◦ Thrill in L second IS
◦ Continuous murmur
(machinary)in 2nd LICS
◦ X-ray: prominent pulmonary
artery with increased
vascular markings, Left heart
36. Patent Ductus Arteriosus
Medical Management
◦ Medical closure in preterm tried with
indomethacin (0.2mg/kg/dose iv for 3 doses 8-
12hr apart) or brufen (ibuprofen).
◦ Start therapy after echo only.
Surgical Management
◦ Ligation and division of ductus is treatment
of choice
◦ In asymptomic patiants before 1year
◦ P.HTN is not contraindication.
37. Coarctation of the Aorta
In boys more than in girls
Almost always juxtaductal in
position.
Weak femoral pulses, Radio
femoral delay, hypotention in
lower parts of body.
High BP in upper body part in
the arm 20mmhg more than
leg, headache, vertigo,
epistaxis.
Murmur at left interscapular
area in back.
Treatment
Digoxin & diuretic PGE1
38. Pulmonary Stenosis
Narrowing in pulmonary valve
RT side heart failure
Ejection Systolic murmur at Left 2nd
ICS radiate to back, S2 widely split
ECG …Echo RT side hypertrophy
Treatment
Balloon valvuloplasty
Surgical repair
39. Aortic stenosis
Increased pressure in the LF side of the
heart (LV hypertrophy)
Easy fatigability, exertional chest pain,
syncope
Ejection systolic murmur at right 2nd ICS
radiate to neck, high HR.
Treatment..
- Beta-blocker or ca channel blocker to
decreased hypertrophy
- Balloon valvoplasty
- Surgical repair
47. Clinical Presentation
Clinical presentation is directly related to the
degree of pulmonary stenosis.
Severe stenosis results in immediate cyanosis
following birth.
Mild stenosis will not present until later.
◦ Growth is retarded – insufficient oxygen and nutrients
◦ SOB on exertion → rest
◦ Digital clubbing
◦ Paroxysmal hypercynotic attacks (tet spells)
◦ Left parasternal heave
◦ Systolic thrill (50%) at left PSE 3 and 4 ICS
◦ S2 is often single
◦ Harsh ejection systolic murmur at left PSE 3rd ICS
48. “Tet Spell”
“Tet spells” at 2-3yo, child
becomes cyanotic,
restless, gasping
respiration,may experience
syncope
More frequently in morning
upon awakening or after
vigorous cry.
Children assume squatting
position
During spell, dec in
intensity or disappearance
of systolic murmur
49. Exams and Tests
CBC
- hematocrit
ECG
-RVH, RAD
CXR
-boot shaped
heart, right sided
aortic arch
Echocardiogram
-VSD, PS, RVH
50. Tetralogy of Fallot
Apex is lifted, concavity in pumonary segment, oligemic lung field.
Boot shaped Heart
51. Treatment
Severe TOF with
worsening cynosis in
early neonatal period
require prostaglandins E
infusion; and surgery
(modified Blalock-
taussing shunt)
Corrective surgery
carried out from 3
months to 2year
depending upon
expertise availablity
Blalock-
Taussig shunt
53. Treatment of the cyanotic spells
Try to calm the patient .
Knee chest position,
O2
Propranolol(0.1-0.2mg/kg slow IV).
Morphine s.c
NaHCO3 iv
Increase IV fluid.
Prevented by oral Propranolol (1mg/kg
every 4hr)
54.
55. Transposition Of great
arteries
Most serious cynotic lesion,
Seen in newborn period (5%)
More common in infants of diabetic
mothers and in males.
Survive when ASD, PDA, or VSD
56. TGA with intact ventricular septum
◦ Cynosis and tachypnea within 1st hours of life.
◦ Single S2, no murmur
◦ PGE1 (o.o5-o.2ug/kg/min infusion)is immediately
started to maintain patency of DA.
◦ CCF is less common
TGA with VSD
◦ Mild cynosis recognised 1st month of life.
◦ Murmur is pansystolic
◦ Many Neonates are large 4kg at birth then
growth retardation occurs.
◦ They need anti-CCF measures
Clinical Features
58. Management
Corrective surgery by
age of 2 weeks
Procedures:
◦ Rashkind or ballon atrial
septoplasty
◦ Mastured procedure
◦ Total repair: Arterial swich
technique.
60. Clinical Features
Progressive Cynosis
Poor feeding
Tachypnea over the first 2 weeks
Holosystolic murmur due to VSD
Single S2
Left axis Deviation and left VH on ECG
characteristics.
Normal heart size
65. Treatment
Medical management:
◦ Anti-CCF measure
Surgical Repair:
◦ VSD closure and
placement of conduit
between right ventricle
and Pulmonary artries.
66. Total Pulmonary venous
return
2%
Pulmonary vein return to the right
atrium or the superior vena cava
instead of the left atrium
Atrial level communication is
required.
Without obstruction: Hyperactive
RV impulse with wide split S2
Systolic ejection murmur at Left
USB
Mid diastolic murmur at left LSB
With obstruction: signs of right
sided heart failure, no murmur, no
change in S2
* Treatment
Give PGE, cath, and surgical
treatment
67. Hypoplastic left Heart
Syndrome
Most common cause of death
from cardiac side in 1st month
Failure of development of
MV,Av,or arch.
Infants may appear healthy at
birth, but signs of HLHS soon
become apparent after the
ductus arteriosus closes. :
Cyanosis minimal, weak pulses,
Cold extremities, greyish
colour(low cardiac output)
S2 single and loud no heart
murmur
Right ventricle Hypertrophy
* Treatment
68. Treatment of C.H.D
This is depend on the type of the C.H.D.
No treatment (observation+reassurance)
Medical treatment(antifailure,antiarythmaic..etc).
Surgical treatment (palliative or curative).
Cardiac transplant or lung heart transplant.
69. 1-General measures
Special positions. (semisiting ,knee chest position (
O2 (most patients need O2 and other need little O2).
IVF(again depend on type of CHD ).
Salt restriction.
Exercise restriction.
Rx of anemia.
Rx of polycythemia. PCV>65
Avoidances of dehydration mainly polycythemic patients.
Avoidances of high altitude.
Avoidance of contraceptive “thrombosis+hypertension”.
Correction of acidosis.
Correction of electrolyte disturbances .
Careful monitoring during surgery.
71. Acute rheumatic fever (ARF)
in response to infection with group A
B-haemolytic streptococcus
aged 5–15yrs
incidence is highest in those from
socially and economically
disadvantaged areas
72. Clinical features
• There is a latent
period of 2–6wks
between onset of
symptoms and
previous streptococcal
infection (e.g.
pharyngitis).
Symptoms are non-
specific.
The grouping together
of clinical features
makes the diagnosis
more likely (Jones
criteria)
73.
74.
75. Management
In the acute phase treatment will include: • bed rest;
• anti-infl ammatory drugs (e.g. aspirin);
• corticosteroids (2–3wks);
• diuretics/ACE inhibitors if in heart failure;
• antibiotics (e.g. penicillin V for 10 days).
Sedatives may be helpful early in the course of chorea;
◦ phenobarbital (16-32 mg every 6-8 hr PO) drug of
choice.
◦ If ineffective, then haloperidol (0.01-0.03 mg/kg/24hr divided
bid PO) or
◦ chlorpromazine (0.5 mg/kg every 4-6 hr PO) should be
initiated
Long-term therapy
◦ prevention of further attacks of acute rheumatic
◦ development of chronic rheumatic heart disease.
78. Infective endocarditis
Children at risk are those
◦ with turbulent blood flow through the heart or
◦ where prosthetic material has been inserted
following surgery: e.g.
• PDA or VSD;
• coarctation of aorta;
• previous rheumatic fever
special risk groups have emerged,
including
intravenous drug users;
patients taking immunosuppressant medications;
79. Most common pathogens
• Streptococcus viridans
(50% cases): often after
dental procedures.
• Staphylococcus aureus:
often related to central
venous catheters.
• Group D streptococcus
(enterococcus): often
after lower GI surgery
80.
81.
82.
83.
84.
85. Treatment
Antibiotic therapy:.
Empirical therapy: vancomycin plus gentamicin
◦ in patients without a prosthetic valve
◦ when there is a high risk of S. aureus, enterococcus, or
viridans streptococci
◦ 4-6 wk of treatment is usually recommended.
Fubgal infection: amphotericin B and 5-fluorocytosine
signs of heart failure
◦ diuretics,
◦ afterload reducing agents,
◦ digitalis, in some cases
Bed rest is recommended and heart failure should be
treated.
Surgery
86.
87.
88. Surgery indications
◦ severe aortic,
◦ mitral or prosthetic valve involvement
with intractable heart failure
◦ failure to sterilize the blood despite
adequate antibiotic levels in 7-10 days in
the absence of extracardiac infection,
◦ myocardial abscess,
◦ recurrent emboli,
◦ Increasing size of vegetations while
receiving therapy
89.
90. Prognosis
mortality may be as high as 20– 25%
complications (50–60%) include
◦ heart failure.
◦ Myocardial abscesses and toxic myocarditis
◦ arrhythmias
◦ Systemic emboli from left-sided vegetations
(>10-15 mm) may result in
brain abscess
stroke.
Fungal endocarditis is difficult to manage
and has a poorer prognosis