Congenital Heart Diseases in Children.pptxAshik Alvee
This document provides an overview of congenital heart disease in children. It discusses the epidemiology, risk factors, classification, and approach to diagnosis and management. Common congenital heart defects such as ventricular septal defect, atrial septal defect, patent ductus arteriosus, and tetralogy of Fallot are described in detail, including their typical presentation, physical exam findings, investigations, and treatment. The document is intended to educate medical students and trainees about pediatric congenital heart disease.
The document discusses cardiovascular disorders in children, including congenital heart diseases like ventricular septal defect (VSD). It provides details on the anatomy and physiology of the cardiovascular system in children, changes after birth, and diagnostic techniques for congenital heart diseases such as echocardiography and catheterization. VSD is described as a hole in the septum between the right and left ventricles allowing left-to-right shunting, which can cause congestive heart failure or pulmonary hypertension.
Congenital heart disease is the most common birth defect, affecting 0.8% of newborns. The document outlines the prevalence, etiology, evaluation, specific lesions, pathophysiology, clinical manifestations, diagnosis, management, and prognosis of various congenital heart defects. Key defects discussed include atrial septal defect, ventricular septal defect, patent ductus arteriosus, coarctation of the aorta, tetralogy of Fallot, and transposition of the great arteries. Physical exam findings, diagnostic tools, treatment options, and complications are described for each condition.
The document discusses atrial septal defect (ASD), including its embryology, types, pathophysiology, natural history, evaluation, and management. ASD is a congenital heart defect characterized by an opening in the interatrial septum that causes blood to flow from the left atrium to the right atrium. The size and location of the defect determines symptoms and treatment, which may include medical management, interventional closure, or surgical repair.
The document provides information on congenital heart defects, including their causes, types, signs and symptoms, diagnosis, and treatment. It discusses several specific defects in detail, including aortic stenosis, coarctation of the aorta, pulmonary stenosis, and patent ductus arteriosus. The key points are:
1. Congenital heart defects can involve the heart's chambers, valves, or vessels and have various causes including genetic syndromes.
2. Specific defects like aortic stenosis and pulmonary stenosis can cause obstruction to blood flow while others like patent ductus arteriosus allow extra blood flow to the lungs.
3. Symptoms depend on the severity of the defect but may include heart failure,
This document presents information from a presentation on acyanotic congenital heart disease. It begins with objectives that cover fetal circulation, defining CHD and risk factors, classifying CHD, explaining acyanotic heart disease and specific defects. It then provides detailed information on ventricular septal defect, atrial septal defect, patent ductus arteriosus, aortic stenosis, pulmonary stenosis, and coarctation of aorta. For each defect, it discusses clinical manifestation, diagnostic criteria, management, and complications. It also includes summaries of two research papers on neurodevelopmental outcomes after surgery for acyanotic CHD and a comparison of renal function between cyanotic and acyanotic CHD in children.
Congenital Cardiac Disease types and pathophysiology .pptdoctorunreserved
This document discusses congenital heart disease (CHD) and provides details on various types of defects including left-right and right-left shunts. It covers the prevalence, etiology, clinical features, diagnosis, and treatment of atrial septal defects, ventricular septal defects, patent ductus arteriosus, atrioventricular septal defects, and other conditions. Preoperative evaluation and management of patients with CHD is also summarized.
This document provides information on congenital heart disease (CHD), including epidemiology, classification, diagnosis, and treatment. It discusses several specific types of CHD such as atrial septal defect (ASD), ventricular septal defect (VSD), patent ductus arteriosus (PDA), coarctation of the aorta, tetralogy of Fallot, transposition of the great arteries, tricuspid atresia, truncus arteriosus, and hypoplastic left heart syndrome. It describes the clinical presentation, investigations, and management approaches for each condition.
Congenital Heart Diseases in Children.pptxAshik Alvee
This document provides an overview of congenital heart disease in children. It discusses the epidemiology, risk factors, classification, and approach to diagnosis and management. Common congenital heart defects such as ventricular septal defect, atrial septal defect, patent ductus arteriosus, and tetralogy of Fallot are described in detail, including their typical presentation, physical exam findings, investigations, and treatment. The document is intended to educate medical students and trainees about pediatric congenital heart disease.
The document discusses cardiovascular disorders in children, including congenital heart diseases like ventricular septal defect (VSD). It provides details on the anatomy and physiology of the cardiovascular system in children, changes after birth, and diagnostic techniques for congenital heart diseases such as echocardiography and catheterization. VSD is described as a hole in the septum between the right and left ventricles allowing left-to-right shunting, which can cause congestive heart failure or pulmonary hypertension.
Congenital heart disease is the most common birth defect, affecting 0.8% of newborns. The document outlines the prevalence, etiology, evaluation, specific lesions, pathophysiology, clinical manifestations, diagnosis, management, and prognosis of various congenital heart defects. Key defects discussed include atrial septal defect, ventricular septal defect, patent ductus arteriosus, coarctation of the aorta, tetralogy of Fallot, and transposition of the great arteries. Physical exam findings, diagnostic tools, treatment options, and complications are described for each condition.
The document discusses atrial septal defect (ASD), including its embryology, types, pathophysiology, natural history, evaluation, and management. ASD is a congenital heart defect characterized by an opening in the interatrial septum that causes blood to flow from the left atrium to the right atrium. The size and location of the defect determines symptoms and treatment, which may include medical management, interventional closure, or surgical repair.
The document provides information on congenital heart defects, including their causes, types, signs and symptoms, diagnosis, and treatment. It discusses several specific defects in detail, including aortic stenosis, coarctation of the aorta, pulmonary stenosis, and patent ductus arteriosus. The key points are:
1. Congenital heart defects can involve the heart's chambers, valves, or vessels and have various causes including genetic syndromes.
2. Specific defects like aortic stenosis and pulmonary stenosis can cause obstruction to blood flow while others like patent ductus arteriosus allow extra blood flow to the lungs.
3. Symptoms depend on the severity of the defect but may include heart failure,
This document presents information from a presentation on acyanotic congenital heart disease. It begins with objectives that cover fetal circulation, defining CHD and risk factors, classifying CHD, explaining acyanotic heart disease and specific defects. It then provides detailed information on ventricular septal defect, atrial septal defect, patent ductus arteriosus, aortic stenosis, pulmonary stenosis, and coarctation of aorta. For each defect, it discusses clinical manifestation, diagnostic criteria, management, and complications. It also includes summaries of two research papers on neurodevelopmental outcomes after surgery for acyanotic CHD and a comparison of renal function between cyanotic and acyanotic CHD in children.
Congenital Cardiac Disease types and pathophysiology .pptdoctorunreserved
This document discusses congenital heart disease (CHD) and provides details on various types of defects including left-right and right-left shunts. It covers the prevalence, etiology, clinical features, diagnosis, and treatment of atrial septal defects, ventricular septal defects, patent ductus arteriosus, atrioventricular septal defects, and other conditions. Preoperative evaluation and management of patients with CHD is also summarized.
This document provides information on congenital heart disease (CHD), including epidemiology, classification, diagnosis, and treatment. It discusses several specific types of CHD such as atrial septal defect (ASD), ventricular septal defect (VSD), patent ductus arteriosus (PDA), coarctation of the aorta, tetralogy of Fallot, transposition of the great arteries, tricuspid atresia, truncus arteriosus, and hypoplastic left heart syndrome. It describes the clinical presentation, investigations, and management approaches for each condition.
The document discusses congenital heart diseases, which occur in approximately 1% of live births. It describes several types of congenital heart defects including atrial septal defect (ASD), ventricular septal defect (VSD), atrioventricular canal defect, and patent ductus arteriosus - all of which involve increased pulmonary blood flow. It also discusses obstructive defects like aortic stenosis and pulmonary stenosis. The document provides details on the pathophysiology, clinical manifestations, diagnosis, and treatment of these various congenital heart conditions.
The document discusses several types of congenital heart diseases that can present in adults, including atrial septal defects, ventricular septal defects, patent ductus arteriosus, coarctation of the aorta, tetralogy of Fallot, Ebstein's anomaly, and transposition of the great arteries. It provides details on the anatomy, clinical presentation, diagnostic workup, and treatment options for each condition.
Mr. Surendra Sharma discusses several congenital heart diseases including their definitions, causes, pathophysiology, clinical manifestations, diagnostic evaluations, and management. He provides details on ventricular septal defect (VSD), atrial septal defect (ASD), patent ductus arteriosus (PDA), tetralogy of Fallot, transposition of the great arteries, coarctation of the aorta, and pulmonary stenosis. The document contains in-depth information on the incidence, characteristics, and treatment of these common congenital heart conditions.
Mr. Jayesh Soni discusses congenital heart defects in children. He notes that approximately 8-12 children per 1000 are born with congenital heart defects. The document then describes the fetal circulation patterns and their remnants post-birth. It provides classifications for acyanotic and cyanotic heart defects and discusses specifics such as atrial septal defects and ventricular septal defects in more detail. For VSDs, the document outlines signs, symptoms, diagnostic evaluations, and management approaches including indications for surgery. Complications are also listed.
Mr. Jayesh Soni discusses congenital heart defects in children. He notes that approximately 8-12 children per 1000 are born with congenital heart defects. The document then describes the fetal circulation patterns and how they normally close after birth. It provides classifications for acyanotic and cyanotic heart defects and discusses specifics such as atrial septal defects (ASD), ventricular septal defects (VSD), signs/symptoms, diagnostic evaluations, and management including medical, interventional, and surgical options. Complications are also outlined.
The document discusses various congenital heart defects including their definition, etiology, classification as acyanotic or cyanotic, signs and symptoms, diagnosis, and treatment. Specific defects covered include atrial septal defects, ventricular septal defects, patent ductus arteriosus, and atrioventricular septal defects. The treatment sections provide guidelines for managing each defect medically or surgically depending on its size and severity.
Ebstein's anomaly is a rare heart defect where the tricuspid valve, which separates the right atrium and ventricle, is abnormally located low in the right ventricle. This causes the right atrium to enlarge and the right ventricle to have two sections - an upper atrialized section and a lower functional section. Symptoms range from none in mild cases to cyanosis, heart failure and arrhythmias in severe cases. Diagnosis involves echocardiogram, ECG and chest x-ray. Treatment options include medications, surgery to repair or replace the valve, and management of complications like heart failure. Prognosis depends on severity of symptoms, with earlier presentation indicating poorer prognosis.
This document provides an overview of congenital heart disease (CHD) and anesthesia considerations for CHD. It begins with definitions and classifications of CHD, including acyanotic and cyanotic defects. Specific conditions discussed include atrial septal defect, ventricular septal defect, patent ductus arteriosus, pulmonary stenosis, aortic stenosis, and coarctation of the aorta. For each condition, the document outlines etiology, pathophysiology, clinical presentation, diagnosis, and treatment considerations.
Congenital heart disease (CHD) refers to problems in heart structure present at birth. It affects 3-5% of births and causes up to 33% of neonatal deaths. Symptoms depend on the specific defect but may include cyanosis, difficulty breathing, and failure to thrive. Diagnosis involves a physical exam, ECG, echocardiogram, and other tests. Treatment ranges from surgery to correct defects like ventricular septal defects, patent ductus arteriosus, and tetralogy of Fallot to multi-stage procedures for single ventricle conditions like hypoplastic left heart syndrome. Nursing care focuses on nutritional support, infection prevention, reducing heart workload, monitoring for heart failure, and educating families
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
This document provides an overview of congenital heart disease, including prevalence, circulatory adjustments at birth, hemodynamic classifications, and descriptions of specific conditions like atrial septal defect (ASD) and ventricular septal defect (VSD). It notes that congenital heart defects affect 6-8 per 1000 live births and can range widely in severity. Diagnosis typically occurs by 1 week or 1 month of age. After birth, clamping of the umbilical cord and expansion of the lungs cause pressure changes and closure of passages between circulations. Conditions are classified as acyanotic or cyanotic depending on oxygen saturation levels. ASD and VSD are both described in detail including typical clinical features, imaging findings, and management
This document provides an outline and overview of congenital heart disease. It defines CHD and discusses incidence rates. It covers the development of the heart, fetal circulation, classification of CHD types, etiology, associated syndromes, signs to suspect CHD, diagnostic steps, management approaches, and details several specific types of CHDs like PDA, VSD, ASD, pulmonary stenosis, bicuspid aortic valve, and coarctation of the aorta.
This document summarizes several types of congenital heart disease and how they are impacted by pregnancy. It discusses defects that cause volume overload like atrial and ventricular septal defects. It also discusses defects involving obstruction like pulmonary stenosis. Complications in pregnancy can include increased strain on the heart and potential need for termination or surgical correction before pregnancy. Management may involve antibiotics and monitoring for complications like heart failure.
This document discusses cardiac disorders in pediatrics, including congenital and acquired disorders. The two major groups are congenital disorders present at birth, and acquired disorders that develop later in life such as bacterial endocarditis. Common congenital defects include atrial and ventricular septal defects, tetralogy of Fallot, transposition of the great arteries, and hypoplastic left heart syndrome. Management involves medications, oxygen management, nutrition, and surgery depending on the specific defects. Post-operative care focuses on pain management, cardiac monitoring, and family support.
This document discusses several congenital heart diseases including their incidence, etiology, pathophysiology, clinical manifestations, diagnosis, and management. It provides details on ventricular septal defect (VSD), atrial septal defect (ASD), patent ductus arteriosus (PDA), tetralogy of Fallot, transposition of the great arteries, coarctation of the aorta, and pulmonary stenosis. The overall incidence of congenital heart diseases is about 8-10 per 1000 live births with VSD being the most common type, accounting for 25-30% of cases. Etiologies may include hereditary factors, infections, chromosomal or genetic abnormalities. Clinical exams, imaging tests, and cardiac catheterization
This document discusses congenital heart disease, specifically atrial septal defect (ASD), ventricular septal defect (VSD), and patent ductus arteriosus (PDA). It defines each condition, describes their signs and symptoms, risk factors, pathophysiology, diagnosis, and management including both medical and surgical treatment options. The prognosis for each condition with and without treatment is addressed. The document provides a detailed yet concise overview of these three common types of acyanotic heart disease.
This document discusses congenital heart disease, specifically atrial septal defects and ventricular septal defects. It defines what each condition is, describes the causes and types, and outlines the pathophysiology, clinical features, diagnosis, and management. Atrial septal defects are abnormalities where blood passes from the left atrium to the right atrium, while ventricular septal defects allow blood to pass from the left ventricle to the right ventricle through a hole in the ventricular septum. Treatment may involve medication, surgery to repair the defects, or in some small cases, simply monitoring for spontaneous closure of the hole.
The document discusses several congenital heart diseases including ventricular septal defects (VSD), atrial septal defects (ASD), patent ductus arteriosus (PDA), pulmonary stenosis, aortic stenosis, and coarctation of the aorta. It describes the pathophysiology, clinical presentation, investigations, and management of each condition. Cyanotic heart diseases are defined as those involving a right-to-left or left-to-right shunt leading to low oxygen saturation. The document provides classification, epidemiology, etiology and detailed information about specific lesions causing cyanosis.
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.
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Semelhante a Approach to Pediatric Cardiovascular diseases.pptx
The document discusses congenital heart diseases, which occur in approximately 1% of live births. It describes several types of congenital heart defects including atrial septal defect (ASD), ventricular septal defect (VSD), atrioventricular canal defect, and patent ductus arteriosus - all of which involve increased pulmonary blood flow. It also discusses obstructive defects like aortic stenosis and pulmonary stenosis. The document provides details on the pathophysiology, clinical manifestations, diagnosis, and treatment of these various congenital heart conditions.
The document discusses several types of congenital heart diseases that can present in adults, including atrial septal defects, ventricular septal defects, patent ductus arteriosus, coarctation of the aorta, tetralogy of Fallot, Ebstein's anomaly, and transposition of the great arteries. It provides details on the anatomy, clinical presentation, diagnostic workup, and treatment options for each condition.
Mr. Surendra Sharma discusses several congenital heart diseases including their definitions, causes, pathophysiology, clinical manifestations, diagnostic evaluations, and management. He provides details on ventricular septal defect (VSD), atrial septal defect (ASD), patent ductus arteriosus (PDA), tetralogy of Fallot, transposition of the great arteries, coarctation of the aorta, and pulmonary stenosis. The document contains in-depth information on the incidence, characteristics, and treatment of these common congenital heart conditions.
Mr. Jayesh Soni discusses congenital heart defects in children. He notes that approximately 8-12 children per 1000 are born with congenital heart defects. The document then describes the fetal circulation patterns and their remnants post-birth. It provides classifications for acyanotic and cyanotic heart defects and discusses specifics such as atrial septal defects and ventricular septal defects in more detail. For VSDs, the document outlines signs, symptoms, diagnostic evaluations, and management approaches including indications for surgery. Complications are also listed.
Mr. Jayesh Soni discusses congenital heart defects in children. He notes that approximately 8-12 children per 1000 are born with congenital heart defects. The document then describes the fetal circulation patterns and how they normally close after birth. It provides classifications for acyanotic and cyanotic heart defects and discusses specifics such as atrial septal defects (ASD), ventricular septal defects (VSD), signs/symptoms, diagnostic evaluations, and management including medical, interventional, and surgical options. Complications are also outlined.
The document discusses various congenital heart defects including their definition, etiology, classification as acyanotic or cyanotic, signs and symptoms, diagnosis, and treatment. Specific defects covered include atrial septal defects, ventricular septal defects, patent ductus arteriosus, and atrioventricular septal defects. The treatment sections provide guidelines for managing each defect medically or surgically depending on its size and severity.
Ebstein's anomaly is a rare heart defect where the tricuspid valve, which separates the right atrium and ventricle, is abnormally located low in the right ventricle. This causes the right atrium to enlarge and the right ventricle to have two sections - an upper atrialized section and a lower functional section. Symptoms range from none in mild cases to cyanosis, heart failure and arrhythmias in severe cases. Diagnosis involves echocardiogram, ECG and chest x-ray. Treatment options include medications, surgery to repair or replace the valve, and management of complications like heart failure. Prognosis depends on severity of symptoms, with earlier presentation indicating poorer prognosis.
This document provides an overview of congenital heart disease (CHD) and anesthesia considerations for CHD. It begins with definitions and classifications of CHD, including acyanotic and cyanotic defects. Specific conditions discussed include atrial septal defect, ventricular septal defect, patent ductus arteriosus, pulmonary stenosis, aortic stenosis, and coarctation of the aorta. For each condition, the document outlines etiology, pathophysiology, clinical presentation, diagnosis, and treatment considerations.
Congenital heart disease (CHD) refers to problems in heart structure present at birth. It affects 3-5% of births and causes up to 33% of neonatal deaths. Symptoms depend on the specific defect but may include cyanosis, difficulty breathing, and failure to thrive. Diagnosis involves a physical exam, ECG, echocardiogram, and other tests. Treatment ranges from surgery to correct defects like ventricular septal defects, patent ductus arteriosus, and tetralogy of Fallot to multi-stage procedures for single ventricle conditions like hypoplastic left heart syndrome. Nursing care focuses on nutritional support, infection prevention, reducing heart workload, monitoring for heart failure, and educating families
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
This document provides an overview of congenital heart disease, including prevalence, circulatory adjustments at birth, hemodynamic classifications, and descriptions of specific conditions like atrial septal defect (ASD) and ventricular septal defect (VSD). It notes that congenital heart defects affect 6-8 per 1000 live births and can range widely in severity. Diagnosis typically occurs by 1 week or 1 month of age. After birth, clamping of the umbilical cord and expansion of the lungs cause pressure changes and closure of passages between circulations. Conditions are classified as acyanotic or cyanotic depending on oxygen saturation levels. ASD and VSD are both described in detail including typical clinical features, imaging findings, and management
This document provides an outline and overview of congenital heart disease. It defines CHD and discusses incidence rates. It covers the development of the heart, fetal circulation, classification of CHD types, etiology, associated syndromes, signs to suspect CHD, diagnostic steps, management approaches, and details several specific types of CHDs like PDA, VSD, ASD, pulmonary stenosis, bicuspid aortic valve, and coarctation of the aorta.
This document summarizes several types of congenital heart disease and how they are impacted by pregnancy. It discusses defects that cause volume overload like atrial and ventricular septal defects. It also discusses defects involving obstruction like pulmonary stenosis. Complications in pregnancy can include increased strain on the heart and potential need for termination or surgical correction before pregnancy. Management may involve antibiotics and monitoring for complications like heart failure.
This document discusses cardiac disorders in pediatrics, including congenital and acquired disorders. The two major groups are congenital disorders present at birth, and acquired disorders that develop later in life such as bacterial endocarditis. Common congenital defects include atrial and ventricular septal defects, tetralogy of Fallot, transposition of the great arteries, and hypoplastic left heart syndrome. Management involves medications, oxygen management, nutrition, and surgery depending on the specific defects. Post-operative care focuses on pain management, cardiac monitoring, and family support.
This document discusses several congenital heart diseases including their incidence, etiology, pathophysiology, clinical manifestations, diagnosis, and management. It provides details on ventricular septal defect (VSD), atrial septal defect (ASD), patent ductus arteriosus (PDA), tetralogy of Fallot, transposition of the great arteries, coarctation of the aorta, and pulmonary stenosis. The overall incidence of congenital heart diseases is about 8-10 per 1000 live births with VSD being the most common type, accounting for 25-30% of cases. Etiologies may include hereditary factors, infections, chromosomal or genetic abnormalities. Clinical exams, imaging tests, and cardiac catheterization
This document discusses congenital heart disease, specifically atrial septal defect (ASD), ventricular septal defect (VSD), and patent ductus arteriosus (PDA). It defines each condition, describes their signs and symptoms, risk factors, pathophysiology, diagnosis, and management including both medical and surgical treatment options. The prognosis for each condition with and without treatment is addressed. The document provides a detailed yet concise overview of these three common types of acyanotic heart disease.
This document discusses congenital heart disease, specifically atrial septal defects and ventricular septal defects. It defines what each condition is, describes the causes and types, and outlines the pathophysiology, clinical features, diagnosis, and management. Atrial septal defects are abnormalities where blood passes from the left atrium to the right atrium, while ventricular septal defects allow blood to pass from the left ventricle to the right ventricle through a hole in the ventricular septum. Treatment may involve medication, surgery to repair the defects, or in some small cases, simply monitoring for spontaneous closure of the hole.
The document discusses several congenital heart diseases including ventricular septal defects (VSD), atrial septal defects (ASD), patent ductus arteriosus (PDA), pulmonary stenosis, aortic stenosis, and coarctation of the aorta. It describes the pathophysiology, clinical presentation, investigations, and management of each condition. Cyanotic heart diseases are defined as those involving a right-to-left or left-to-right shunt leading to low oxygen saturation. The document provides classification, epidemiology, etiology and detailed information about specific lesions causing cyanosis.
Semelhante a Approach to Pediatric Cardiovascular diseases.pptx (20)
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.
This document provides an overview of diseases of the blood, including various types of anemias and disorders of hemostasis. It discusses topics like hematopoiesis, iron deficiency anemia, sickle cell disease, thalassemia, immune thrombocytopenic purpura, and hemophilia. For each condition, it outlines causes, clinical features, laboratory findings, diagnosis, and treatment approaches. The document thus serves as a comprehensive reference for pediatricians on blood disorders commonly encountered in clinical practice.
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
This document discusses the approach to assessing and treating upper respiratory tract infections (URTIs) in children. It begins by introducing URTIs as a common problem, then describes the anatomy of the respiratory tract. It outlines symptoms of URTIs and the approach to taking a history and examining the patient. It discusses common causes of URTIs like the common cold, allergic rhinitis, sinusitis, pharyngitis, and more severe conditions like croup, epiglottitis and diphtheria. For each condition, it covers symptoms, diagnosis, treatment and prevention.
This document summarizes vaccination programs in Pakistan, including the Expanded Program on Immunization (EPI) and non-EPI vaccines. It outlines the objectives of EPI to increase immunization coverage for children under 5 and reduce incidence of targeted diseases. The current EPI schedule in Pakistan includes vaccines for BCG, hepatitis B, oral polio, rotavirus, pneumococcal, pentavalent, IPV, typhoid, measles-rubella, and tetanus toxoid for women. Non-EPI vaccines discussed include those for COVID-19, influenza, mumps, varicella, hepatitis A, HPV, meningococcal, and dengue. The document stresses the importance of cold
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
This particular slides consist of- what is hypotension,what are it's causes and it's effect on body, risk factors, symptoms,complications, diagnosis and role of physiotherapy in it.
This slide is very helpful for physiotherapy students and also for other medical and healthcare students.
Here is the summary of hypotension:
Hypotension, or low blood pressure, is when the pressure of blood circulating in the body is lower than normal or expected. It's only a problem if it negatively impacts the body and causes symptoms. Normal blood pressure is usually between 90/60 mmHg and 120/80 mmHg, but pressures below 90/60 are generally considered hypotensive.
End-tidal carbon dioxide (ETCO2) is the level of carbon dioxide that is released at the end of an exhaled breath. ETCO2 levels reflect the adequacy with which carbon dioxide (CO2) is carried in the blood back to the lungs and exhaled.
Non-invasive methods for ETCO2 measurement include capnometry and capnography. Capnometry provides a numerical value for ETCO2. In contrast, capnography delivers a more comprehensive measurement that is displayed in both graphical (waveform) and numerical form.
Sidestream devices can monitor both intubated and non-intubated patients, while mainstream devices are most often limited to intubated patients.
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Hypertension and it's role of physiotherapy in it.Vishal kr Thakur
This particular slides consist of- what is hypertension,what are it's causes and it's effect on body, risk factors, symptoms,complications, diagnosis and role of physiotherapy in it.
This slide is very helpful for physiotherapy students and also for other medical and healthcare students.
Here is summary of hypertension -
Hypertension, also known as high blood pressure, is a serious medical condition that occurs when blood pressure in the body's arteries is consistently too high. Blood pressure is the force of blood pushing against the walls of blood vessels as the heart pumps it. Hypertension can increase the risk of heart disease, brain disease, kidney disease, and premature death.
The facial nerve, also known as cranial nerve VII, is one of the 12 cranial nerves originating from the brain. It's a mixed nerve, meaning it contains both sensory and motor fibres, and it plays a crucial role in controlling various facial muscles, as well as conveying sensory information from the taste buds on the anterior two-thirds of the tongue.
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