Pediatric nursing

1. CHAPTER IV
Systemic Disorders
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2. CONGENITAL HEART DISEASES
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3. LEARNING OBJECTIVES
At the end of this class you will be able to
Define CHD
List the common cyanotic and acyanotic heart conditions
Discuss CHF
Explain infective endocarditis in children
Explain ARF in children
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4. NORMAL BLOOD FLOW
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5. CONGENITAL HEART DISEASE
A problem in the structure of the heart that is present at birth
Symptoms can vary from none to life-threatening
symptoms include:- Rapid breathing, bluish skin, poor
weight gain, and feeling tired.
- It does not cause chest pain
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6. ETIOLOGY
Genetic - Chromosomal abnormality
 Adverse maternal conditions (environmental)
- Maternal infections – rubella
- Maternal diseases – DM
- Drugs – valproate
- Advance maternal age
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7. CONT…
Syndrome complexes
- VACTREL syndrome - Vertebral, Anorectal,
Cardiac(VSD,TOF and others),Tracheal, Renal, Oesophageal
and Limb abnormalities
But the majority of cases of the congenital heart diseases are
unknown cause
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8. TYPES OF CHD
1. Acyanotic congenital heart disease
Ventricular septal defect
Atrial septal defect
Patent ductus arteriosus
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9. CONT…
2. Cyanotic congenital heart disease (4T’S)
Tetralogy of fallot
Truncus arteriosus
Transposition of great arteries
Tricuspid atresia
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10. ACYANOTIC CONGENITAL HEART
DISEASE
Blood is shunted (flows) from the left side of the heart to the
right side of the heart due to a structural defect (hole) in the
inter-ventricular septum.
Communication between the systemic and pulmonary sides
of the circulation, which results in shunting of fully
oxygenated blood back into the lungs.
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11. VENTRICULAR SEPTAL
DEFECT (VSD)
Is a defect in the ventricular septum, the wall dividing the
left and right ventricles of the heart.
Cause
Other congenital conditions, such as Down syndrome
Incomplete looping of the heart during days 24-28 of
development
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12. CONT…
Clinical Manifestation
Symptomless at birth - usually manifests a few weeks after
birth.
Infant with a large VSD will fail to thrive and become
sweaty and tachypnoeic (breathe faster) with feeds.
Pulmonary hypertension due to the increased blood flow
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13. CONT…
Diagnosis
Can be detected by cardiac auscultation - pansystolic murmur
Treatment
Most cases do not need treatment and heal at the first years of
life.
Smaller congenital VSDs often close on their own
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16. CONT…
Surgical Intervention:- Indications
1. Failure of congestive cardiac failure to respond to medications
2. VSD with pulmonic stenosis
3. Large VSD with pulmonary hypertension
4. VSD with aortic regurgitation
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17. ATRIAL SEPTAL DEFECT
Blood flows between the atria (upper chambers) of the heart
Causes
Down syndrome
Ebstein's anomaly
Fetal alcohol syndrome
Holt–Oram syndrome
Lutembacher's syndrome
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18. CONT…
Clinical Presentation
Shortness of breath, especially when exercising.
Fatigue.
Swelling of legs, feet or abdomen.
Heart palpitations or skipped beats.
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19. CONT…
Frequent lung infections.
Stroke.
Heart murmur, a whooshing sound that can be heard through
a stethoscope
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20. CONT…
Diagnosis
Individuals with a significant ASD are diagnosed in utero or
in early childhood with the use
of ultrasonography or auscultation of the heart
sounds during physical examination
Chest X-ray, ECG or EKG, Cardiac catheterization
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21. CONT…
Treatment
Surgical closure
Medical Treatment
- Digoxin - strengthen the heart muscle
- Diuretics. help the kidneys remove excess fluid from the body.
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22. PATENT DUCTUS ARTERIOSUS (PDA)
Is a condition where the ductus arteriosus fails to close
after birth.
Resulting in irregular transmission of blood between
the aorta and the pulmonary artery
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23. CONT…
Cause
PDA is sometimes idiopathic. Known risk factors include:
Preterm birth
Congenital rubella syndrome
Chromosomal abnormalities (e.g., Down syndrome)
Genetic conditions such as Loeys-Dietz syndrome (would also
present with other heart defects)
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24. CONT…
Sign and symptom
Tachycardia
Respiratory problems - Dyspnea (shortness of breath)
Continuous "machine-like" (also described as "rolling-thunder"
and "to-and-fro") heart murmur
Cardiomegaly (enlarged heart, reflecting ventricular
dilation and volume overload)
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25. CONT…
Left subclavicular thrill
Bounding pulse
Widened pulse pressure
Poor growth
Differential cyanosis, i.e. cyanosis of the lower extremities
but not of the upper body.
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26. CONT…
Diagnosis
Noninvasive techniques:- Echocardiography and associated
Doppler studies
Electrocardiography (ECG)
Chest X-ray
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27. CONT…
Treatment
PDA can be treated with both surgical and non-surgical
methods
 Non surgical treatment
- Indomethacin or a special form of ibuprofen have
been used to initiate PDA closure
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28. CONT…
Prevention
Some evidence suggests that indomethacin administration on the
first day of life to all preterm infants reduces the risk of developing a
PDA and the complications associated with PDA. Indomethacin
treatment in premature infants also may reduce the need for surgical
intervention
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29. CYANOTIC HEART DEFECT
 Is a group-type of congenital heart defect (CHD) that occurs
due to deoxygenated blood bypassing the lungs and entering
the systemic circulation or a mixture of oxygenated and
unoxygenated blood entering the systemic circulation.
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30. CONT…
Clinical feature
Clubbing
The patient assuming a crouching position
Cyanosis - facial discolouration (particularly the lips) and
digit discolouration (fingers & toes).
Crying
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31. CONT…
Crabbiness/irritability
Tachycardia
Tachypnea
A history of inadequate feeding.
Unusually large toe & fingernails.
Delayed development (both biological & psychological).
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32. TETRALOGY OF FALLOT (TOF)
The primary defect is an anterior deviation of the
infundibular septum (the muscular septum that separates the
aortic and pulmonary outflows).
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33. TOF CONT…
The consequences of this deviation are the 4 components:
1. Obstruction to right ventricular outflow (pulmonary
stenosis),
2. Ventricular septal defect (VSD),
3. Dextroposition of the aorta so that it overrides the
ventricular septum (overriding aorta), and
4. Right ventricular hypertrophy
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34. CONT…
Clinical manifestation
Episodes of bluish color to the skin.
When affected babies cry or have a bowel movement they may
develop a "tet spell" where they turn very blue,
Have a hard time breathing, become limp, and
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35. CONT…
Occasionally lose consciousness.
Other symptoms may include a heart murmur, finger
clubbing, and easy tiring with breastfeeding.
Cause
Typically not known.
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36. CONT…
Risk factors include
- A mother who uses alcohol,
- Has diabetes,
- Is over the age of 40,
- Rubella during pregnancy
- Down syndrome
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37. CONT…
Treatment
Treated by open heart surgery
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38. TRANSPOSITION OF THE GREAT VESSELS
Is a group of congenital heart defects involving an abnormal
spatial arrangement of any of the great vessels.
Risk factors
Preexisting diabetes mellitus of a pregnant mother
Diagnosis
Chest X-ray
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39. CONT…
Treatment
 Prostaglandins can be given to keep the ductus arteriosus open
Arterial switch operation is the definitive treatment for dextro-
transposition
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40. TRUNCUS ARTERIOSUS
Also called Common arterial trunk
Is a rare form of congenital heart disease that presents at
birth.
In this condition, the embryological structure known as
the truncus arteriosus fails to properly divide into
the pulmonary trunk and aorta
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41. CONT…
Clinical Manifestations
Cyanosis presents at birth
Heart failure may occur within weeks
Systolic ejection murmur is heard at the left sternal border
Widened pulse pressure
Bounding arterial pulses
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42. CONT…
Loud second heart sound
Biventricular hypertrophy
Cardiomegaly
Increased pulmonary vascularity
Hypocalcemia
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43. CONT…
Treatment
Neonatal surgical repair,
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44. TRICUSPID ATRESIA
There is a complete absence of the tricuspid valve
Therefore, there is an absence of right atrioventricular
connection. This leads to a hypoplastic (undersized) or
absent right ventricle.
Causes
Causes of Tricupsid atresia are unknown.
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45. CONT…
Clinical manifestations
progressive cyanosis
poor feeding
tachypnea over the first 2 weeks of life
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46. CONT…
Holosystolic murmur due to the VSD
left axis deviation on electrocardiography and left ventricular
hypertrophy (since it must pump blood to both the pulmonary
and systemic systems)
normal heart size
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47. CONT…
Treatment
PGE1 to maintain patent ductus arteriosus
Modified Blalock-Taussig shunt to maintain pulmonary blood
flow.
Cavopulmonary anastomosis to provide stable pulmonary flow
Fontan procedure to redirect inferior vena cava and hepatic
vein flow into the pulmonary circulation
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48. CONGESTIVE HEART FAILURE
Cardiac output--- Stroke volume X Heart rate
Heart rate varies with age
Stroke volume is the amount of blood ejected per beat
Preload– the amount of blood returning to the heart during
diastole
After load—the amount of pressure exerted against ventricular
ejection during systole
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49. CHF
Definition: It is a state of decreased cardiac output with failure to
met metabolic needs
Decreased cardiac output could be due to
1. Poor contractility
2. Decreased preload
3. Increased after load
4. Decreased in heart rate #222 49

50. CLINICAL MANIFESTATIONS
OF CHF
History
Progressive fatigue and cough
Sweating and failure to feed
Bilateral pretibial and pedal pitting edema
Older children complains dyspnea and chest pain
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51. CONT…
 Facial puffiness
 Ascites in severe cases
 Progressive weight loss
 Anorexia
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52. CLINICAL MANIFESTATIONS OF
CHF
Physical examination
Tachycardia, Tachypnea, week pulse
Pitting edema, cold extremeties
Raised JVP
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53. CONT…
Precordial examination may show
Bulged chest, hyperdynamic precordium
Diastolic and or Systolic murmur
Hepatomegaly, ascites
Crepitations and wheezing due to pulmonary edema
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54. ETIOLOGIES OF CHF
1. Acquired heart diseases
Rheumatic heart disease (valvular heart disease)
Myocarditis
Pericarditis with effusion
Heart rhythm disturbances
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55. CONT…
2. Congenital heart diseases (CHD)
A. Acyanotic CHD (Left to right shunt)
PDA, VSD, ASD etc
B. Cyanotic CHD (right to left shunt)
Tetralogy of fallot, Truncus arteriosus
Tricuspid atresia, Transposition of great arteries
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56. DIAGNOSIS OF CHF
Clinical examination
CXR: to show cardiomegaly, pulmonary edema etc
Echocardiography: differentiate acquired from congenital heart
diseases, severity, presence of infective endocarditis
ECG: Detection of rhythm disturbances, cavity dilatation, axis
deviation and hypertrophy
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57. CARDIOMEGALY
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58. TREATMENT OF CHF
A. Medical therapy
1. Reduction of volume overload
Furosemide, chlorthiazide, reduce salt intake
2. Increase heart contractility
Digoxin, Dopamine
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59. CONT…
3. Inhibit salt and water reabsorption
Captopril, enalapril, Spironolactone
4. Decrease afterload (resistance)
Captopril, enalapril
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60. TREATMENT OF CHF
Surgical therapy
Correction of structural defect in congenital heart disease
(PDA, VSD, ASD, TOF, TGA, TA)
Closed surgery to correct septal defects
Open surgery to correct complicated heart defects
Valve repair or replacement for rheumatic heart disease
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61. INFECTIVE ENDOCARDITIS
Infectious Endocarditis (IE): an infection of the heart’s
endocardial surface
Classified into four groups:
• Native Valve IE
• Prosthetic Valve IE
• Intravenous drug abuse (IVDA) IE
• Nosocomial IE
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62. Acute
• Affects normal heart valves
• Rapidly destructive
• Metastatic foci
• Commonly Staph.
• If not treated, usually fatal
within 6 weeks
FURTHER CLASSIFICATION
Sub-acute
• Often affects damaged heart
valves
• Indolent nature
• If not treated, usually fatal by
one year
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63. ETIOLOGIC AGENTS IN PEDIATRIC
INFECTIVE ENDOCARDITIS
COMMON: NATIVE VALVE OR OTHER CARDIAC
LESIONS
• Viridans group streptococci (S. mutans, S. sanguis, S.
mitis)
• Staphylococcus aureus
• Group D streptococcus (enterococcus) (S. bovis, S.
faecalis)
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64. EPIDEMIOLOGY
Often a complication of congenital or rheumatic heart disease
Can also occur in children without any abnormal valves or
cardiac malformations.
Rare in infancy; in this age group, it usually follows open heart
surgery or is associated with a central venous line
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65. EPIDEMIOLOGY
Patients with congenital heart lesions in which blood is
ejected at high velocity through a hole or stenotic orifice are
most susceptible to endocarditis.
Vegetations usually form at the site of the endocardial or
intimal erosion that results from the turbulent flow
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66. PATHOPHYSIOLOGY
1. Turbulent blood flow disrupts the endocardium making it
―sticky‖
2. Bacteremia delivers the organisms to the endocardial
surface
3. Adherence of the organisms to the endocardial surface
4. Eventual invasion of the valvular leaflets
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67. CLINICAL MANIFESTATIONS
HISTORY
• Prior congenital or rheumatic heart disease
• Preceding dental, urinary tract, or intestinal
procedure
• Intravenous drug use
• Central venous catheter
• Prosthetic heart valve
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68. CLINICAL MANIFESTATIONS
SYMPTOMS
• Fever, Chills
• Chest and abdominal pain
• Arthralgia
• Dyspnea
• Night sweats, Weight loss
• CNS manifestations (stroke, seizures, headache
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69. CLINICAL MANIFESTATIONS
SIGNS
• Elevated temperature
• Tachycardia
• Vascular- Embolic phenomena (Roth spots, petechiae,
splinter nail bed hemorrhages, CNS or ocular lesions)
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70. CONT…
• Immune complex phenomena (glomerulonephritis,
arthritis, Osler nodes, Roth spot, )
• Janeway lesions
• New or changing murmur
• Splenomegaly
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71. CLINICAL MANIFESTATIONS
• Arthritis
• Heart failure
• Arrhythmias
• Metastatic infection (arthritis, meningitis, mycotic arterial
aneurysm, pericarditis, abscesses, septic pulmonary
emboli)
• Clubbing
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72. PETECHIAE
Photo credit, Josh Fierer, M.D.
medicine.ucsd.edu/clinicalimg/ Eye-Petechiae.html
Harden Library for the Health Sciences
www.lib.uiowa.edu/ hardin/
md/cdc/3184.html
1.Nonspecific
2.Often located on extremities
or mucous membranes
dermatology.about.com/.../
blpetechiaephoto.htm
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73. SPLINTER HEMORRHAGES
1.Nonspecific
2.Nonblanching
3.Linear reddish-brown lesions found under the nail bed
4.Usually do NOT extend the entire length of the nail
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74. OSLER’S NODES
1.More specific
2.Painful and erythematous nodules
3.Located on pulp of fingers and toes
4.More common in sub-acute IE
American College of Rheumatology
webrheum.bham.ac.uk/.../ default/pages/3b5.htm www.meddean.luc.edu/.../
Hand10/Hand10dx.html
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75. JANEWAY LESIONS
1.More specific
2.Erythematous, blanching macules
3.Nonpainful
4.Located on palms and soles
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76. LABORATORY
• Positive blood culture
• Elevated erythrocyte sedimentation rate
• Elevated C-reactive protein
• Anemia
• Leukocytosis
• Immune complexes
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77. • Hematuria
• Renal failure: azotemia, high creatinine
(glomerulonephritis)
• Chest radiograph: bilateral infiltrates, nodules, pleural
effusions
• Echocardiographic evidence of valve vegetations,
prosthetic valve dysfunction or leak, myocardial abscess,
new-onset valve insufficiency
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78. DIAGNOSTIC (DUKE) CRITERIA
Definitive infective endocarditis
• Pathologic criteria
• microorganisms or pathologic lesions: demonstrated by
culture or histology in a vegetation, or in a vegetation that
has embolized, or in an intracardiac abscess
• Clinical criteria
• two major criteria, or one major and three minor criteria, or
five minor criteria
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79. DIAGNOSTIC (DUKE) CRITERIA
Possible infective endocarditis
• findings consistent of IE that fall short of ―definite‖, but not ―rejected‖
Rejected
• firm alternate Dx for manifestation of IE
• resolution of manifestations of IE, with antibiotic therapy for  4 days
• no pathologic evidence of IE at surgery or autopsy, after antibiotic therapy
for  4 days
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80. DIAGNOSTIC (DUKE)
CRITERIA
Major criteria
• Positive blood culture for IE
• Echocardiographic evidence of endocardial involvement
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81. CONT…
Minor criteria
• Predisposing conditions (heart condition or IV drug use)
• Fever of 100.40F or higher
• Embolic – vascular phenomena
• Immunologic phenomena
• Microbiologic evidence not meeting major criteria
• Echocardiographic evidence not meeting major criteria
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82. THE ESSENTIAL BLOOD TEST
Blood Cultures
• Minimum of three blood samples
• Three separate venipuncture sites
• Obtain 10-20mL in adults and 0.5-5mL in children
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83. CONT…
Positive Result
• Typical organisms present in at least 2 separate samples
• Persistently positive blood culture (atypical organisms)
• Two positive blood cultures obtained at least 12 hours apart
• Three or a more positive blood cultures in which the first
and last samples were collected at least one hour apart
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84. DUKE’S MAJOR CRITERIA
Evidence of endocardial involvement (Echocardiography)
• Intracardiac mass on a valve or other site
• Regurgitant flow near a prosthesis
• Abscess
• Partial dehiscence of prosthetic valves
• New valve regurgitant flow
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85. COMPLICATIONS
Four mechanisms
• Embolic
• Local spread of infection
• Metastatic spread of infection
• Formation of immune complexes – glomerulonephritis and
arthritis
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86. EMBOLIC COMPLICATIONS
Occur in up to 40% of patients with IE
Predictors of embolization
• Size of vegetation
• Left-sided vegetation
• Fungal pathogens, S. aurous, and Strep. Bovis
Incidence decreases significantly after initiation of effective
antibiotics
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87. EMBOLIC COMPLICATIONS
Stroke
Myocardial Infarction
• Fragments of valvular vegetation or vegetation-induced
stenosis of coronary ostia
Hypoxia from pulmonary emboli
Abdominal pain (splenic or renal infarction)
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88. LOCAL SPREAD OF INFECTION
Heart failure
• Extensive valvular damage
• Myocardial abscesses
• Toxic myocarditis
Paravalvular abscess (30-40%)
• Most common in aortic valve, IVDA, and S. aureus
• Higher rates of embolization and mortality
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89. LOCAL SPREAD OF INFECTION…
Arrythmias
Heart block
Valve obstruction
Pericarditis
Fistulous intracardiac connections
E.g. , acquired VSD
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90. METASTATIC SPREAD OF
INFECTION
Metastatic abscess
• Kidneys, spleen, brain, soft tissues
Meningitis and/or encephalitis
Vertebral osteomyelitis
Septic arthritis
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91. TREATMENT
Medical
Surgical
• Intra-cardiac complications
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92. MEDICAL TREATMENT
Pre-antibiotic era - a death sentence
Antibiotic era
• microbiologic cure in majority of patients
Parenteral antibiotics
• High serum concentrations to penetrate vegetations
• Prolonged treatment to kill dormant bacteria clustered in
vegetations
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93. MEDICAL TREATMENT
A total of 4–6 wk of treatment is recommended, with
serumcidal levels by tube dilution of at least 1:8 after a dose of
antibiotic.
Depending on the clinical and laboratory responses, antibiotic
therapy may require modification and, in some instances, more
prolonged treatment is required.
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94. MEDICAL TREATMENT
In nonstaphylococcal disease, bacteremia usually resolves in
24–48 hr, whereas fever resolves in 5–6 days with appropriate
antibiotic therapy.
Resolution with staphylococcal disease takes longer
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95. MEDICAL TREATMENT
Determinants of choice of antibiotics
• Type of endocarditis
• Native valve
• Prosthetic valve
• Etiologic agent
• Sensitivity of the etiologic agent to drugs
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96. MEDICAL TREATMENT:
BACTERIAL
Commonly used antibiotic combination:
Aqueous crystalline penicillin G sodium
or
Ceftriaxone sodium
plus
Gentamicin sulfate
Plus
Vancomycin hydrochloride
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97. MEDICAL TREATMENT: FUNGAL
Amphotericin B
5-fluorocytosine
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98. MEDICAL TREATMENT
Treatment of complications
• Heart failure
• Digitalis
• Salt restriction
• Diuretic therapy
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99. SURGICAL TREATMENT
Removal of vegetations
Valve replacement
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100. SURGICAL TREATMENT :
INDICATIONS
• Severe aortic or mitral valve involvement with intractable
heart failure
• Rupture of an aortic sinus
• Dehiscence of an intracardiac patch
• Failure to sterilize the blood despite adequate antibiotic
level
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101. SURGICAL TREATMENT :
INDICATIONS
• Recurrent emboli
• New heart block
• Myocardial abscess
• Increasing size of vegetation.
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102. PROGNOSIS
In the pre-antibiotic era, infective endocarditis was a fatal
disease.
Despite the use of antibiotic agents, mortality remains at 20–
25%.
Serious morbidity occurs in 50–60% of children with
documented infective endocarditis
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103. Female
S. aureus
AVegetation size
ortic valve
Prosthetic valve
Older age
POOR PROGNOSTIC FACTORS
Diabetes mellitus
Low serum albumen
Heart failure
Paravalvular abscess
Embolic events
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104. PREVENTION.
In patients with high or moderate risk heart conditions,
antimicrobial prophylaxis before various procedures:
• dental and oral procedures
• surgery of the upper respiratory tract
• Surgery of the GI tract
• Urinary tract procedures
Continuing education regarding the important of prophylaxis
Proper general dental care and oral hygiene
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105. PREVENTION
Vigorous treatment of sepsis and local infections
Careful asepsis during heart surgery and catheterization .
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106. ACUTE RHEUMATIC FEVER
–Acute rheumatic fever: inflammatory disease with
devastating sequelae
–Link to pharyngeal infection with group A beta hemolytic
streptocci
–Continues to be a problem worldwide:
–sporadic outbreaks in developed countries
–frequent occurrences in developing countries
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107. CONT…
–Still gaining understanding of etiology
–link between genetic predisposition and clinical
manifestations
–Best prevention still correct use of antibiotics
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108. Etiology
• Rheumatogenic strains of GAS serotypes (M 1, 3, 5, 6, 18,
24)
• ⅔ of the patients with an acute episode of rheumatic fever
have a history of an upper respiratory tract infection several
weeks before
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109. Epidemiology
• Most common form of acquired heart disease in all age
groups world wide
• Important cause of chronic heart disease and death in
developing world
• Estimated 30 million people suffer from ongoing heart
disease from ARF, 70% dying at average age 35 years old
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110. CONT…
• Accounts for
• 50% of all cardiovascular disease
• 50% of all cardiac admissions in many developing countries
In some developing areas of the world, the annual incidence is
282/100,000 population
Males and females equally affected
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111. Factors associated with acute rheumatic fever
• Socioeconomic status
• Overcrowding,
• poverty,
• lack of access to medical care
• Virulence of strain of GAS
• serotypes of GAS (M types 1, 3, 5, 6, 18, 24) are
associated with ARF
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112. Host factors
• Age : peak incidence in children 5 - 15 years old
• Previous history of acute rheumatic fever
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113. Pathogenesis
Still not clearly defined
Group A strep pharyngeal infection precedes clinical
manifestations of ARF by 2 - 6 weeks
Two seriously considered theories:
The cytotoxicity theory
• suggests that cytotoxic effect of GAS streptolysin O toxin
may be responsible for the pathogenesis.
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114. CONT…
The immunologic theory (theory of molecular mimicry)
• Antibodies made against group A strep cross-react with
human tissue (e.g., heart, brain, joint).
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115. Clinical Features
Following upper airway infection with GAS
- Silent period of 2 - 6 weeks
- Sudden onset of fever, pallor, malaise, fatigue
#222 115

116. Clinical Features (continued)
Characterized by:
• Arthritis
• Carditis
• Sydenham’s chorea
• Erythema marginatum
• Subcutaneous nodules
Called ―major manifestations‖ of Jones criteria either because
of frequency or specificity
#222 116

117. Minor manifestations
Clinical features
• Fever
• Arthralgia
Laboratory features
• Elevated c-reactive protein or
• Erythrocyte sedimentation rate
• Prolonged PR interval on EKG
#222 117

118. Diagnosis
 Jones criteria
• Criteria developed to prevent overdiagnosis
• Some criticism regarding validity but still important as guidelines
Probability of ARF high with
• Evidence of previous infection with streptococcal upper
respiratory infection & 2 major criteria or 1 major criteria and 2
minor criteria #222 118

119. Diagnosis: Jones Criteria
• Major criteria
• polyarthritis
• Carditis
• Sydenham’s chorea
• Erythema marginatum
• Subcutaneous nodlues
#222 119

120. Diagnosis: Jones Criteria (continued)
• Minor manifestations
• Fever
• Arthralgia
• Elevated c-reactive protein or
erythrocyte sedimentation rate
• Prolonged PR interval on EKG
#222 120

121. There are 3 circumstances in which the diagnosis of acute
rheumatic fever can be made without strict adherence to the
Jones criteria.
• Chorea .
• Indolent carditis.
• Recurrences of acute rheumatic fever .
#222 121

122. Treatment
Supportive
• bed rest .
• For carditis with heart failure
• digoxin,
• fluid and salt restriction,
• diuretics,
• Oxygen
#222 122

123. CONT…
Antibiotic therapy
• 10 days of orally administered penicillin or erythromycin,
or
• single intramuscular injection of benzathine penicillin
#222 123

124. Anti-Inflammatory Therapy
• Agents such as acetaminophen can be used to control pain
and fever while the patient is being observed for more
definite signs of acute rheumatic fever or for evidence of
another disease.
#222 124

125. • ASA in patients with typical migratory polyarthritis and
those with carditis
• The usual dose of aspirin is 100 mg/kg/day in 4 divided
doses PO for 3–5 days, followed by 75mg/kg/day in 4
divided doses PO for 4 wk.
#222 125

126. • In patients with carditis and cardiomegaly or congestive heart
failure , corticosteroids.
• The usual dose of prednisone is 2 mg/kg/day in 4 divided
doses for 2–3 wk followed by a tapering of the dose that
reduces the dose by 5 mg/24 hr every 2–3 days.
• At the beginning of the tapering of the prednisone dose,
aspirin should be started at 75 mg/kg/day in 4 divided
doses for 6 wk.
#222 126

127. Prevention
Primary Prevention
• Appropriate antibiotic therapy instituted before the
9th day of symptoms of acute GAS pharyngitis
#222 127

128. Secondary Prevention
 Penicillin g benzathine , every 4 wk intramuscular
 < 27 kg: 600,000 units
 >27 kg: 1,200,000 units
or
 Penicillin v 250 mg, twice a day oral
or
 Sulfadiazine or sulfisoxazole
#222 128

129. Common Hematologic
disorders in pediatrics
#222 129

130. ANEMIA
130
#222

131. ANEMIA
Definition:-
- Physiological (functional) definition:-
- is a decrease in red cell mass and corresponding
decrement in oxygen carrying capacity.
- Laboratory definition:- when Hgb level in the blood is below
the reference level for age and sex.
#222 131

132. INTRODUCTION AND
GENERAL ASPECTS
Blood consists of: Red cells, white cells and platelets
Plasma:- the liquid component of blood, which contains
soluble fibrinogen is the place where the above elements are
suspended.
Serum is what remains after the formation of the fibrin clot.
132
#222

133. THE RED CELLS:
Red Blood Cells (Erythrocytes):
The major function of red blood cells is to transport
hemoglobin, which in turn carries oxygen from the lungs
to the tissues.
133
#222

134. ANEMIA
Mild: Hgb 12-10gm/dl female
14-10gm/dl male
Moderate: 7-10 gm/dl
Severe: less than 7gm/dl
#222 134

135. CAUSES OF ANEMIA…
1. Deceased red cell production :- generally develops gradually
and cause chronic anemia. This can be due to:-
a) Marrow failure ;- 2ndry to
-Marrow aplasia/hypoplasia.
- marrow infiltration.
- Transient erytroblastopenia.
#222 135

136. CAUSES OF ANEMIA
b) Impaired erythropoietin production.
- anemia of chronic disease.
-Chronic inflammatory disease.
-HIV infection
c) Defect in RBC production
- Nutritional anemia , deficiency of
Iron , folic acid, Vitamin B-12…..
#222 136

137. CAUSES OF ANEMIA…
2. Hemolysis (Increased red cell destruction)
a) extrinsic:- enlarged spleen, hepatitis, leukemia, lymphoma,
tumors
b) drug-induced:- antibiotics, such as penicillin, ampicillin, or
methicillin, ibuprofen
c) Intrinsic:- inherited, red blood cells produced by the body are
defective.
#222 137

138. CAUSES OF ANEMIA…
3. Blood loss
- GI loss
- Pulmonary loss
- Bleeding disorder.
#222 138

139. TYPES OF ANEMIA
The most common types of anaemia are:-
- Iron deficiency anaemia
- Sickle cell anaemia
- Thalassaemia - Pernicious anaemia
- Aplastic anaemia - Fanconi anaemia
- Haemolytic anaemia
#222 139

140. ANAEMIA
Most common form of anaemia, is caused by:-
Chronic blood loss: Most commonly due to excessive
menstruation or bleeding into or from the gut as a result of a peptic
ulcer, gastritis, haemorrhoids or in children, worm infestation.
#222 140

141. TYPES, IRON…
Increased use of iron: In pregnancy, due to the growth of the
foetus or children undergoing rapid growth spurts in infancy and
adolescence.
Decreased absorption of iron: lack of stomach acid; chronic
diarrhoea; or malabsorption.
#222 141

142. TYPES, IRON…
Treated with iron supplementation(dietary changes and
supplements, medicines) as well as the treatment of the
underlying cause of the iron deficiency.
#222 142

143. APLASTIC ANAEMIA
Blood disorder in which the body's bone marrow doesn't make
enough new blood cells
Causes:- damage to the bone marrow's stem cells
Treatment:- blood transfusions, blood and marrow stem cell
transplants, and medication
#222 143

144. HAEMOLYTIC ANAEMIA
A condition in which red blood cells are destroyed and removed
from the bloodstream before their normal lifespan is up.
Cause: disease conditions
Treatment: blood transfusions, medicines, blood and marrow
stem cell transplants and lifestyle changes.
#222 144

145. THALASSAEMIA
Inherited blood disorders which cause the body to make fewer
healthy red blood cells and less haemoglobin.
Treatment: blood transfusions, iron chelation therapy, and folic
acid supplements
#222 145

146. SICKLE CELL ANAEMIA
A serious disease in which the body makes sickle-shaped
("C"-shaped) red blood cells.
Normal red blood cells are disk-shaped and move easily
through your blood vessels.
An inherited, lifelong disease
#222 146

147. SICKLE…
Treatment: The goals of treating sickle cell anaemia are to
relieve pain, prevent infections, eye damage and strokes, and
control complications.
Bone marrow transplants may offer a cure in a small number of
sickle cell anaemia cases
#222 147

148. PERNICIOUS ANAEMIA
A condition in which the body can't make enough healthy red
blood cells because it doesn't have enough vitamin B12.
Cause: certain diseases that interfere with vitamin B12
absorption; certain medicines; surgical removal of part of the small
intestine; and tapeworm infection.
Treatment: treated by replacing the missing vitamin B12 in the
body.
#222 148

149. CLINICAL FEATURES
 Pallor,Weakness, malaise, and easy fatigability are common
complaints.
 Dyspnea on mild exertion.
The nails can become brittle, lose their usual convexity, and
assume a concave spoon shape (koilonychia).
149
#222

150. CLINICAL CONT…
Anoxia can cause fatty change in the liver, myocardium, and
kidney.
With acute blood loss and shock, oliguria and anuria can
develop due to renal hypoperfusion.
Central nervous system hypoxia can cause headache, dimness
of vision, and faintness.
#222 150

151. LAB.DX
Hgb and Hct
Peripheral morphology
Bone marrow aspration cytology
#222 151

152. TREATMENT PRINCIPLES
A. Treatment of underlying cause
B. Dietary conselling
C. Iron theraphy
D. Blood transfusion
- Sever anemia
- anemia leading to CHF
#222 152

153. LEUKAEMIAS
Leukaemias are malignant disorders of the haematopoietic
stem cell compartment, characteristically associated with
increased numbers of white cells in the bone marrow and/or
peripheral blood.
153
#222

154. CONT…
The course of leukaemia may vary from a few days or weeks
to many years, depending on the type.
The most common malignant neoplasms in childhood
#222 154

155. FACTORS ASSOCIATED WITH THE
DEVELOPMENT OF LEUKAEMIA
Ionising radiation- An increase in leukaemia was observed
after the use of radiotherapy: eg-diagnostic X-rays of the fetus
in pregnancy
Cytotoxic drugs, Retroviruses
Genetic -There is a greatly increased incidence of leukaemia
in the identical twin
Immunological -Immune deficiency states. 155
#222

156. CLASSIFICATION
Leukaemias are traditionally classified into four main
groups:
• Acute lymphoblastic leukaemia (ALL)
• Acute myeloid leukaemia (AML)
• Chronic lymphocytic leukaemia (CLL)
• Chronic myeloid leukaemia (CML).
156
#222

157. CLINICAL FEATURES
The majority of patients with acute leukaemia, regardless of
subtype present with symptoms arising from:
 Anaemia - shortness of breath on effort; excessive tiredness,
weakness
Leucopoenia - recurrent infections
157
#222

158. CLINICAL CONT…
Thrombocytopenia - bleeding and bruising (particularly
acute promyelocytic leukaemia)
Marrow infiltration - bone pain.
#222 158

159. CLINICAL FEATURES…
Examination may be unremarkable, but features include:
Pallor
Fever (due to infection, not the disease itself)
159
#222

160. CLINICAL FEATURES…
Petechiae, purpura, bruises, fundal haemorrhage (particularly
acute promyelocytic leukaemia)
Lymphadenopathy, hepatosplenomegaly (more notable in
lymphoblastic leukaemia)
Violacious skin lesions (acute myelomonocytic leukaemia).
#222 160

161. PRINCIPLES OF
MANAGEMENT
Untreated acute leukaemia is invariably fatal, most often
within months, though with judicious palliative care it may be
extended to perhaps a year.
161
#222

162. CONT…
Treatment with curative intent may be successful, or may fail,
either because the leukaemia cannot be eradicated or because the
patient cannot sustain the therapy, death occurring as early as if
treatment had not been initiated.
#222 162

163. TREATMENT OUT LINE
Treatment of complications
- Anemia – transfusion
- Infection-antibiotics
- Thrombocytopenia- platelate transfusion
Anti- neoplastic medication
BM - transplantation
#222 163

164. HAEMOPHILIA
Inherited genetic disorder that impairs the body's ability
to make blood clots, a process needed to stop bleeding.
X-linked recessive disorders females are very rarely severely
affected
#222 164

165. CONT…
Types:- two main types of haemophilia:-
Haemophilia A, which occurs due to not enough
clotting factor VIII,
Haemophilia B, which occurs due to not enough
clotting factor IX
#222 165

166. CLINICAL FEATURE
Spontaneous bleeding, most characteristic type of internal
bleed is a joint bleed where blood enters into the joint spaces.
Children with mild to moderate haemophilia may not have
any signs or symptoms at birth especially if they do not
undergo circumcision.
#222 166

167. CONT…
Their first symptoms are often frequent and large bruises
and haematomas from frequent bumps and falls as they learn to
walk
Diagnosis:- is by testing the blood for its ability to clot and its
levels of clotting factors
#222 167

168. COMPLICATIONS
Deep internal bleeding, e.g. deep-muscle bleeding, leading to
swelling, numbness or pain of a limb.
Joint damage from haemarthrosis potentially with severe
pain, disfigurement, and even destruction of the joint and
development of debilitating arthritis.
#222 168

169. CONT…
Transfusion transmitted infection from blood transfusions
that are given as treatment
Adverse reactions to clotting factor treatment, including the
development of an immune inhibitor which renders factor
replacement less effective.
#222 169

170. CONT…
Intracranial haemorrhage is a serious medical emergency
caused by the buildup of pressure inside the skull. It can cause
disorientation, nausea, loss of consciousness, brain damage,
and death.
#222 170

171. TREATMENT
Factor replacement can be either isolated from human blood
serum, recombinant, or a combination of the two.
Anticoagulants such as heparin and
warfarin are contraindicated for people with haemophilia as
these can aggravate clotting difficulties
#222 171

172. CNOT…
Medicines which contain aspirin, ibuprofen, or naproxen
sodium should not be taken because they are well known to
have the side effect of prolonged bleeding
#222 172

173. Orthopedics in
Pediatrics
#222 173

174. • Fracture is break in the continuity of the cortex of a bone
• Causes:- Traumatic (High Vs Low energy Injury), Atraumatic
or Pathological
• Mechanism of injury
• Direct trauma
• Indirect trauma or Combined
Fracture
#222 174

175. CLASSIFICATION
Based on :-
A) Site of involvement
metaphysis, diaphysis ,articular
B)Soft tissue involvement
- Closed(simple):- Fracture is not exposed to the
environment
- Open (compound) #222 175

176. CONT…
B) Compound (Open) fracture
A break in the skin and underlying soft tissue leading
(directing) into or communicating with the fracture and its
hematoma
#222 176

177. History:-
- Trauma
- Deformity
- Pain
DIAGNOSIS
Physical examination
- Deformity
- Mobility
- tenderness
#222 177

178. INVESTIGATION
X-ray should be taken in at least two planes (AP and lateral)
Should always include the joints proximal and distal to the
fracture
Look in the X-ray for: Presence of fracture, The part of bone
fractured
#222 178

179. #222 179

180. MANAGEMENT OF
FRACTURE
Primary survey
• ABC
Secondary survey
• Head-to-toe examination
– Sign of fracture, dislocation,
– ST injury
#222 180

181. MANAGEMENT OF
FRACTURE…
– Including vascular and neurological status
– Record all your finding
• Emergency treatment of fractures and dislocation
– Align the fracture
– Splint
– Analgesics
#222 181

182. MANAGEMENT OF
FRACTURE…
Investigation
– X- ray
• PA and lateral X- ray (Include one joint above & one
below)
• Special view if necessary
• If difficulty of interpretation take X-ray of opposite side
#222 182

183. DEFINITIVE TREATMENT
1. Reduction
2. Immobilization
3. Soft tissue management
4. Rehabilitation
#222 183

184. METHODS OF
IMMOBILIZATION
1- Plaster of Paris (POP) cast
- Is the safest and cheapest method of immobilization
- Immobilization should always include the two adjacent
joints
- Joints should be immobilized in a functional position
#222 184

185. IMMBILIZATION
TECHNIQUES
Complications include joint stiffness and compartment
syndrome.
#222 185

186. IMMBILIZATION
TECHNIQUES…
2. Immobilization by traction method
1. Skin traction
– Used
• for children
• for adults temporarily
– Weight more than 3 Kg result in skin slough
#222 186

187. REHABILITATION
 Start immediately
 Phase of rehabilitation
• Resting
• Properioceptive training
• Strengthening exercise
• Work related training
#222 187

188. PRINCIPLES OF COMPOUND
FRACTURE MANAGEMENT:
Early wound debridement and thorough irrigation with saline
Antibiotics: Broad spectrum e.g. Penicillin +
Aminoglycoside should be given IV at least for 48 hrs.
Tetanus prophylaxis
#222 188

189. CONT…
Rigid immobilization with access to the wound e.g. external
fixation
Delayed wound closure!
Never close a compound fracture immediately in an attempt
to convert it to a closed one. You’ll cause a severe anaerobic
infection
#222 189

190. CLUB FOOT
CTEV
#222 190

191. CONGENITAL TALIPUS EQUINO
VARUS ( CTEV)
• The hill is inverted
• Fore foot & mid foot –inverted & adducted (Varus)
• Ankle is equines
191
• Twist of calcaneum and navicular around the
talus
#222

192. INCIDENCE
Common
1-3/1000
Varies with - Race (ethnicity )
• Highest among black Africans
• Sex
• M:F 2:1
50% bilateral 192
#222

193. ETIOLOGY
Unknown
Multifactorial
• Genetic
• + family Hx
• Neuromuscular defect
193
#222

194. CONT…
• Mechanical theory
• Environmental
• Oligohydraminosis
• Drugs
• Tubocurarine
#222 194

195. CLASSIFICATION
Based on reducibility
• Mild (Grade I)
• To neutral
• postural
195
#222

196. CONT…
• Moderate (Grade II)
• 0-20° from neutral
• Tendon contracture
• Severe (Grade III)
• >20°, deformity, Joint contracture
#222 196

197. DIAGNOSIS
 C/F
• Club like appearance
• Foot point plantar
• Small heal, drown up &
inverted
• Deep creases at posterior
ankle
197
#222

198. CONT…
• Lateral side is convex, absent creases
• Medial concave with creases
• Mid & fore foot – adducted & inverted
• Posteriorly displaced lateral malleoli
• Calf muscle atrophy
• Radiography
#222 198

199. TREATMENT
 Start as soon as possible
 Extend until skeletal maturity
 Never be completely normal
1. Conservative
• Streaching – count 10/20-30 times/
several times per day
199
#222

200. TREATMENT
Strapping- change every 2-3 days .Serial
cast
2. Operative
• Timing
• 8 month (6-12 month)
200
•
#222

201. FOLLOW UP
After operation
• 3 serial cast
• Club foot shoe
201
Neglected CTEV – Triple fusion (after the age of 10-
12yrs)
• Talo-Calcanial
• Talo-Navicular
• Calcaneo-cuboid
#222

202. OSTEOMYELITIS
#222 202

203. OSTEOMYELITIS
Inflammation of the bone due to pathogenic infection
Epidemiology
Common in children
Males are affected twice more than girls
Direct inoculation in older children
Bactremia in neonates and infants
#222 203

204. OSTEOMYELITIS
Pathogenesis
Bactremia seeding the bone
Metaphyseal involvement due to sluggish blood flow
Acquired via blood stream or direct inoculation
#222 204

205. CONT…
Long bones of the extremities are affected most
Etiology
S. aureus, S. pneumoniae, H. influenzae
Pseudomonas, M. tuberculosis, salmonella
#222 205

206. OSTEOMYELITIS
Clinical presentation
Prolonged and increasing fever
Localized bone pain and irritability
Localized skin edema and erythema
Limping (painful walking)
Muscle spasm
#222 206

207. OSTEOMYELITIS
#222 207

208. OSTEOMYELITIS WITH
PERIOSTEAL REACTION
#222 208

209. OSTEOMYELITIS
Diagnosis
Physical examination
Complete blood count
ESR
Blood culture
X-ray of the affected bone
Bone scan #222 209

210. OSTEOMYELITIS
Complications
Bactremia and sepsis
Secondary - infection (pneumonia, meningitis,
endocarditis)
Septic arthritis
Chronic osteomyleitis
#222 210

211. OSTEOMYELITIS
Treatment
Pain control
Treatment depends on culture and sensitivity
Cloxacillin IV for 10-14 days cover s. aureus
#222 211

212. CONT…
Ceftriaxone for H. influenzae, S. pneumoniae
Surgical debridement of the wound and dead
bone
#222 212

213. SEPTIC ARTHRITIS
#222 213

214. SEPTIC ARTHRITIS
Bacterial inflammation of the joint space
Epidemiology
Common in children
Involve mostly knee , hip and ankle joint
Etiology
S. aures, H. influenzae, S. pneumoniae
GBS, gram-ve rods in neonates
#222 214

215. SEPTIC ARTHRITIS
Pathogenesis
Acquired mostly due to bactremia and seeding of the joint
space
Osteomyelitis and penetrative joint injury cause direct
bacterial inoculation
Bacterial proliferation, host reaction with joint neutrophilic
infiltration---joint abscess
#222 215

216. SEPTIC ARTHRITIS
Clinical manifestation
Acute joint pain, fever and irritability
Joint erythema, swelling and hotness
Tenderness on manipulation of the joint
Limitation of joint movement
#222 216

217. SEPTIC ARTHRITIS
#222 217

218. SEPTIC ARTHRITIS
Diagnosis
Clincial presentation
CBC, ESR
Arhtrocentesis
Blood culture
U/S of the joint
#222 218

219. SEPTIC ARTHRITIS
Differential diagnosis
Tuberculosis
Reactive arthritis
Rheumatoid arthritis
Rheumatic heart disease
Gonococcal arthritis
#222 219

220. SEPTIC ARTHRITIS
Treatment
Pain control
Joint aspiration for treatment and diagnosis
Initiate Cloxacillin and ceftraxione
Change antibiotics based on culture
Follow for clinical response
#222 220

221. SEPTIC ARTHRITIS
Complication
Secondary infection of other organs
Oseomyelitis
Joint destruction
Deformity
#222 221

222. END
#222 222