3. Neonatal Conjunctivitis
Chemical Conjunctivitis (most common) - due to
silver nitrate
Mild palpebral edema and clear, sterile Eye Discharge
Onset <24 hours within eye prophylaxis at birth
Resolves within 48 hours of birth
HSV Conjunctivitis
Onset within 14 days of birth
Up to 20% of HSV infected infants are affected
Risk of disseminated Herpes Simplex Virus
Findings
Keratitis or Cataracts
Chorioretinitis
Optic Neuritis
4. Neonatal conjunctivitis
Gonorrheal Conjunctivitis
Onset within 2-5 days of life
Severe lid edema, and purulent exudates next step , obtain
gram stain may reveal intracellular gram –ve diplococci
Rx Ceftriaxone x 1 dose, saline irrigation of eyes
Chlamydia Conjunctivitis
Onset within 7-14 days of birth
Initial mild watery discharge Progresses to copious and
purulent discharge
Diagnosis Giemsa staining of epithelial cell scrapings from
tarsal conjunctivae will reveal intracytoplasmic inclusions
Rx Oral erythromycin x 2 weeks
8. Erythema Toxicum
Sterile papules and yellow vesicles on a
erythematous base
Distributed on face and body
Wright’s stain reveals eosinophils
Do not rx with antibiotics
9. Q
A 2 –day old child was brought for general examining
and while examining you notice several yellow vesicles
and papules on an erythematous base. They are
distributed on the neonate’s face and the chest. The
vesicular fluid obtained for analysis and a wrights stain
reveals numerous eosinophils. Most likely diagnosis:
A. Milia
B. Staphylococcal folliculitis
C. Candida dermatitis
D. Miliaria rubra
E. Erythema toxicum
ANS. E
Next step reassure mother and observe
10. Diaper Dermatitis
Diaper rashes are common between 9 to
12 months of age
Etiology
Diaper Irritant Dermatitis
Candida diaper dermatitis
Bacterial diaper dermatitis
Seborrheic Dermatitis
Acrodermatitis Enteropathica
11. Irritant Diaper dermatitis
Most common cause of diaper rash
Etiology : Iirritation by urine, feces, moisture and friction
Rash is seen mainly in the areas in contact with the diaperbuttocks, medial thighs, labia and scrotum. The skin fold areas are
not involved because there is no contact with the diaper
Erythema, papules, and areas of scaling are present.
Secondary infections with bacteria and yeast are common.
How to prevent Irritant diaper dermatitis?
a. Keep the diaper area dry :
Use disposable diapers or frequently change the wet diapers
Apply petroleum jelly after each diaper change to decrease skin contact with
moisture.
Apply powder in the area to keep it dry and decrease friction
If above measures fail, use low-potency steroids
12. Candida Dermatitis
One of the etiologies of diaper dermatitis
Involves deep skin folds ( Skin folds
spared in irritant dermatitis)
Characterized by bright red rash with
peripheral scaling and satellite papular
lesions
Rx ketoconazole, nystatin local creams
13. Bacterial Diaper dermatitis
Bacterial infection complicationg the
irritant dermatitis
Etilogy : S.aureus
Charecterized by pustules and crusted
lesions
Rx : Topical Mupirocin or Neosporin.
14. Seborrheic Dermatitis
Can occur in the diaper area.
Red and scaly waxy patches. Usually, there is
concomitant involvement of axillary & neck folds
and skin behind the ears referred to as
“Cradle cap” appears at 2-3 weeks of life and
disappears by 3-4 month.
Rx : In severe cases, use Ketoconazole or
hydrocortisone cream
15. Acrodermatitis Enteropathica
Etiology : zinc deficiency
Scales and crusty papules in the peri-oral and the diaper
area.
Infant may be withdrawn and may have loss of appetite
Paronychia and loss of scalp hair, eyebrows, and
eyelashes may occur.
There might be associated diarrhea indicating an
underlying malabsorption syndromes.
Rx :
Completely response to zinc supplements.
17. Choanal Atresia
Complete obstruction of one or both nares
Pathophysiology remember that Infants are obligate nose
breathers until 4 months old
Signs
Bilateral Choanal atresia
Cyanosis that is relieved with crying
Unilateral Choanal atresia
Diagnosis usually delayed by years
Foul mucus discharge from affected nares
Upper Respiratory Infection may result in distress
Diagnosis
Check patency with stethoscope (listen over nares)
Try passing Small feeding tube unable to pass via nares
Lubricate 5 french tube and insert Normally should meet no
resistance
Management: Bilateral Choanal Atresia
Bilateral Choanal Atresia in newborn is an emergency
Stabilization Oral Airway
Surgical repair Laser burrowing of bony palate
18. CLEFT LIP
Occurs in 1 in 700 births. Occurs due to failure of closure of medial
nasal and maxillary processes leads to cleft lip. Often, associated
with cleft palate. Failure of fusion of palatal processes leads to cleft
palate. Etiology :
Family History
Asian ethnicity
Maternal ETOH consumption
Maternal anti-convulsant use ( eg: Phenytoin)
Maternal Diabetes
Associations:
Pierre Robin Syndrome Micrognathia , Cleft Palate and
Glossoptosis
Trisomy 13 Syndrome Holoprosencephaly
Cleft palate may be associated with Pituitary abnormalities
(Panhypopituitarism) & Hypothalamus anomalies (Kallmann's
Syndrome)
Problems with Cleft Lip/ palate
Recurrent otitis media often requiring ear tubes
Hearing loss with cleft palate
Speech problems with cleft palate
Dental issues like tooth dislocation
19. Management – cleft lip/palate
Feeding of Newborn
Isolated cleft lip usually does not cause feeding problem
Encourage breast feeding breast feeding strengthens facial muscles of
the kid and eases repair
Cleft lip associated with cleft palate or isolated cleft palate may require
special nipples or a palatal obturator plate (Plastic dental appliance that
covers cleft in palate and improves sucking)
Surgical Treatment
Cleft lip:
Cleft lip alone Usually repaired at 10 to 12 weeks ( 3 months)
Remember "Rule of Tens " a rule of thumb used by surgeons to
determine a child’s readiness for surgery ten weeks of age, ten
pounds in weight and ten grams of hemoglobin. If the child meets all
the three criteria, child reaches all three criteria, surgical risks are
greatly minimized
Cleft palate :
Surgical repair before age 2 years ( best age is usually
between 9 to 18 months) i.e; before speech develops ( to
ensure normal speech) Its is a complicated surgery and is done
when the baby is bigger and better able to tolerate it (between 9 and 18
months)
Surgical revision may be needed at 4 to 5
years
20. Q.1
During your rotation in the birth rooms, you come across
a full term baby that is delivered and noted to have cleft
lip and palate. The baby is otherwise healthy. The
mother is very concerned and anxious. She asks you if
there is any treatment available immediately. What is the
most appropriate response?
A. Surgery needs to be done urgently to prevent permanent
defect
B. Your baby is healthy. Does not need any therapy
C. Your baby will benefit from surgery between 9 to 12
months.
D. Your baby should get cleft palate repair by 3 months to
prevent speech defects
E. Your baby has a permanent defect for which no
treatment options are available.
21. Ans. C
Baby has cleft palate. Surgery for cleft palate is
more complicated than the cleft lip and requires
the baby to be big enough to tolerate it. The goal
is to do the surgery between 9 & 18 months in
order to facilitate normal speech development.
Surgery for cleft lip can be done at 10 weeks ( 3
months) not cleft palate. Choice D is incorrect
Baby will not be able to tolerate these surgeries
now choice A is incorrect
23. Rh Sensitization
Pathophysiology (Rh- mom , Rh+ father,
Rh+baby)
Maternal antibody Formation to fetal Rh ( first
baby not affected usually mother gets access
to fetal RBCs suring delivery. Second baby if
Rh+ve will get affected)
Results in Hemolytic Disease of the Newborn
IgM forms in 7 days Does not cross placenta
IgG forms in 21 days Crosses placenta easily
Neonatal Hemolytic Anemia
Fetal Hydrops
If mother Rh- , always check father’s Rh type
24. Rh Sensitization
Indications for giving RhoGAM (xD) to Rh
Negative Mother
Standard Timing
Additional Indications
Week 28 gestation
Postpartum (under 3 days postpartum if baby Rh+)
Placenta Separation
Labor Third Stage
Termination or Spontaneous Abortion after 6 weeks
Antepartum bleed
Abruptio Placenta
Abdominal Trauma
Procedures (Give RhoGAM within 72 hours of
procedure)
Amniocentesis or Cordocentesis
Chorionic Villus Sampling
External version
25. RHOGAM Dosing
Dosing
Standard RhoGAM Dosing
Before 12 weeks gestation: RhoGAM 50 mcg
IM
RhoGAM 50 mcg IM has limited availability
Now RhoGAM 300 mcg IM is given at this time
After 12 weeks gestation: RhoGAM 300 mcg
IM
First Trimester Bleeding or Late
Pregnancy Bleeding
RhoGAM dose based on Kleihauer-Betke
Test
26. Kleihauer-Betke
Indications
Measures fetal cells in maternal circulation
Used in assessing for Rh Sensitization
If Maternal blood Rh negative and if there is Large antepartum bleed
Mechanism
Blood Film stained with acid elution
Fetal Hgb more acid resistant
Fetal RBC darkly stained, Maternal RBC "ghosts"
Technique
Count Fetal cells per 50 low power fields
Five cells per 50 (lpf) = 0.5 ml bleed
Interpretation
Calculate Maternal Blood Volume (ml) =
Calculate Fetal Whole Blood (ml) =
(Pre-pregnant weight in kg) x 70 ml/kg x (1.0 + (0.5 x weeks
gestation/36)) - Estimated Blood loss (ml) at time of test
(Fetal Cell Count/Maternal Cell Count) x Maternal Blood Volume
Rh Immune Globulin (RhoGAM) Dose
Give 300 ug per 30 ml fetal whole blood or 15 ml pRBC
28. Duodenal Atresia
Presents soon after birth
Persistent vomiting
Associated with Downs
Do AXR – Double bubble appearance
Confirm with ultrasound
Surgery as soon as possible
duodenoduodenostomy
29. Congenital Pyloric Stenosis
Presents at 6 to 8 weeks with vomiting
Hypochloremic metabolic alkalosis,
hypokalemia
Physical – olive shaped epigastric mass
Ultrasound confirmatory
Rx – Surgery/ Pyloromyotomy
30. Failure to pass Meconium
By 48 hours. Consider following
differential
Cystic fibrosis
Imperforate Anus
Hirschprung disease
31. Hirschprung disease
Congenital megacolon
Lack of intramural ganglionic cells
C/F :
Submucosa level (Meissner's Plexus)
Myenteric level (Auerbach's Plexus
Presentations: Age dependant
Newborn No meconium in 24-48 hours of birth
First month of life Progressive abdominal distention, Small caliber stools (pencil-thin)
& failure to thrive
Two to three months of life Enterocolitis (fever, explosive bloody Diarrhea) Initial
presentation in 33% of patients
Older Childhood progressive Constipation, Fecal Impaction & Abdominal distention
Rectal exam Reveals no stool in the ampulla
Diagnosis can be made with barium enema, revealing a transition zone between the
constricted aganglionic segment and the proximal, normally dilated segment. Anal
manometry useful in daignosis. Rectal biopsy shows lack of ganglion cells and
confirms the daignosis
Rx : ilio-anal anastomosis, in severe cases colostomy
33. Physiological Jaundice
Never Never occurs less than 24hrs after birth ( NOT ON DAY 1
consider from 2 to 14 days. Usually does not persist more
than 1 week in duration )
Breast Feeding Jaundice
Physiologic Jaundice Transient limitation of Bilirubin conjugation (
due to immature glucuronyl transferase) , Increased Hemolysis
Hemoglobin drops from 20 to 12 in first week
Exaggerated Physiologic Jaundice : occurs with
Low glucuronyl transferase (Hepatic immaturity)
Risk factors
Breast Feeding Jaundice
Prematurity
Asian ethnicity
Weight loss
Complications : Kernicterus most seen with pathological jaundice,
however can be seen with breastfeeding jaundice or exaggerated
physiological jaundice
34. Breast Feeding Jaundice
Pathophysiology
Early Breast Feeding Jaundice
Same as mechanism as exaggerated physiologic Jaundice
Late Breast Feeding Jaundice
Nonesterified long-chain fatty acids in breast milk
Competitively inhibit glucuronyl transferase
Labs
Early-Onset Breast Milk Jaundice – within 3-4 days of
birth
Same course as exaggerated physiologic Jaundice
Total Bilirubin peaks < 17 mg/dl by day 4 of life
Late-Onset Breast Milk Jaundice
Bilirubin peaks between day of life 6 to 14
Total Bilirubin often 12 to 20 mg/dl
Hyperbilirubinemia may persist 2-3 months
35. Breast Feeding Jaundice - Management
Early onset Breast Feeding Jaundice ( bili < 17)
Encourage mothers to nurse frequently (8-10x per day)
Avoid supplementation if possible
Monitor Serum Bilirubin daily as outpatient
Do not supplement with glucose or sterile water
Continue Breast Feeding even if supplementing
Formula indicated only for inadequate milk production
Phototherapy when Indicated
Mothers may express milk after feedings
Increases milk volume
Management: Late onset Jaundice (Bilirubin 17-20 mg/dl )
Diagnosis
Interrupt Breast Feeding for 24-48 hours
Monitor Serum Bilirubin levels every 12-24 hours Bilirubin should
decrease by 3 mg/dl per day and this confirms diagnosis of brest milk
jaundice.
Resume Breast Feeding after decreased Serum Bilirubin
This management if improves jaundice, confirms Breast Feeding
Jaundice
36. Pathological Jaundice
Criteria
Jaundice in first 24 hours of life or after day 14
Serum Bilirubin rises > 5 mg/dl in the first 24 hours
Direct Bilirubin (conjugated) >2mg/dl ( even during the period of
physiological jaundice, when u see high direct bilirubin suspect
biliary obstruction)
Term Infant
Serum Bilirubin >17 mg/dl
Any Jaundice that persists longer than 1 week
Preterm Infant
Serum Bilirubin >15 mg/dl
Any Jaundice that persists longer than 2 weeks
Except in Breast Feeding Jaundice
Except in Breast Feeding Jaundice
Complications : Kernicterus, Anemia, Failure to thrive
Rx : Phototherapy ( contraindicated in conjugated
hyperbilirubinemia) , Exchange transfusion if phototherapy is not
effective or if bili is very high ( > 30mg%)
37. Phototherapy
Mechanism
Bilirubin absorbs light – very ensitive to blue light and undergoes
photoisomerization
Photoisomerization
Converts toxic bilurubin to non toxic which is then excreted in bile
Contraindications
Conjugated Hyperbilirubinemia
Risk of bronze baby syndrome
Adverse Effects
Loose stools , Skin Rashes , Overheating , Dehydration ( due to
Insensible water loss , Diarrhea) Electrolyte disturbance
( Hyponatremia, Hypokalemia)
Bronze baby syndrome
Dark, grayish brown discoloration of skin
May persist for months
Associated with Conjugated Hyperbilirubinemia
39. Clavicle # from Birth Trauma
Most common newborn orthopedic injury
Signs
Pain with movement and Moro reflex
Pseudoparalysis of extremity on fracture side
Sternocleidomastoid muscle spasm on affected side
Crepitus at fracture site
Palpable bony irregularity at fracture site
Precautions
Assess concurrent injury to adjacent structures Cervical spine , Brachial
plexus & Humerus
Radiology Chest XRay
Management
Immobilize arm and shoulder 7-10 days
Safety pin infants sleeve to shirt
Prognosis
Excellent, even for displaced fractures
Course
Palpable callus formation in 7 to 10 days
Fracture heals in 4 to 6 weeks
40. Torticollis from Birth Trauma
Etiologies
Sternocleidomastoid muscle injury from Birth Trauma Hematoma
and fibrosis results in muscle shortening
Muscle adaptation from abnormal intrauterine position
Cervical vertebral abnormalities Suggested by limited neck ROM
at birth
Pathophysiology
Unilateral shortening of sternocleidomastoid muscle
Associated Conditions
Congenital asymmetric contractures of hip abductors
Unilateral Congenital Hip dysplasia
Signs
Head Tilt toward the affected side
Limited neck range of motion
May suggest cervical vertebral abnormality
Face and skull asymmetry from lack of position change
Palpable mass within sternocleidomastoid muscle
Gradually disappears and is replaced by fibrous knot
41. Torticollis - Management
Radiology
Neck XRay Indicated for significantly limited neck ROM
Ultrasound Hips
Remember to Assess for concurrent Congenital Hip dysplasia
Indicated for significant hip abductor tightness
Management
Positioning head opposite affected side Padded bricks ,
Sandbags
Passive Stretching
Rotate infants head to affected side
Tilt head backwards (extend) away from affected side
Surgical release of sternocleiodomastoid muscle
Indicated for limited range of motion at 1 year
Course
Minimal signs at birth
Torticollis will be evident by 2 to 3 weeks
Recovery over 3 to 4 months with therapy
Complete resolution by 1 year with therapy
42. Brachial Plexus Injury from Birth Trauma
Injuries may occur intrapartum prior to delivery: 50%
Unrelated to Shoulder Dystocia or excessive traction
Possibly from fetal shoulder against symphysis pubis
General
Follows difficult or prolonged delivery
Mechanism of injury
Upper plexus Injury Lateral flexion of neck against fixed head, shoulder
Lower plexus Injury Arm forced upward
Types
Duchenne-Erb Paralysis (Waiter's Tip Deformity)
Klumpke's Paralysis (Clawhand Deformity)
Whole Arm Paralysis (uncommon) Limb completely flaccid , Hands dry and
atrophic & All reflexes absent
Signs: General
Arm motionless at side with elbow extended
Moro Reflex absent on affected side
Swelling above clavicle due to hemorrhage
Traumatic neuritis
Thoracic root injury
Tenderness to palpation
Horner's Syndrome
Differential Diagnosis: Pseudoparalysis Clavicle Fracture & upper
humerus#
43. Brachial Plexus Injury from Birth Trauma
Associated Conditions
Phrenic Nerve palsy from Birth Trauma
Horner's Syndrome
Radiology: XRay Shoulder and XRay arm
Assess for concurrent fracture ( r/o pseudoparalysis )
Management
Prevent fixed soft tissue contractures
Gentle repetitive range of motion shoulder and elbow
Supportive splints for wrist and fingers
Reconstructive surgery for late deformities
Prognosis ( what to tell the mother ???)
Improvement in first week suggests full recovery
No improvement by 6 months suggests permanent deficit
No improvement expected after 2 years
Older patients
Underdevelopment of Upper extremity
Humerus shortened
Contractures and disuse atrophy
44. Erb-Duchenne Palsy
Most common type associated with Brachial Birth
Trauma
Pathophysiology Upper Roots (C5 to C6) Injury
Signs: Waiter's Tip
Arm adducted and internally rotated
Forearm pronated
Wrist flexed
Finger function and grasp reflex are normal
Moro Reflex and biceps reflex absent on affected side
Waiter's Tip position if C7 involvement
Prognosis
Fair to good recovery of arm function: 50-80%
45. Klumpke’s Palsy
Least common form of Brachial Birth Trauma
Pathophysiology
Injury to C7, C8, and T1 spinal nerves
Signs: Clawhand deformity
Hand Intrinsic Muscle Weakness
Grasp reflex absent on affected side
Biceps reflex and radial reflex present
Horner's Syndrome may be associated
Occurs if T1 sympathetic fibers are affected
Upper part of arm unaffected
46. Phrenic Nerve Injury – Birth Trauma
Pathophysiology Associated with Brachial Birth
Trauma leads to Unilateral diaphragm paralysis
Signs
Respiratory distress
Diminished breath sounds on affected side
Radiology: Ultrasound or Fluoroscopy of
diaphragm
Diaphragm elevated on affected side
Affected diaphragm moves upward with inspiration
Management
Pulmonary toilet while resolving
Refractory cases
Diaphragmatic plication
Course
Resolves over 1 to 3 months
47. Moro Reflex
A normal reflex present in newborn infants.
Absence of the Moro reflex in an infant is
abnormal. Presence of a Moro reflex in an older
infant, child, or adult is also abnormal.
Two-sided absence of the Moro reflex suggests
damage to the central nervous system (brain or
spinal cord).
One-sided absence of the Moro reflex the
possibility of a fractured clavicle or injury to the
brachial plexus, which can occur because of birth
trauma. Conditions associated with brachial
plexus injury include Erb's palsy and ErbDuchenne paralysis.
Paralysis on one side of the body may also
produce an asymmetrical Moro reflex .
50. Omphalocele
Covered abdominal wall defect at Umbilicus in newborn
Defect at base of Umbilical Cord (2 to 10 cm)
Normal abdominal viscera and contained within sac ,
Abdominal contents herniate via defect ( Intestine , Liver,
Gall Bladder Stomach, Bladder , Pancreas , Spleen )
Associated conditions (67% of cases) Trisomy
13 , Trisomy 18 , Congenital Heart Disease (VSD up to
25% of cases), Gastrointestinal disorders ( Midgut
volvulus , Malrotation , Meckel's Diverticulum &
Imperforate anus), Renal anomalies
Diagnosis : Usually diagnosed by prenatal Obstetric
Ultrasound
RX Apply warm dressing over the defect
Rx is surgery on first day of life
Prognosis : chromosomal abnormalities associated with
poor prognosis
51.
Gastroschisis
Open peri-umbilical abdominal wall defect in newborns
Risk factors : Intrauterine Growth Retardation , Prematurity &
Young mother (< 20 yrs age)
Pathophysiology Abdominal wall defect lateral to Umbilicus
with evisceration of small intestine and ascending colon , Bowel
may be abnormal - matted and thickened
Diagnosis : Usually diagnosed by prenatal Obstetric Ultrasound
Complications Necrotizing enterocolitis, Bowel perforation
Management Initial step Apply warm fluid-impermeable
dressing over defect
Orogastric Tube for decompression
Fluid Resuscitation (high evaporative losses)
Blood Culture & Broad spectrum antibiotic coverage
Maintenance IV fluids: D10W or 1/4NS
Start with 20 cc/kg bolus over 30 minutes
Fluid requirements in gastroschisis 2.5x normal
Ampicillin + Gentamicin
Surgical repair on first day of life
Parenteral Feeding
53. Advantages of breast feeding
Lower Incidence of Infantile Colic
Most Important method of maternal-infant bonding
Easier to digest than formula (related to protein)
Human milk is digested in 1.5 hours where asFormula is
digested in 4 hours
Does not induce allergic response (contrast to formula)
no Diarrhea, Gastrointestinal tract bleeding or Atopic
Dermatitis
Lower Incidence of feeding problems like
Gastroesophageal Reflux (Regurgitation) & Constipation
Colostrum contains multiple immune factors
Macrophages ( Complement, Lysozyme & Lactoferrin )
Secretory IgA antibodies Infant receives 0.5 to 1g
Secretory IgA per day thru breast milk provides
Bacterial, Viral, and protozoal protection
Lower Incidence of infection Bacteremia , Meningitis ,
Botulism Gastrointestinal infection , Lower respiratory
infection , Otitis Media & Urinary Tract Infection
54. Advantages of breast feeding
Advantages to mother
Faster return to pre-pregnancy weight
Decreased postpartum bleeding
Increased Bone Mineral Density
Lower Incidence of Ovarian Cancer
Lower Incidence of premenopausal Breast
Cancer
Remember breast feeding is not
guaranteed contraception
55. Contraindications - breastfeeding
Contraindications: Absolute
Maternal HIV Infection
Chemical Dependency ( drug abuse )
Important medication use that contraindicates lactation
( chemo rx, ergot alkaloids) Cardiovascular
medications to avoid in Lactation are Acebutolol &
Amiodarone
Untreated syphilis
Active/ untreated TB
Herpes only if there are active lesions on breast
Contraindications: Relative
Tobacco Smoking in lactation Significant nicotine
exposure via breast milk , 10x greater exposure than in
bottle fed infants
56. Herbs and Teas considered safe in
Lactation!
Avoid Caffeine more than 2 beverages per day
Herbs
Chamomile
Garlic
Ginger
Ginseng
Teas
Chicory
Orange Spice
Peppermint
Raspberry
Red bush tea
Rose hips
58. Amblyopia ( Lazy Eye )
Poor vision that cannot be corrected by eye glasses
which has no organic cause
Etiologies
Strabismus (most common cause of amblyopia)
Anisometropia (Refractive Amblyopia)
Misalignment of eyes
Large difference in Refractive Error between eyes
Deprivation Amblyopia
Congenital Cataract
Retinoblastoma
Corneal scarring
Vitreous opacity
Severe Ptosis
Optic atrophy
Iatrogenic patching
59. Amblyopia ( Lazy Eye ) Pathophysiology
Occurs in developmentally immature eye
Occurs in developmentally immature eye
during first 6 months of life
Normally visual acuity improves rapidly after birth
20/400 => 20/80 and Eye fully matures by age 9
years
However, normal maturity requires clear, equal,
aligned image for each eye if at all there is
conflicting data with Strabismus (2 competing
images) or Anisometropia (1 clear, 1 blurred image)
the brain suppresses information from the "bad"
eye
Continued suppression leads to permanent vision
loss in the bad eye.
Children should be screened for visual acuity/
strabismus to take measures to prevent
Amblyopia
60. Amblyopia
Management: Relies on forcing the
child to use amblyopic eye
Patch "good", dominant eye
May use Atropine to blur dominant eye
Prognosis
Remember that Amblyopia irreversible
after age 9 years
63. Breath Holding Spells
Characteristics
Transient episodes of breath holding
Associated with child becoming limp and unresponsive
Seizure-type activity may occur
Spells can occur as often as several times a day or as rarely as
once a year.
Types
Cyanotic Breath Holding Spell (most common)
Pallid Breath Holding Spell
Diagnostics
Electroencephalogram (EEG) normal
Evaluation
Do a Thorough history and examination
Consider the differential and Rule-out other pediatric spell
because life-threatening conditions may present similarly to BHS,
diagnosis of the benign condition can be difficult Therefore,
evaluation of breath-holding episodes requires the consideration
and elimination of other, more worrisome explanations.
64. Cyanotic BHS
More common Breath Holding Spell than Pallid
Spell
Episode onset after age 6 months, resolve by 5
years
Triggers
Occurs following a stressor such as scolding
Course
Initial: Brief, shrill cry
Next: Forced expiration and apnea ensues
Next: Cyanosis and loss of consciousness
Variable: Clonic movements may occur
65. Pallid BHS
Less common than Cyanotic Breath Holding Spell
Age of onset 12-24 months
Trigger: Pain
Strike body part on falling
Startled
Course
Initial: Stops breathing
Next: Immediate loss of consciousness
Next: Infant becomes limp and pale
Variable: Tonic Seizure, Bradycardia, Asystole >2 sec
66. Table 1. Differentiation of severe BHS from generalized seizures and cardiac
disturbances
Feature
Severe BHS
Generalized
seizures
Cardiac
disturbances
Age at onset
Often infancy
Rarely infancy
Variable
Family history of
BHS
Often positive
None
None
Precipitating event Usually present
Usually absent
Usually absent
Sleep state
Always awake
Asleep or awake
Awake, often with
stressor
Pallor or cyanosis
Always; before
syncope
Variable; after
syncope
Variable
Myoclonic jerks
Variable; few beats
Usually
Absent
67.
BHS - Management
Reassure parents that although BHS are frightening to observe children
will outgrow them By the time patients are 4 years old, 50% of BHS
resolve; by age 6 - 90% have done so; and by age 7 or 8, virtually all of
them resolve.
Are there any long term effects ? parents should be told that evidence
suggests no serious long-term effects of benign BHS in otherwise healthy
children these patients do not have increased risk of epilepsy or other
neurologic problems The only significant finding on subsequent follow-up
of children with BHS was a mildly increased incidence of syncope later in
life, especially in childhood or adolescence.
When a child with hx of BHS becomes upset and cries reasonable efforts
to calm the child should be made If an episode occurs despite these
measures, observation of the child and prevention of injury are generally all
that is required
If child loses consciousness place the child in a lateral supine position to
help avoid injury and possible aspiration
Once an episode has resolved, the child should be reassured.
Avoid drawing excessive attention to the event or expressing extreme worry
to the child as this may encourage the behavior
Medications are not usually indicated
In severe BHS associated with Bradycardia or Asystole or in patients with
multiple daily episodes 0.1 mg Atropine tid is effecive in preventing BHS
Referral to a pediatrician should be made in all cases in which
pharmacologic therapy is being considered.
69. Acute Epiglottitis
Caused by H.influenzae. Incidence has gone down dramatically since the
introduction of HiB vaccine.
Common age 2 months to 7 years
Onset Acute
Classic presentation is open mouth, protruding tongue and drooling
( dysphagia/ difficulty swallowing occurs due to swollen
epiglottis manifests as drooling)
Stridor may be present. Voice sounds “Muffled”
The child is often agitated and appears toxic, fever often present.
Spontaneous cough is absent( in contrast to Croup where there is “Barky”
cough Remember Epiglottitis patients actually “Look” worse than they
“Sound” where as croup patients “sound” worse than they look)
Look for signs of upper airway obstruction : flaring of the nasal alae,
suprasternal/ supraclavicular retraction, use of accessory muscles and
intercostal retractions (these signs may be absent at initial presentation)
Direct exam of Epiglottis by tongue depression shows cherry red,
swollen epiglottis. ( BUT AVOID TONGUE DEPRESSION AS ANY
IRRITATION OF EPIGLOTTIS CAN PRECIPITATE COMPLETE AIRWAY
OBSTRUCTION )
70. Thumb sign on lateral neck x-ray
Black arrow the tip of the epiglottis. White arrow pre-epiglottic space (vallecula). The normal epiglottis is thin or
triangular in appearance. Here, it appears enlarged and rounded looks like a thumb-print ( path gnomonic x-ray
appearance of epiglottitis)
71. Acute Epiglottitis
Diagnosis :
Clinical ( differentiate from Croup).
Supportive diagnosis can be obtained by lateral neck radiographs if the
child is stable to be transported to x-ray department shows enlarged
epiglottis protruding from the anterior wall of the hypopharynx (thumb
sign). Negative lateral radiographs do not rule out the diagnosis.
CBC reveals marked leucocytosis with left shift ( croup can have
leucocytosis but bandemia is usually absent)
Diagnosis can be confirmed by direct visualization but do not use tongue
depressors. Visualization should only be done by laryngoscopy with
anesthetist at the bedside and child prepared for intubation. Direct
laryngoscopy is pathognomonic demonstrates a large, almost
spherical, edematous, cherry-red epiglottis.
Rx :
Once Epiglottitis confirmed (laryngoscopy) First step INTUBATE!
( Remember ABCs)
Antibiotics DOC is Ceftriaxone. Ampicillin is alternative. Cultures
should be obtained from the epiglottis and from blood.
Racemic epinephrine and Corticosteroids can be potentially harmful here
( unlike in “Croup”)
72. Croup
Laryngotracheobronchitis leading to subglottic edema ( in
epiglottitis, supraglottic area is involved)
Etiology : MCC parainfluenza viruses, other causes – influenza,
RSV, Adenoviruses
Onset – insidious ( preceded by URI symptoms)
Common age 3 months to 3 years
Spontaneous “BARKY” Cough is present.
Inspiratory stridor that is increased by crying is seen.
Child usually does not appear toxic ( Sounds worse than he looks)
No droolong or dysphagia
On examination, Epiglottis is red but not swollen.
Lateral neck x-ray negative for thumb sign. A posterior-anterior view
of the neck may demonstrate a classic “Steeple” sign in only 50%
cases (a narrowed column of subglottic air)
73. “Steeple” Sign
The arrow points to
the narrowed column
of subglottic air ( due
to subglottic edema).
A lateral neck x-ray in
croup may show
overdistended
hypopharynx
74.
Treatment
Mild cases Humidified air at home, use humidifiers ( humidity can
reduce subglottic edema). If child is hypoxic or cyanotic hospitalize
use humidified oxygen
Moderate to severe cases Racemic epinephrine by nebulizer &
Systemic Corticosteroids ( dexamethasone).
With nebulized epinephrine and dexamethasone, improvement can be
seen in 2 to 3 hours. Observe for improvement and if improves,
discharge home.
DO NOT GIVE ANTIBIOTICS
Indications for admission in Croup:
Croup
Child less than 1 year
Cyanosis
No improvement/ worsening despite above therapy
Worsening stridor/ accessory muscle use ( intercostals, neck muscles)
Decreased alertness
Follow-up cannot be guaranteed
Use of racemic epinephrine and corticosteroids has almost eliminated
the need for intubation. However, if no improvement seen and if there is
evidence of worsening respiratory compromise despite above therapies
intubation
In severe croup that failed to respond to racemic epinephrine use
Heliox ( mixture of helium and oxygen)
75. Q
A 2 year old boy is brought to the emergency department with
complaints of throat pain, inability to swallow and drooling. The
throat pain, difficulty swallowing, and drooling started in the
afternoon and have worsened over the night. There is mild cough
and nasal congestion for 2 days now. His past history is significant
for frequent ear infections. Mother is not very sure if he received all
his immunizations. On examination, he looks tired, his temperature
was 102F, blood pressure 100/60, respiratory rate was 32 with
some accessory muscle use, saturating 100% on room air. He
coughs occasionally. Rest of the physical exam is benign. A lateral
neck x-ray was negative. CBC reveals leucocytosis with left shift.
The most appropriate next step in management:
A. Ceftriaxone
B. Examination of epiglottis by tongue depression
C. Racemic epinephrine
D. Corticosteroids
E. Laryngoscopy followed by Urgent intubation
F. Humidified air
76. Ans. E
Presence of dysphagia, drooling, absence of
typical “barky” cough and CBC with left shift
favors Epiglottitis more than Croup.
A negative lateral neck x-ray does not rule out
epiglottitis.
First step is always intubation ( patient is already
in distress with respiratory rate 32)
Next step after securing airway is Ceftriaxone.
Racemic epinephrine and corticosteroids are
contraindicated in epiglottitis.
77. Q2
A 2 year old girl presents to the emergency room with
fever, cough, runny nose, stridor and difficulty breathing.
The child has been having nasal congestion and
rhinorrhea for past 3 days. Temperature is 101, RR 30.
No cyanosis. Child looks restless and anxious. She has
an audible continuous stridor even at reat and a barky
cough. On examination, she has bilaterally significantly
decreased breath sounds and moderate intercostal
retractions. The most appropriate next step in
management:
A. Humidified air
B. Humidified oxygen
C. Laryngoscopy followed by Urgent Intubation
D. Racemic Epinephrine and Dexamethasone
E. Ceftriaxone
78. Croup Score
Calculate Croup score to determine whether croup is mild, moderate or severe then take a decision on treatment.
Scoring
Level of Consciousness
Alert: 0
Restless, anxious: 2
Disoriented : 3
Cyanosis
None: 0
When crying : 2
At Rest: 3
Stridor
None: 0
With Agitation: 1
Intermittent at Rest: 2
Continuous at rest : 3
Air Entry
Normal: 0
Decreased: 1
Moderately decreased: 2
Severely decreased : 3
Retractions
None: 0
Mild: 1
Moderate: 2
Severe: 3
Interpretation of score
Very mild < 2
Mild to moderately severe – 2 to 9
Severe croup > 9
PRESENCE OF PULSUS PARADOXUS INDICATES SEVERE CROUP
NO NEED TO REMEMBER EVERYTHING, REALIZE THE COMPONENTS OF SCORE AND QUICKLY
ASSESS SEVERITY IN THE QUESTION !!
79. Ans.D
This is a severe croup.
For moderate to severe croup, use
Racemic epinephrine + steroids
For Mild croup use Humidified air. If
child hypoxic – use supplemental oxygen,
humidified.
Intubation used only if racemic
epinephrine+ steroid combination fails to
improve symptoms.
82. Congenital Heart Disease
Common Etiologies
Cyanotic Congenital Heart Disease (5 T's)
Transposition of the Great Vessels
Tetralogy of Fallot ( decreased pulmonary circulation on cxr)
Tricuspid valve atresia
Total anomalous pulmonary venous return
Truncus arteriosus
Acyanotic Congenital Heart Disease: Left to right shunt
Ventricular Septal Defect – pan systolic murmur
Atrial Septal Defect – fixed split of s2
Patent Ductus Arteriosus – machinary murmur
83. Causes of Pediatric CHF–
Remember age of presentation!
Presentation: Week 1
Arteriovenous fistula
Aortic Coarctation (Interrupted aortic arch)
Decreased pulses
Left Ventricular Hypertrophy
Hypoplastic left heart Syndrome
Asymmetric pulses
Aortic Stenosis
Increased Pulses
Most common CHF cause in first week
Decreased pulses
Right Ventricular Hypertrophy
Hyperactive precordium
Myocarditis
Decreased pulses
Right Ventricular Hypertrophy
Decreased precordium
84. Causes of Pediatric CHF
Presentation: Weeks 2 to 4
Acyanotic (PaO2 >150 on 100% O2)
Onset occurs with drop in pulmonary vascular resistance Pressure
drops allowing left to right shunt
Coarctation of Aorta Most common CHF cause in first 2-4 weeks
Aortic Stenosis
Myocarditis
Patent Ductus Arteriosus
Arteriovenous fistula
Ventricular Septal DefecT
Cyanotic (PaO2 <150 on 100% O2)
Hypoplastic left heart Syndrome (Uniformly fatal)
Total Anomalous pulmonary venous return
Truncus arteriosus
Transposition and VSD
Tricuspid atresia and VSD
Single Ventricle
86. Causes of Limp in Kids
Age under 2 years
Ages 3-5 years
Toxic or Transient Synovitis (most common)
Ages 5-9 years
Congenital Hip dysplasia (most common)
Toddler's Fracture
Tibial Stress Fracture
Cerebral Palsy
Legg-Calve-Perthes Disease (most common)
Muscular Dystrophy
Ages 11-16 years
Slipped Capital Femoral Epiphysis (most common)
Legg-Calve-Perthes Disease
Juvenile Rheumatoid Arthritis
Osteochondritis Dissecans of the Knee
87. SCFE
Occurs during maximal pubertal growth spurt - age 13 to 15 years
in males and age 11 to 13 years in females
Most common hip disorder in adolescents
Blacks are more affected
Child is usually overweight/ obese
Mechanism – Femoral epiphysis can slip before the closure of
epiphyseal plate
Signs Hip is held in abduction and external rotation and
internal rotation is extremely limited
Dx: clinical and then,obtaion Hip XRay may show Widened
epiphyseal plate and displacement of femoral head
Management – SCFE is an Orthopedic Emergency!
Immediately hospitalize and schedule internal fixation
Use spica hip casting for 6 to 8 weeks Decreases risk of Femoral Neck
Fracture and protects epiphyses
In case of severe chronic Slipped Capital Femoral Epiphyses , osteotomy
needed to realign and stabilize
88. Leg-Calve Perthes Disease
Osteonecrosis of the femoral head
Age group affected : 4 to 9 yrs
Exam reveals trendelenberg gait and
internal rotation is affected
Diagnosis : x-ray hip
Orthopedic consult
89. Transient Tenosynovitis of the Hip
Most common cause of limp and hip pain
in children under 10 yrs of age
Afebrile, non toxic child
ROM of hip – abduction, internal/external
rotation are affected
ESR only slightly elevated, Arthrocentesis
fluid clear. ( unlike septic cases
Make sure to rule out septic arthritis
90. Congenital Dislocation of Hip
Common in girls > boys
Common with breech deliveries
Screen all kids with ortolani & Barlow
maneuvers
Ultrasound is confirmatory
Management – Very Important
94. Diverticultis
Left lower quadrant pain, tenderness,
leucocytosis, fever +/Complications LGI bleed, perforation –”walled
off”, diverticular abscess, sepsis, shock ( ?
Imaging, ?when ) ( when someone has
pneumaturia it’s a complicated diverticulitis)
Medical management – NPO, ivf, antibiotics
Surgery : only for complicated diverticulitis
( abscess, perforation) or recurrent diverticultis >
1 episode ( i.e; surgery should be considedered
following 1st episode)
95. Emergency Surgery in Diverticulitis
Stage patients with acute diverticulitis and perforation
with the following classifications:
Stage I: confined pericolic abscess
Stage II: distant abscess (retroperitoneal or pelvic)
Stage III: generalized peritonitis (noncommunicating)
Stage IV: fecal peritonitis (communicating)
Treat patients according to their respective stage:
In patients with Stage I abscess, begin with conservative therapy
but individualize treatment as needed, noting that abscesses <2
cm and confined to the mesocolon are most likely to respond to
conservative therapy
In patients with Stage II abscess or nonresolving Stage I
abscess, carry out surgical or percutaneous drainage under
radiological guidance ( consider percutaneous drainage if pt is
too unstable to undergo surgery)
Send patients with peritonitis (Stage III or IV) to surgery as soon
as possible
96. Elective Surgery - diverticulitis
Consider elective colon resection in patients
who:
Have had two resolved episodes of acute
diverticulitis
Are under age 40 ( its believed that
complication rate is high in the young)
Are immunocompromised
97. Prognosis counselling - diverticulitis
Counsel patients that:
Only 10% to 25% of patients with diverticula will
ever develop acute diverticulitis
Only one third of patients will ever develop a
recurrence following a single episode of acute
diverticulitis
Patients are less likely to respond to medical
therapy with each recurrent episode of acute
diverticulitis
Surgery should be considered following the
second episode of acute diverticulitis
98. Follow Up - Diverticulitis
Follow-up
Colonoscopy 6 weeks after diverticulitis
episode
Define extent of Diverticulosis
Evaluate for Colon Cancer
Barium Enema may be used as alternative
option
99. Cholelithiasis
Remember indications for emergency
surgery vs. Elective surgery
When do you do percutaneous drainage
of gall bladder
When do you ERCP with Stenting –
elective vs. emergent
