Infection and Tropical Diseases

The Study of Pediatric Infectious Diseases

Why is there a need to know pediatric infectious diseases?
We live in a germ filled world. Microbes of infinite variety and
complexity colonize our body surfaces and orifices.

Infectious diseases will continue to plague human beings as

long as they live in the world we know.
Infectious problems cut across every discipline and
subdiscipline of medicine.

What is the responsibility of a physician in relation to treating

infectious diseases?
The task of the physician is to meet these challenges with confidence
borne of increased understanding of the principles of microbiology and
immunology and of how these principles are essential to rational
decision-making in the clinical areas.
Causes of 105 million deaths among children <5 in
developing countries, 1999

Ten Leading Causes of Morbidity

No. and Rate/100,000 Population, Philippines, 2002

Special Problems of Children

1. First exposure

Exposure to an agent for the first time often

produces fever and a severe illness

Reexposure likely to produce a mild illness,

modified by the serum antibodies from the first
infection
2. Small passages

The smaller passages are more easily obstructed by

edema or secretions
3. Young cells

Rapid growth rates of cells (e.g., fetal tissue) make

cells more susceptible to infection with most viral
agents

Decreased interferon production may be observed

in young cell cultures and newborn animals
4. Immature immunologic defenses

IgM are not usually synthesized by the fetus unless

exposed to maternal infection

Other immature immunologic functions in the

newborn
o Decreased complement activity
o Decreased neutrophil chemotaxis
o Less effective cell-mediated immunity

1 - Pediatrics 2

Clinical Approach to Infectious Diseases Basic Tenets

1. Infectious diseases intertwined with microbiology
o Immunology, virology and genetics
o Microbiology concentrates on the study of
microorganisms
o Discipline of infectious diseases concerns itself with
the study of patients
2. All living cells appear to be parasitized by microbes
throughout their lifetimes
o The infection of all external and many internal
surfaces of man begins at birth and results in
indigenous microbiota, or normal bacterial flora
3. Pathogenesis both of virulence of infecting microbes and of
defense of invaded host
o Clinically manifest infectious disease usually
develops as a consequence of transitory breakdown
of host defense mechanisms instead of coincidental
exposure to and colonization by organisms
possessing specific disease-producing attributes
rendering them pathogenic
4. In-depth knowledge of the immune system indispensable in
understanding the basic nature of management and
prevention of human diseases
o Our understanding of host immune defense
mechanisms is opening a new era of immunologic
therapy (e.g., immunoglobulins)
5. Microbial infection may be responsible for most human
diseases
o Conventional viruses (e.g., measles and rubella)
responsible for certain neurologic disorders
o Atypical infectious agents found to be the cause of
progressive degenerative CNS disease
(e.g., scrapie and kuru, Creutzfeldt-Jacob disease)
Two Approaches to the Study

Etiologic Agent Approach

o Student learns to identify the characteristics of the
infecting organism and the disease it may cause
o When clinical experience begins, he must shift
viewpoints in terms of

Anatomic Syndrome Approach

o Can be defined in purely empirical and mutually
exclusive terms and a patients illness often can be
classified into a single anatomic syndrome

Etiologic Agent vs. Anatomic Syndrome

1st semester || AY 2012-2013

rainwater@mymelody.com

The Diagnostic Process

It is important to make the anatomic syndrome diagnosis

before trying to determine the specific etiologic agent

Clinical diagnosis is an intellectual process in analyzing a

patients disease
o A judgment that begins when the patient is first
seen; observed signs and symptoms and ends when
the diagnosis cannot be refined further
Steps in Diagnosis

History and physical examination

o The experienced clinician forms a hypothesis or
tentative diagnosis from the given history
o The physical examination can be completed in a
brief period relative to the disease suspected

Working or presumptive diagnosis

o Basis for laboratory exams and therapy
Approach to Diagnosis by Symptoms and Signs

Fever of unknown origin

Fever and seizures

Fever and lymphadenopathy

Fever and abdominal pain

Fever and diarrhea

Fever and hepatosplenomegaly

Fever and limp

Fever and neutropenia

Fever and petechiae

Fever

Elevation of body temperature to above normal

(37.4C orally or 38C rectally)
Challenge
o To establish the causative agent distinguish viral
from bacterial disease
o Identify the site of a localized infection

Temperature Variability

Individual to individuals

Diurnal variation in temperature

o Circadian rhythm

Oral, axillary or rectal temperatures

Responses among children and adults

Physiological and pathologic states causing fever

Physiologic Fever States

Digestion

Exercise

Ovulation

Pregnancy

Warm environment

Emotion

General Approach to the Child with Possible Infection

A. Detailed history and PE is essential
a. History:

Present illness, significant medical

history, travel and animal contact,
medications, unusual food ingestions and
risk of infection with HIV (e.g., IVDU,
remote history of blood transfusion,
unprotected sexual intercourse)
b. Comprehensive physical examination:

Special attention to general appearances,

rashes, skin manifestations of
endocarditis, hepatosplenomegaly,
evidence of joint effusion, lymph node
enlargement
B. Use of the laboratory:
Pathogens identified through:
a. Direct methods

Cultures of bacteria and viruses

Microbiologic stains, including:

Gram stain

Ziehl-Neelsen stain (AFB)

Silver stain (fungal elements)

Wright stain (stool WBCs)

Fluorescent antibody-antigen staining for

HSV1 & 2, VZV, RSV, Influenza A and B,
parainfluenza

Direct observation including wet mount

for fungal elements, dark-field
microscopy for T. pallidum

PCR
b. Indirect methods

Intradermal skin testing for

Mycobacterium tuberculosis and
Coccidioides immitis

Antibody testing for viruses: EBV, CMV,

VZV, HIV; Toxoplasma gondii, Bartonella
henselae and Mycoplasma pneumoniae
c. Nonspecific laboratory indications of infection
typically include elevation of acute-phase reactants:
CRP and ESR

2 - Pediatrics 2

Fever and Fever of Unknown Origin

Pathologic Causes

Infection

Inflammation (e.g., connective tissue disease)

Neoplasms

Vaccines

Dehydration
Common Causes of Fever
Minor Illnesses
URTI
Viral exanthema
Gastroenteritis

Major Illnesses
Bacterial meningitis
UTI
Pneumonia
Malaria

Mechanisms of a Protective Effect of Fever

Enhanced neutrophil migration

Increased production of antibacterial substances by

neutrophils

Increased production of interferon

Increased antiviral and antitumor activity of interferon

Increased T-cell proliferation

Decreased growth of microorganisms in iron-poor

environment
Extreme Hyperpyrexia (>41C) and Hypothermia
Extreme Pyrexia
Hypothermia
Central fevers
Elderly and the newborn
(neoplastic, trauma, or infection)
(poikilotherms)
Drug fever
Cold exposure
Heat stroke
Hypothyroidism
HIV
Overwhelming infection
Malignant hyperthermia
Sepsis in CRF
Malignant neuroleptic syndrome
Overzealous treatment
with antipyretics
Pathogenesis of Fever

1st semester || AY 2012-2013

rainwater@mymelody.com

Fever Patterns

Intermittent exaggerated circadian rhythm that includes a

period of normal temperature on most days
o High spikes with return to normal

Remitting persistent and varies by more than 0.5C for >24

hours (like intermittent but never returns to normal)

Sustained persistent and does not vary more than 0.5C for
>24 hours (like remittent but with less marked swings of
temperature)

Relapsing febrile periods that are separated by intervals of

normal temperature
o Tertian 1st and 3rd days (P. vivax)
o Quartan 1st and 4th days (P. malariae)
Spectrum of Fever Syndromes

Fever without localizing signs

Fever of short duration associated with infection

Recurrent and prolonged fever associated with infection

Fever with a rash

Fever in association with a chronic disease

Fever associated with a collagen diseases

Fever associated with malignancy

Drug fever

Factitious fever

Hospital-acquired
Classic Working Definition

Continuous fever of at least 3 weeks duration with daily

temperature elevation above 38.3C and remaining
undiagnosed after 1 week of intensive study in the hospital
Working Definition (Pediatric)

Fever >38C persisting as a predominant feature for more

than 7-10 days in a child in whom a careful, thorough history
and physical examination and preliminary laboratory data
fail to establish a diagnosis
Fever of Unknown Origin in:
Infectious Causes
Common
Mastoiditis (chronic); Sinusitis
Salmonellosis
Subdiaphragmatic abscess
Cytomegalovirus, EBV, Hepatitis viruses
Tuberculosis
Malaria
VLM
Uncommon
Perinephric abscess
Pyelonephritis
Psittacosis
Rare
Disseminated Histoplasmosis
Toxoplasmosis
SBE
Leptospirosis

Noninfectious Causes
Common
Leukemia
Lymphoma
JRA
SLE
Periodic fever

Uncommon
Polyarteritis nodosa
Neuroblastoma
Serum sickness
Rare
Pancreatitis
Drug fever

Etiology
1. Infectious causes
2. Collagen-vascular

Juvenile rheumatoid arthritis

SLE

HSP

Vasculitis
3. Malignancies/Neoplasms

Occult solid tumors (neuroblastoma,

Wilms tumor, retinoblastoma)

Hematologic tumors
(leukemia, lymphoma, Hodgkins)
4. Miscellaneous

Factitious fever

Metabolic (drug fever, milk allergy,

dehydrated diabetes insipidus)

Genetic (familial Mediterranean fever,

Caffeys disease, hypothalamic
dysfunction, hemoglobinopathy crisis)
5. Unknown/undiagnosed

40-50%
10-20%
10%
3%
1%
1%
5-10%

What is the Eventual Etiology of FUO in Children?

No. of Cases
Infection
198
Respiratory
102
Others
96
Collagen disease
57
Inflammatory bowel disease
7
Neoplasm
25
No diagnosis
48
Resolved
56
Miscellaneous
54

Infectious

Most frequent
o Typhoid fever, malaria, disseminated/miliary TB,
UTI, hidden (cryptic) abscesses, septicemia

Typhoid fever
o Stepladder pattern (sustained, progressive)
o Fever will not be shorter than five days to a week
o Faget sign pulse-fever disproportion
Differential Diagnosis
Salmonella Infection (Typhoid Fever)

Seriously and obviously ill with no apparent cause

Abdominal tenderness

Shock

Confusion

Child with sickle-cell disease

Osteomyelitis/arthritis infant

Anemia associated with malaria

Malaria

Residence in an endemic area

Blood film positive
Severe anemia
Enlarged spleen
Jaundice

Miliary (Disseminated) Tuberculosis

Weight loss

Anorexia, night sweats

Systemic upset

Enlarged liver and/or spleen

Cough

Tuberculin test positive or negative

Sterile pyuria

X-ray shows very widespread small discrete shadows in both

lung fields

Sequel of hematogenous dissemination of the organism,

which may develop in the post-primary phase or in patients
with long-standing latent infection

Also encountered in patients with immunosuppression

Pyelonephritis

CVA or suprapubic tenderness

Crying on passing urine

Passing urine more frequently than usual

Incontinence in previously continent child

White blood cells and/or bacteria in urine on microscopy

Abscess

10-15%

20-30%

% of Cases
44.4
22.9
21.7
12.8
1.6
5.6
10.7
12.6
12.1

Fever with no obvious focus of infection (deep abscesses)

Local tenderness or pain
Fluctuant mass
Specific signs depend on site subphrenic, psoas, lung, renal,
retroperitoneal
Follows surgical operations or manipulation/
umbilical catheterization

Septicemia

Seriously and obviously ill, highly-febrile child with no focus of

infection

Purpura, petechiae

Shock or hypothermia in a young infant

(+) blood cultures

Adage
FUO is more likely to be caused by an unusual presentation of a
common disorder than a common manifestation of a rare disorder.

3 - Pediatrics 2

1st semester || AY 2012-2013

rainwater@mymelody.com

Evaluation
History

Thorough history essential

Careful description of the fever pattern
Attention to associated findings at the time of fever, including
tachycardia, skin warmth, and diaphoresis

Approach to the Diagnosis

Exclude factitious fever

Observation of fever in the hospital for 48 hours without

antipyretics and observing the pattern

Laboratory studies should be organized towards the most

likely diagnosis after complete history and physical
examination

Exposure to ill contacts

Animal exposure
Travel history (recent and remote)
Dietary history (raw meat/fish ingestion;
unpasteurized milk; pica)
Family history (genetic-ethnic background)

Laboratory

The most broadly-based, highest-yield, and most

cost-effective testing is done first, and the lowest-yield, most
esoteric testing is done last if no diagnosis is made despite
persistence of symptoms

Directed toward the most likely diagnostic studies

History of Exposures
Ill persons
TB, salmonellosis, viral
Animals
Zoonosis, bartonellosis (cat scratch disease),
leptospirosis, toxoplasmosis
Travel
Malaria, fungi, others
Food
Trichinosis
Soil
VLM, toxoplasmosis
Drugs
Drug fever (antibiotics)
Insects
Rickettsia, malaria, others
Clues in the History that may Localize the Infection
Sore throat
Strep tonsillitis
Cough, rusty sputum
Lobar pneumonia
Severe joint pain/swelling
Pyogenic arthritis
Severe pain in head and back of the neck
Meningitis
with stiffness
Severe pain in a bone
Osteomyelitis
Tender liver
Amebic liver abscess
Viral hepatitis
Ill-defined subcutaneous inflammation
Cellulitis, pyomyositis
Bloody diarrhea
Shigella, Campylobacter
Chronic Diseases
Congenital heart diseases
Cyanotic heart disease
Rheumatic fever
Shunted hydrocephalus
Chronic renal disease
Congenital or acquired
immunodeficiency
Recent surgery

Complications
Bacterial endocarditis
Cerebral abscess
Bacterial endocarditis
Recurrence of RF
Shunt infection
Ventriculitis, septicemia
Urinary tract infection
Opportunistic organisms, fungi,
parasites
Concealed abscesses

Physical Examination

Complete, detailed, thorough and diligent

Repeated frequently. Constant reassessment for specific focal

signs can pick up growing tumors/masses/abscesses, changing
murmurs or early jaundice

Look for a focus of infection or findings to suggest an occult

infectious process; findings suggesting a non-infectious
disease

Scalp

Pallor

Eyes

Jaundice

Fundi

Rashes/purpura

Ear drums

Mucocutaneous manifestations

Nose
of systemic diseases

Throat

Murmurs or changing murmurs

Gums

Abdominal masses or tenderness

Teeth

Hepatomegaly

Sinuses

Splenomegaly

Bones

Lymphadenopathy

Joints

Muscles

External genitalia,
pelvic organs

Urine

4 - Pediatrics 2

Temperature Chart

Document genuine fever

Clues often overlooked or their significance not appreciated

o Review by someone without prior knowledge of
previous finding simportant

Discern fever pattern

Laboratory Data and Ancillary Procedures

Preliminary
o CBC with differential count, platelet count
o ESR
o Aerobic and anaerobic blood cultures
o Urinalysis and urine culture
o Chest x-ray film
o Tuberculin test
o Serologic testing useful in salmonellosis,
brucellosis, tularemia, rickettsial infections
o Any other tests indicated by the history or physical
findings

Analyze all data

How helpful are CT scans and nuclear medicine studies to determine
diagnosis?

Minimally
o In prospective study of 109 patients with FUO,
scanning procedures have very low utility in the
absence of clinical findings that suggested a
localized process
o Bone marrow examination had little value when
hematologic abnormalities were lacking in the
peripheral blood
Treatment

Stop all medications

Therapeutic (empirical) trials

o Suspected disseminated TB
o Systemic JRA
o Malaria
o Rheumatic fever
o Culture-negative endocarditis

Diagnosed conditions treat accordingly

1st semester || AY 2012-2013

rainwater@mymelody.com

Gram-Positive Organisms Causing Pyogenic and other Infections

1.

2.

Staphylococcus species
a. S. aureus
b. S. epidermidis
Streptococcus
a. S. pneumonia (Pneumococcus)
b. Group A Streptococcus (S. pyogenes)

Staphylocccus species

Aerobic cocci that grow in pair or clusters

Either coagulase-positive (S. aureus) or coagulase-negative (S.

epidermidis, S. saprophyticus, S. haemolyticus)

Part of the normal flora of humans

Pathogenesis

Disease may result from tissue invasion or injury caused by

various toxins and enzymes produced by the organisms

Virulent factors
o Loose polysaccharide capsule (slime layer)
o Coagulase (clumping factor)
o Protein A
o Catalase, Panton-Valentine leukocidin (PVL),
hemolysins
o Penicillinase or -lactamase
o Exotoxins ( Exfoliatin A and B)
o Enterotoxins (A, B, C1 , C 2 , D, E)
o Toxic shock syndrome toxin-1 (TSST-1)
Staphylococcus aureus

The most common cause of pyogenic infections of the skin

and soft tissue
o Impetigo, furuncle (boils), cellulitis, abscess,
lymphadenitis, paronychia, omphalitis, and wound
infection
o Bacteremia osteomyelitis, suppurative arthritis,
deep abscesses, pneumonia, empyema,
endocarditis, pyomyositis and pericarditis

Toxin-mediated diseases
o Food poisoning
o Staphylococcal scarlet fever
o Staphylococcal skin scalded syndrome (SSSS)
o Toxic shock syndrome (TSS)
Clinical Manifestations

The signs and symptoms vary with the location of the

infection, which is most commonly the skin but may be any
tissue

Skin infections are more prevalent among person living in low

socioeconomic circumstances and particularly those in
tropical climates
Staphylococcus epidermidis
(Coagulase-Negative Staphylococci) (CONS)

Cause infections in patients with indwelling foreign devices

intravenous catheters, hemodialysis shunts and grafts, CSF
shunts, peritoneal dialysis catheters, prosthetic cardiac valves
and prosthetic joints.

Common cause of nosocomial neonatal infection

Impetigo contagiosa

Honey-colored crusts
Impetigo Contagiosa and Impetigo Bullosa

Impetigo contagiosa
o The classic lesion begin as erythematous papules in
traumatized areas. They quickly evolve into honeycolored crusted plaques with surrounding erythema
o GAS and S. aureus are the chief causative agents

Impetigo bullosa
o Exclusively staphylococcal in origin
o The characteristic lesion are caused by
epidermolytic toxin

Impetigo contagiosa

Impetigo bullosa

Other Staphylococcal Localized Skin Infections

Abscess

Cellulitis

Staphylococcal Pneumonia

Direct Invasion: Infections Originating from Hair Follicles

Folliculitis

Carbuncle

5 - Pediatrics 2

Furunculosis

Furunculosis

1st semester || AY 2012-2013

A.

5 year old child with S. aureus

pneumonia initially demonstrated
consolidation of the right middle and
lower zone.

B.

Seven days later, multiple lucent areas

are noted as pneumatoceles develop.

C.

Two weeks later, significant resolution is

evident, with a rather thick-walled
pneumatocele persisting in the right
midzone associated with significant
residual pleural thickening.

rainwater@mymelody.com

Toxin Mediated Disease: Staphylococcal Scalded Skin Syndrome

(Ritter disease)

Occurs predominantly in infants and children < 5yr of age

The onset of the rash may be preceded by a prodrome of

malaise, fever, and irritability associated with exquisite
tenderness of the skin or the appearance of generalized
erythema may be abrupt without preceding symptoms.

The erythematous skin may rapidly acquire wrinkled

appearance and sterile, flaccid blisters and erosions develop

Circumoral erythema or radial crusting and fissuring around

the eyes, mouth, and nose (sunburst pattern)

Areas of epidermis may separate in response to gentle shear

force (Nikolsky sign)

Caused by phage group 2 staphylococci, strains 71 and 55

Pathogenesis direct invasion

Common clinical syndromes otitis media, sinusitis,
pneumonia and sepsis (bacteremia)
The diagnosis is established by recovery of S. pneumoniae
from the site of infection or the blood.
Treatment
o Depends on severity, sites of infection, presence of
resistance
o Empirical treatment is based on susceptibility
pattern in the communities
o
Cefotaxime or ceftriaxone, Cefuroxime
(pneumonia & meningitis)

Pneumococcal Pneumonia
Chest X-ray of11 month old girl
showing a round, nodular
area of consolidation in the
midlung.

Sunburst pattern

Lateral view showing the

triangular consolidation in the
right middle lobe

Management of Staphylococcal Infection

Appropriate antibiotics
o Oral cloxacillin
o Parenteral oxacillin, Cefazolin, vancomycin
[MRSA]+ clindamycin

Incision and drainage

Other supportive measures (toxin-mediated)

o
fluid replacement
o Application of emollient
Streptococccus pneumoniae (Pneumococcus)

Gram positive, lancet-shaped polysaccharide encapsulated

diplococcus

Encapsulated strains cause most serious disease in humans

(otitis media, life threatening pneumonia, bacteremia, and
meningitis)

Capsular polysaccharides impede phagocytosis

Virulence is related in part to capsular size

Invasive strains 4, 6B, 9V,14, 18C, 19F & 23F

Most healthy individuals carry various S. pneumoniae

serotypes in their upper respiratory tract (>90% of children 6
mo and 5 yr)

Children <2 yr of age are susceptible to pneumococcal

infection because of decreased ability to produce antibody
against the T-cell independent antigens and the high
prevalence of colonization.

Pneumococcal co-pathogenicity may be important in disease

caused by other respiratory viruses (influenza)

High risk groups - Patients with sickle cell disease, asplenia,

deficiencies in humoral (B cell) and complement-mediated
immunity, HIV infection, certain malignancies (leukemia,
lymphoma),chronic heart, lung, or renal disease, CSF leak and
cochlear implants.

6 - Pediatrics 2

Group A Streptococcus (GAS) (Streptococcus pyogenes)

Gram-positive coccoid-shaped bacteria that tend to grow in

chains

Classified on the basis of the M protein antigen, the virulent

factor, located on the cell surface and in fimbriae - >100
serotypes

Types 1, 12, 28, 4, 3, and 2 the most common causes of

uncomplicated streptococcal pharyngitis

M types associated with pharyngitis rarely cause skin

infections

M types associated with skin infections rarely cause

pharyngitis

Pharyngeal strains (M type 12) is associated with

glomerulonephritis, while others are associated with
rheumatic fever

More of the skin strains (M types 49, 55, 57 and 60)

nephritogenic

Produces a large variety of enzymes and toxins (Streptococcal

pyrogenic exotoxins A, B, and C)

Common cause of infections of the upper respiratory tract

(pharyngitis) and the skin ( impetigo, pyoderma) in children

Also cause distinct clinical entities (scarlet fever and

erysipelas), as well as toxic shock syndrome and necrotizing
fasciitis

Causes potentially serious nonsuppurative complications:

rheumatic fever and acute glomerulonephritis

Pathogenesis: Direct invasion and toxin mediation

Diagnosis:
Throat swab culture or rapid antigen detection test

Non-specific pharyngotonsillitis

Highly suggestive of group A -streptococcal infection: palatal petechiae

1st semester || AY 2012-2013

rainwater@mymelody.com

Scarlet Fever

Toxin-mediated disease

Rash appears within 24-48 hours after onset of symptoms

Begins around the neck and spread over the trunk and
extremities

It is a diffuse, finely papular, erythematous eruption

producing a bright red discoloration of the skin, which
blanches on pressure.

More intense along the creases of the elbows, axillae, and

groin

The skin has a goose-pimple appearance and feels rough

The face is usually spared, although the cheeks may be

erythematous with circumoral pallor

After 3-4 days, the rash begins to fade and is followed by

desquamation

The tongue is usually coated and the papillae are swollen

(strawberry tongue)

An Overview of Mucocutaneous Symptom Complex

An exanthem is a skin eruption occurring as an integral part of an
infectious disease. The corresponding changes in the mucous
membranes is an enanthem.
Accurate diagnosis is not always possible on preliminary examination
judgment should be deferred until the rash develops.
Classification

Maculopapular eruption

Vesiculobullous or vesiculopustular

Petechial or purpuric eruption

Measles

Conjunctivitis with photophobia

Kopliks spots graying white dots usually as small as grains

of sand, with slight, reddish areola

Distribution of rash
o Starts behind the ears along the hairline, face the
spreads downward over the body
o More confluent on the upper part, discrete on the
lower part

Brownish discoloration and branny desquamation

Rubella (German Measles)

Distribution of rashes are similar to measles but they are

discrete and not associated with desquamation
o Rash starts from the trunk and spreads to the neck,
face and proximal extremities

Forchheimer spots red spots are often seen on the palate

Congenital Rubella Syndrome

Congenital defects occur in >80% of infants infected in the

first trimester and virtually no defects are identified in infants
infected after the first 16 weeks of gestation

Infants infected in the first trimester are more likely to have

multiple congenital defects, whereas those infants infected
after 11-12 weeks of gestation are more likely to have only
deafness or retinopathy

White strawberry tongue

Red strawberry tongue

Treatment of Streptococcal Infection

Non-invasive: Penicillin

Invasive: Penicillin + Clindamycin

Debridement

Clinical Findings in Congenital Rubella Syndrome

General: IUGR, hepatosplenomegaly, chemical evidence of

hepatitis

CNS: Mental retardation, behavioral disorders, hypotonia,

seizures, CSF protein

Cardiac: PDA, peripheral and valvular pulmonary stenosis,

aortic stenosis, VSD

Ocular: Cataracts, salt and pepper retinopathy, corneal

clouding, glaucoma

Orthopedic: Radiolucencies in long bones

Hematologic: Transient thrombocytopenia with purpura

Dermatologic: Blueberry muffin spots, dermatoglyphic

Endocrine: Diabetes in 2nd or 3rd decase

Prevention

Active immunization (15 months, 4-6 years)

Passive immunization for exposed pregnant woman

o Gamma-globulin (.55 mL/kg)
Enteroviral Exanthem
Infectious Mononucleosis

Exudative pharyngitis

Cervical lymphadenopathy

Hoaglands sign lid edema

Typical Serologic Findings Related to the Stage of EBV Infection
Stage of Infection
Presence of Antibody
Primary
VCA IgM or IgG (usually high)
EA (usually high), no EBNA
Convalescent or Past VCA IgG EA (low), EBNA
Reactivation
VCA IgG (high) EA (high), EBNA

7 - Pediatrics 2

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rainwater@mymelody.com

Fever with Vesicular/Bullous and Pustular Rash

Risk Factors for Progressive Varicella

Immunodeficiency

Malignancy

Corticosteroid therapy

Pregnant

Newborns

Adolescents and adults

Treatment

Neonatal varicella
o VZIG and acyclovir

Herpes zoster
o Acyclovir (oral) 20 mg/kg/dose max 800 tid to
shorten the course (optional)

Primary varicella
o Option of no treatment in a healthy child, unless
with complications treatment with IV acyclovir at
500 mg/m2 or 10 mg/k/dose every 8 hours for 7
days
Prevention

Varicella vaccine live attenuated vaccine given in 2 doses

(12-18 months and at 4-6 years)

Post-exposure prophylaxis options

o Varicella vaccine within 3-5 days from exposure
o VZIG within 96 hours from exposure (recommended
for immunocompromised children, pregnant
women, and exposed newborns)
o Pooled IVIG within 96 hours from exposure
Pathogenesis

Viral infection begins at a cutaneous portal of entry such as

the oral cavity, genital mucosa, conjunctiva, or breaks in
keratinized epithelia

Replicate in the sensory neurons, released in nerve endings

and replicate again on the skin

Viremia does not play a role in immunocompetent hosts

HSV Encephalitis

Leading cause of non-epidemic, sporadic encephalitis in

children and adults

It is an acute necrotizing infection involving the frontal and/or

temporal and limbic system.

Beyond the neonatal period, it is almost always caused by

HSV-1.

Symptoms are non-specific but focal signs are common. If

untreated, it can progress to come and death in 75% of cases.
Non-Polio Enteroviruses

Picornaviridae family

Very common viruses with a worldwide distribution

Produce a broad range of important illnesses

The genus name reflects the importance of the GI tract as a

primary site of viral invasion and replication and transmission
Enteroviral Exanthems
Maculopapular

Rubelliform
(Size 1-3 mm)

Roseola-like
(Size 5-15 mm)

Vesicular

Hand, foot
and mouth

Herpangina

Insect bite-like

Non-pustule
forming

Echovirus 9, also 2, 4, 11, 19, 25

Coxsackie virus A9
Echovirus 16 (Boston exanthema)
Echovirus 11, 25
Coxsackie virus B1, B5

Coxsackie virus A16,

also A5, A7, A9, A10, B2, B5
Coxsackie virus A22, also A1-A10, A16
Coxsackie virus A4; crops, last 1-2 weeks
Coxsackie virus, also Echovirus 11, 30

Petechial

Coxsackie virus B, A9; echovirus 9

Problem separating from meningococcemia

Hand, Foot and Mouth Disease

Most commonly caused by Coxsackie virus A16

8 - Pediatrics 2

The oropharynx is inflamed and contains scattered vesicles on

the tongue, buccal mucosa, posterior pharynx, palate, gingiva
and/or lips
Maculopapular/vesicular lesions appear in the hands/fingers,
feet. Lesions are tender and are common on the dorsal
surfaces but can also occur on the palms and soles.
HFMD caused by Enterovirus 71 is more severe with increased
rates of neurologic disease.

Herpangina

Sudden onset of fever, sore throat, dysphagia

Characteristic lesions present on the anterior tonsillar pillars,

soft palate, uvula and posterior pharyngeal wall, occasionally
posterior buccal mucosa

Discrete vesicles that ulcerate, surrounded by erythematous

rings

Resolves in 3-7 days

Cutaneous Bacterial Infection
Impetigo Contagiosa

Erythematous macules that very rapidly evolve into thinwalled vesicles and pustules

The vesiculopustular stage is brief and following rupture,

sticky, heaped-up, honey-colored crusts are formed

Risk factors: insect bites, scabies, cutaneous injuries, and

preceding dermatitis serve as portals of entry for the
organism, which does not penetrate intact skin

Caused by group A -hemolytic streptococcus or S. aureus

Non-bullous or bullous impetigo

o Bullous impetigo often caused by S. aureus, most
often phage group 2

Mainly an infection of infants and young children

Dengue Fever/Dengue Hemorrhagic Fever
Dengue Virus

Causes dengue and dengue hemorrhagic fever

Transmitted by mosquitos

Has 4 serotypes (DEN-1, 2, 3, 4)

Aedes aegypti

Dengue transmitted by infected female mosquito

Primarily a daytime feeder

Lives around human habitation

Lays eggs and produces larvae preferentially in artificial

containers
Clinical Characteristics of Dengue Fever

Benign syndrome

Biphasic fever

Headache

Myalgia

Arthralgia

Rash morbilliform, maculopapular

Leukopenia

Lymphadenopathy

Petechiae
Dengue Hemorrhagic Fever

Known as Philippine, Thai or Singapore hemorrhagic fever,

hemorrhagic dengue, acute infectious thrombocytopenic
purpura

Severe disease

Occurs where multiple types of dengue virus are

simultaneously or sequentially transmitted

Difference in severity is due to difference in immunologic

status

Characterized by:
o Thrombocytopenia
o Increased capillary permeability
o Coagulopathy
Phases of Dengue

Febrile phase. Fluid-like symptoms and dehydration

Critical phase. Cardiovascular compromise to shock from

leaky capillaries, thrombocytopenia and coagulopathy

Recovery phase. Reabsorption of fluid, may develop

hypervolemia in overly aggressive fluid management.

1st semester || AY 2012-2013

rainwater@mymelody.com

Suggested Dengue Case Classification and Levels of Severity

Course of Dengue Illness

Hemorrhagic Manifestations of Dengue

Skin hemorrhages: petechiae, purpura, ecchymoses

Gum bleeding

Nose bleeding

Gastrointestinal bleeding: hematemesis, melena,

hematochezia

Hematuria

Increased menstrual flow

Warning Signs for Dengue Shock
Four Criteria for DHF

Fever, or recent history of acute fever

Hemorrhagic manifestations

Low platelet count (100,000/mm3 or less)

Objective evidence of leaky capillaries

(excessive capillary permeability)
o Elevated hematocrit (20% or more over baseline)
o Low albumin
o Pleural or other effusions

Immunity

Incubation period is 4-10 days

Primary infection can produce a wide spectrum of disease

Individuals are protected from critical illness with other

serotypes following a primary infection for the first 2-3
months but with no long-term cross-protective immunity
Risk Factors that Determine Disease Severity

Secondary infection

Age

Ethnicity

Co-morbid chronic diseases: cardiac, pulmonary

Children in general are less able to compensate with capillary

leakage than adults
Severe dengue should be considered if the patient is from an area of
dengue risk presenting with fever of 2-7 days plus any of the following
features:

There is evidence of plasma leakage, such as:

o High or progressively rising hematocrit
o Pleural effusions or ascites
o Circulatory compromise or shock (tachycardia, cold
and clammy extremities, capillary refill time greater
than three seconds, weak or undetectable pulse,
narrow pulse pressure or, in late shock,
unrecordable blood pressure)

There is significant bleeding

There is an altered level of consciousness (lethargy or

restlessness, increasing or intense abdominal pain, jaundice)

There is severe organ impairment (acute liver failure, acute

renal failure, encephalopathy or encephalitis,
cardiomyopathy) or other unusual manifestations

9 - Pediatrics 2

Initial Warning Signals

Disappearance of fever

Drop in platelets

Increase in hematocrit
When Patients Develop DSS

3-6 days after onset of symptoms

Alarm Signals

Severe abdominal pain

Prolonged vomiting

Abrupt change from fever to hypothermia

Change in level of consciousness (irritability or somnolence)

Differential Diagnosis

Chickungunya (Africa, India, Southeast Asia)

Onyong-nyon (East Africa)

West Nile fever (Europe, Africa, Middle East, India)

Four arboviral diseases with dengue-like course without rash

o Colorado tick
o Rift valley
o Ross river
o Sandfly

Meningococcemia and rickettsial diseases

Conditions that Mimic the Febrile Phase of Dengue
Flu-like
Influenza, chikungunya,
infectious mononucleosis
Fever with Rash
Rubella, scarlet fever, meningococcal,
drug reactions
Diarrheal diseases
Rotavirus, other enteric infections
Infections
Acute gastroenteritis, malaria, typhoid,
leptospirosis, bacterial sepsis and
septic shock
Malignancies
Acute leukemia and other malignancies

1st semester || AY 2012-2013

rainwater@mymelody.com

Dengue Hemorrhagic Fever

Host Factors

Congenital deficiencies of complement components:

properdin, factor D and terminal components

Acquired complement deficiencies: SLE, nephrotic syndrome,

hepatic failure
Diagnosis

High index of suspicion

Isolation by culture from sterile sites: blood, CSF, synovial fluid

Gram stain and culture of petecchial or purpuric lesions

Gram stain of buffy coat of spun blood

Treatment

Drug of choice: Penicillin G 250,000 to 400,000 u/k/day

Cefotaxime and ceftriaxone alternative treatments

Supportive care fluids, vasopressor support, component

transfusions
Complications

Acute complications related to vasculitis, DIC and hypotension

Gangrene, adrenal hemorrhage, endophtalmitis, arthritis,

endocarditis, pericarditis, pneumonia, renal infarcts, avascular
necrosis of epiphyses

Deafness most frequent neurologic sequelae

(5-10% of children with meningitis)

Complications

Carditis

Encephalitis

Severe pleural effusion

End organ damage in severe shock CNS

Management

No hemorrhagic manifestations, patient is well-hydrated

home treatment

Hemorrhagic manifestations or hydration borderline

consider hospitalization

Warning signs (even without profound shock) or DSS

hospitalize
Meningococcal Infections

Caused by N. meningitides

Cell wall has lipid A-containing lipo-oligosaccharides, with

endotoxin and covered by polysaccharide capsule

At least 13 serotypes identified

Majority of diseases worldwide are caused by serogroups A, B,

C, w 135 and Y

Serogroup B most common in infants

Death usually occurs within 6-18 hours

Clinical Manifestations

Spectrum
o Occult meningococcal bacteremia

Fever with or without symptoms

o Meningitis develops in 58% of cases
o Acute meningococcemia

Meningococcemia

Purpuric viral exanthema

Petechial facial rash

Ecchymotic lesions

Poor Prognostic Factors

Mortality rate as high as 110%

Hypertension, hypothermia or extreme hyperpyrexia on

presentation

Purpura fulminans/ptechiae <12 hours

Seizures

Leukopenia and thrombocytopenia

Acidosis and high levels of endotoxin and TNF alpha

Prevention

Postexposure prophylaxis
o Rifampicin 10 mg/kg q12
o Ceftriaxone
o Ciprofloxacin

Quadrivalent vaccine; serogroups A, C, Y, W135

o Approved for children 2-10 years of age and adults
>55 years

Vaccine is unreliable in <2 years

Epidemiology

Endemic disease

Male predominance

Invasive disease is most common among young children

50% occur in <2 years old

o 9 cases/100,000 in the 1st year of life
o >25 cases/100,000 in the 1st 4 months of life

25% in people >30 years

Pathogenesis

Acquired via respiratory route

Nasopharyngeal colonization usually asymptomatic (because

it produces IgA protease)

Meningococcal pili attach to CD46 proteins that induces

microvilli formation and endocytosis of the microbe which
gain access to the bloodstream

These interactions lead to the production of proinflammatory

cytokines, activation of extrinsic and intrinsic coagulation
cascade

Capillary leak, DIC leads to multiple organ failure, septic shock

and sometimes death

Heart, CNS, skin, adrenals are all affected

Myocarditis >50% of patients

Diffuse adrenal hemorrhage (Waterhouse-Friderichsen

syndrome)

10 - Pediatrics 2

1st semester || AY 2012-2013

rainwater@mymelody.com

Meningitis
Acute
Acute bacterial
meningitis
Viral meningitis

Complications
1. Seizures
2. Subdural effusions
3. SIADH
4. Prolonged fever
5. DIC

Subacute/Chronic
TB meningitis
Fungal meningitis
Partially treated BM

Clinical Presentation

Meningitis produces increased ICP because of cerebral edema,

obstruction to flow and absorption of CSF and impairing
venous outflow

Newborn early and late onset infection

o Initial symptoms are non-specific
o Later: fever, seizures, bulging fontanel, shock

Older children fever, irritability, neck stiffness, seizures

Kernigs sign, Brudzinskis sign

Acute Purulent Bacterial Meningitis: Main Etiologic Agents

Newborn to 3 months
o Group B streptococci
o E. coli
o L. monocytogenes
o Enterococci
o S. pneumonia

3 months to 6 years
o H. influenzae, Type B
o S. pneumonia
o N. meningitides

>6 years
o N. meningitides
o S. pneumonia
Viral Meningitis (Aseptic Meningitis)

Usually accompanying the viral infection

Patient manifests signs of the viral infection, as diarrhea,

respiratory, mumps, measles, varicella

CSF is usually normal, or with slight increase in cells or protein

Treatment is supportive as the course itself is self-limiting

Diagnosis and Treatment

CSF analysis

Neuroimaging if with focal deficits or non-response to tx

Blood, tissue culture

Treatment: antibiotics, antiviral, Anti-Kochs

CSF Findings
Type
Appearance
Acute
Turbid
Bacterial
Viral

Clear, colorless

TB/
Fungal

Xanthochromic

WBCS
Increased with
PMNs
predominating
Normal or
slightly
increased
Increased with
lymphocyte
predominating

Glucose
Low

Proteins
Increased

Normal

Normal
or slightly
increased
Markedly
increased

Low

Lumbar Puncture and CSF Analysis

Opening/closing pressure

Appearance clear, colorless, xanthochromic, bloody, turbid,

purulent

White blood cell count and differential

Glucose concentration

Protein concentration

Gram stain, AFB stain, fungal stain

Culture

PCR
Treatment (Antibiotics used in the treatment of bacterial meningitis
depending on the age of the patient and possible agent)
Amikacin
Ceftriaxone
Nafcillin
Tobramycin
Ampicillin
Gentamicin
Penicillin G
Vancomycin
Cefotaxime
Meropenem
Rifampicin
Duration of Treatment

For uncomplicated PCN sensitive S. pneumonia meningitidis =

10-14 days

For resistant strep vancomycin

For uncomplicated N. meningitidis, IV PCN for 5-7 days

Uncomplicated H. influenza Type B 7-10 days

Gram (-) meningitis 3rd generation cephalosporin, 3 weeks

11 - Pediatrics 2

Sequelae
1.
2.
3.
4.

Epilepsy
Learning disability
Motor deficit
Visual/hearing
impairment

TB Meningitis
Three Stages
1. Prodromal fever, headache, irritability
2. Neurologic signs meningeal signs, decreased level of
sensorium
3. Coma, irregular respiration, rigidity, opisthonus

Diagnosis

Clinical: subacute course, (+) TB exposure, (+) tuberculin test

CSF: ground glass appearance with tendency to coagulate,

increased WBC with lymphocytosis, extrememly high protein,
low sugar

Acid fast staining (+), PCR, ELISA or latex agglutination antigen

Treatment

Quadruple anti-TB regimen (HRZ(S/E) 2 mos, HR 10 mos)

Steroids

Treat complications metabolic

Manage increased ICP, hydrocephalus

Encephalitis

Usually viral
1. Herpes simplex virus. Presents with signs of increased ICP,
infection and deterioration in consciousness. Tx: acyclovir.
2. Dengue encephalopathy/encephalitis.
3. Subacute sclerosing panencephalitis (SSPE). Subacute and
degenerative disease of the entire brain.
Symptoms: behavioral and personality changes, myoclonic
jerks, decrease in cognitive function.
Clinical Features

Subtle changes in behavior

Stage 1. Mild symptoms, fever, headache, irritability.

Stage 2. Myoclonus, jerks, but consciousness retained.

Stage 3. Involuntary movements disappear, rigidity, decreased

sensorium.

Stage 4. Critical stage with breathing and circulatory problems

and death.
SSPE
Diagnosis
Clinical course
(+) measles antibody in the CSF
Characteristic EEG findings

Treatment
No treatment
Antiviral drugs under investigation
Supportive care

Pseudotumor Cerebri

Condition characterized by increased ICP, normal CSF cell

count and protein, normal ventricular size documented by MRI

Causes: metabolic, steroid therapy, hypervitaminosis A,

obesity, intake of tetracycline, among others

Clinical features: headache, diplopia, papilledema

Diagnosis: CT, MRI, lumbar tap, CSF analysis

Treatment: determination of the underlying cause, decreased

ICP, specific treatment

1st semester || AY 2012-2013

rainwater@mymelody.com

Pediatric Neurology:
Seizures in Children
Rosalinda Q. de Sagun
October 4, 2007
** Notes in red are from whoever owned the handout I photocopied.
Thank you! :3
Seizures
- Refers to excessive neuronal discharge with change in motor
activity or behavior (but not always motor manifestation
- Not a diagnosis but a SYMPTOM of an underlying CNS disorder
Convulsions
- Refers more to motor attacks
Partial Seizures
- Classification depends on site and size of focus
- Focal lesions in brain
- From one side/part of brain
A. Simple partial seizures
- Maintained consciousness; may verbalize during the seizure
- Motor (Jacksonian marchfinger, hand, arm, shoulder, face),
sensory (numbness in one area), autonomic, psychic
- Pins and needles somatosensory
- No automatism
- Often referred to as auras which may consist of an abnormal
sensation (e.g., smells, flashing lights) & experimental
phenomena (e.g., dj vu)
- Presence of auras always suggests a focal onset of seizure
- If seizure is restricted to a small area in the motor cortex, there
is focal clonic activity
B. Complex partial seizures
- Also known as temporal lobe seizures (no longer used) &
psychomotor seizures
- With impairment of consciousness (usually starts at prolonged
blank stares; confused, prolonged dream-like state)
- Most often behavioral manifestations (violent, disoriented,
talking nonsense)
- Involves association fibers
- Temporal & partial cortex lesions
- Parietal, frontal, temporal, etc. can also present as this
- With automatism (common feature in children and infants
develop after LOC)
- May begin with a simple partial seizure; when the seizure
activity spreads, there may be impaired consciousness leading
to a complex partial seizure
- Interictal EEG
- (+) aura
- May remember start and end of seizure
C. Partial seizures with secondary generalization
- Spreading of the epileptiform discharge during CPS
- Simple or complex evolving to GTC
Generalized Seizures
- Due to a diffuse lesion in the brain
- Both hemispheres
- Usually from thalamus
- Always with loss of consciousness
A. Absence seizures
- Attacks of fixed blank stares (sometimes with automatisms)
- Always with loss of consciousness
- Typical (usually very short duration; no longer than 30 seconds)
or atypical, only in seconds therefore person does not fall on
the ground
- With automatic movements such as grimacing
- Preschool & early school age renders to have poor academic
performance
- Can occur 20x a days
- Diagnosis: EEG2-3 cycles/sec + manifestations =
typical/atypical, EEG not characteristic
- (-) aura
- (-) post-ictal
- Hyperventilation for 3 minutes can activated absence seizures
- Generalized 3-4 Hz slow spike and wave discharges

12 - Pediatrics 2

B. Tonic clonic
- Grand mal seizure
- e.g. Petit mal/Benign febrile seizure (most benign)
- Most dramatic eyes roll upward/back, entire body
musculature undergoes tonic contractions, rapidly become
cyanotic in association with apnea
C. Tonic
- Extension
D. Clonic
- To and fro movement; seizure
E. Myoclonic
- Sudden jerky movements shock like contractions
- Difficult to treat; use 1 or 2 anticonvulsants
- Can be a seizure or not
- May be a presenting symptom of a hereditary inborn error of
metabolism/ metabolic disease
- Poor prognosis (hard to treat & with underlying abnormality)
Infantile Spasm

Severe epileptic syndrome (lifetime)

Very brief; (-) impairment of consciousness

F. Atonic (Astatic)
- drop attack prone to injury
- Sudden loss of muscle tone, sudden drop down
- Must be differentiated from syncopal attacks
- With no risks or predisposing factors
G. Infantile spasms
- Salams seizure like saluting
- Jerky movements
- Attacks are myoclonic; spasm is flexion/bending
- Very poor prognosis & difficult to treat
- May be seen in babies with previous asphyxia
- Part of the West syndrome
H. Unclassified seizures
- Neonatal seizures rowing movement, grimacing, apnea
- Subtle seizures of the newborn
Notes:
Automatism alimentary including lip smacking, chewing,
swallowing, excessive salivation (infants)
semi-purposeful, incoordinated & unplanned gestrural
automatisms like picking & pulling at clothing (older children)
Seizure-like Events
A. Night terrors
- Sleep disorder
- Wakes up in the middle of the night, does not recognize
parents, does not know what is happening, does not remember
anything the next morning
- Related to stress during the day
- In contrast with nightmares in which case you remember
your dreams
- Like seizures seizures usually occurs during sleep
- Usually seen in school-age children
B. Breath-holding spells
- infants cry holds breath becomes cyanotic (inadequate
H20)
- difficult to manage
- check blood Hgb, if low give Fe
- do not give anticonvulsants
C. Syncopal attacks
- Usually in adolescence
- Related to stress, heat & environment; Autonomics
D. Shuddering attacks
- gigil
E. Pseudoseizures
- adolescents, psychogenic
F. GERD
Note: To differentiate : EEG

Causes of Seizures
Non-neurologic
Metabolic disorders
Electrolyte imbalance (Na, Mg, Ca)
Hypoglycemia (esp. newborn)
Hypoxia
Fever (benign febrile seizure)
Systemic infections (UTI, Roseola
infantum)
Toxins
Drug-related (INH low Vitamin B6
pyridoxine)
*Non-neurologic is easier to confirm

Neurologic
Tumors
CNS malformations
Vascular disorders
Idiopathic epilepsy
CNS infections

Epilepsy
- Recurrent episodes of afebrile seizures
- >2 unprovoked seizures occur at an interval >24 hours
- First attack of unprovoked seizures may not result into epilepsy
- Type depends on the predominant seizure type e.g. grandmal, petit
mal
Status Epilepticus
- Continuous seizures lasting longer than 30 minutes or serial
seizures wherein between each seizure, there is no return of
consciousness
- A medical emergency case
- Prognosis depends on how case was managed
- Subtypes:
- Febrile seizures most common
- Idiopathic status epilepticus e.g. patient with menignits
suddenly have seizures
- Symptomatic status epilepticus (tumor) result of an
underlying neurologic disorder
- Can be caused by sudden discontinuation of anticonvulsants (most
common cause)
- Give circulatory support
- Medications:
- Diazepam: short acting; halt seizure
- Phenytoin: expensive
- Phenobarbital: can have behavioral manifestations
- Valproate: myoclonic seizures
- Phenobarbital coma: for anesthesia
Benign Febrile Seizure
- Temperature >38.4C, evidence of causative disease (CNS infection,
metabolic abnormality)
- Children >1 month of age
- Simple: <15 minutes, generalized, occurs once
- Complex: 15 minutes, focal, recurrent within 24 hours
- Should be ruled out
- Most common seizure disorder during childhood
- Characteristics:
- Grand mal lasting <15minutes
- Occurring once in the same illness
- Age incidence: 3mos-5years (In Nelsons9mos-5yrs with
peak at 14-18mos); does not mean that 1month/7years old
cannot have benign febrile seizures, however in this age
group, must rule out other causes first
- Occurs at temperature 38C & above
- Normal neurologic examination
- Family history: (+) febrile seizures
- CNS infection absent
- Symptomatic between periods of seizures
- Recurrence: 30-50% with fever
Notes:
Pads paresis transient weakness after seizure/ictus
- Autosomal dominant inheritance pattern (some families)
- Followed by brief postictal period of drowsiness
- Most frequent cause of febrile convulsions: viral infection of the
upper respiratory tract, Roseola and acute otitis media
- Management:
- Determine cause of the fever throat/ears/diarrhea
fever?
- No anticonvulsant needed
- Antipyretics
- Education of parents
- Oral diazepam (preventive prophylaxis) at onset of febrile
episode (1mg/kg/24hrs) for 2-3 days: effective and safe;
minor side effects include lethargy, irritability and ataxia; in
such cases, be prompt to adjust the dose
- Rule out CNS infections

13 - Pediatrics 2

- Rule out meningitis (if in doubt, do CSF exam e.g. Lumbar tap)
But remember that seizure-induced CSF abnormalities are
rare in children
- Laboratory Tests
- Not necessary if diagnosis is clear-cut benign febrile seizure
- Lab tests are necessary only to determine cause of ever and
rule out meningitis
- IF done, CSF examination should be normal
- EEG: normal & not useful
- Neuroimaging has no role
- Blood tests, chest x-ray, etc. are done to diagnose cause of
fever, not the benign febrile seizure
Notes:
EEG is usually done for complex febrile seizure
- Children with simple febrile seizures are at no greater risk of later
epilepsy than the general population. However some factors are
associated with increased risk:
- Atypical seizures (>15 mins)
- (+) family history of epilepsy
- Initial febrile seizures < 9 months of age
- Delayed developmental milestones
- Pre-existing neurological disorder
Complex Febrile Seizures
- Atypical
- Occur more than once in an illness or repeated convulsions within
the same day, focal findings during postictal period
- >15minutes in duration
- May need investigation to rule out epilepsy
- With focal manifestations
- Increase risk for later epilepsy with the ff characteristics:
- Presence of atypical features of seizure or postictal period
- (+) family history of epilepsy
- Initial febrile seizure <9 months of age
- Delayed developmental milestones
- Pre-existing neurological disorder
Differential Diagnosis for Fever with Seizures
- CNS Infections
Diagnostic Possibilities
- Benign febrile seizure
- In the presence of fever, pneumonia & seizures, a CNS Infection
should be considered (do lumbar tap)
- Infant may not show any meningeal signs even in the presence of
meningitis Lumbar Tap
Diagnosis of Seizures
- For the 1st afebrile seizure with no abnormal neurological findings:
- FBS, calciuria, magnesium
- Serum electrolytes, toxicology screening
- EEG: for atypical features or presence of risk factors for future
epilepsy; done in unprovoked seizures
- With abnormal neurological findings or abnormal EEG
Neuroimaging
- 1st afebrile seizure: seizure disorder or unprovoked seizure
Treatment
A. Medical (Antiepileptics)
- Phenobarbital
- for febrile seizures has lowering temperature effect
- advantage: can be given IV, cheap
- disadvantage: behavioral changes, which is why no longer
used in the US, still used in the Philippines since it is
cheap; must discipline child due to behavioral changes
- Valproate
- for absence seizures
- also for febrile seizures
- myoclonic seizures
- Diazepam
- for acute seizures
- Topiramate
- New generation drug
- Versatile
- Carbamazepine
- Complex partial seizures
- Phenytoin
- Use for accidents no sedative effect, no behavioral
effect
- expensive

B. Surgical
- for epilepsy
- to cure intractable seizures unresponsive to anticonvulsants
- Vagus nerve stimulation - pacemaker
C. Ketogenic diet
- for epilepsy
- restrict quantity of CHO and CHON and most calories provided
as fat
- e.g. Ketocal milk for epileptic patients; only for intractable
patients
- must monitor acid-base balance
Prophylaxis
- Controversial & prolonged prophylaxis is no longer recommended
- Anti-epileptic drugs (e.g., Phenytoin, Carbamazepine) have no
effect
gum swelling, behavioral changes
- Phenobarbital is effective but can decrease cognitive functioning
- Na Valproate is effective but there is an increased risk of fatal
Valproate-induced hepatotoxicity (highest in <2 y/o)
Transcribed by: Fred Monteverde
Denise Zaballero
Notes from: Emy Onishi
Cecile Ong
Denise Zaballero
Fred Monteverde
Emy Onishi
Cecile Ong
Mitzel Mata
Regina Luz
Section C 2009!
BOYCOTT desperate housewives!!!
Lumbar Puncture

Must be < 12 months

Strongly recommended 12-18 months

S/sx of meningeal irritation

No need >18 months

Complex first febrile seizures

Persistent lethargy

Strongly recommended for children on prior antibiotic therapy

Evaluation

History exact description

PE, neuro exam

Age of onset

Precipitating events: prenatal/postnatal insults to the brain

Occurrences of prior seizures (non-convulsive)

Classify the seizure

Family history of seizure most idiopathic are genetic

PE

Head size, dysmorphic features

Port-wine stain on face
Trauma
Increased ICP
Metabolic disorders r/t feeding

EEG

To classify the seizures

Provide additional clues in making an etiologic diagnosis
(N) EEG is of limited value and does not rule out that seizure
episode has occurred (interictal normal EEG)
SSPE periodic lateralized epileptic discharges
To differentiate paroxysmal events
Generalized vs. partial
(+) abnormality
o 10-40% absent epileptic
o 1-5% present non-epileptic
(may be a genetic variant carrier)

Epilepsy

0-4 years old, >70 y/o (bimodal

Pediatric primary (idiopathic)

Older secondary
Manifestations

NB hypoxia, metabolic, birth trauma

1-5 febrile seizures, intracranial infection

5-13 genetic epilepsies

Neuroimaging

Partial onset (especially adult)

Progressive neurologic disease loss of milestones

Intractable seizures

Seizures increase in frequency and intensity despite adequate

treatment

MRI > CT in sensitivity for structural epileptogenic foci

Other ILAE Dx Scheme

Syndromic
o Predominant seizure type
o Age of onset
Infantile Spasm (West Syndrome)

Age-specific

3-12 months, peak 4-7 months

Infantile spasm, MR, hypsarrythmia on EEG

Brief but recurrent spasm (50-100x/d)

Flexor, extensor/mixed

Associated with perinatal injury

Lennox-Gastaut Syndrome

Continuum of West

Seizure disorder, MR, atypical pattern on EEG (slower)

Seizure types are variable

Tonic more frequent

Resistant to therapy
Benign Rolandic Epilepsy

3-13 years old, peak 9-10

Males > females

More frequent 2-3 hours (p-?) sleep

Grunting, facial twitching secondary generalized (bed wet?)

(focal)

EEG: characteristic cortico-temporal spikes

Affected children otherwise normal

Complete remission 15-16 years old

Lab tests (no routine lab tests, to r/o provoked seizures)

Serum glucose determination

Electrolytes

Drug screens

BUN and creatinine

Thyroid function test

Childhood Absence

6-7 years old

Female > male

Simple (blank stare) or complex (automatism/motor

component)

Diagnosis

Usually clinical

EEG

Neuroimaging

Videotelemetry
o Extended EEG (4 hours)

Increased Risk for Occurrence in Febrile Seizures

Complex febrile seizures

Family history

<18 months 1st seizure

Lower maximum temperature

Short duration or ____

2-3% risk of epilepsy (1% of general population

10% risk neuroimpairment, family history

Management

If clearly metabolic, EEG is unnecessary

Treatment with antiepileptic drugs may be needed to control

seizures until the underlying pathology responsible for acute
encephalopathy is corrected
o 2 weeks seizure free

14 - Pediatrics 2

Seizures in Children: An Overview

Abnormalities of Tone and Movement in Children

** Additional notes from Panda Manilas photos.

Developmental Delay

Delayed acquisition of milestones expected for chronological

age

Important to distinguish from progressive neurological

disorders, which manifest as loss of previously acquired skills

Delays can involve any developmental parameter/s:

motor, language, psychosocial

Seizure. An abnormal excessive neuronal discharge arising

from the brain, capable of causing alteration in function
and/or behavior.
Convulsion. A type of seizure with a motor component.
Epilepsy. Recurrent unprovoked seizures (operational
definition more than two.)

Diagnosis of Epilepsies

Everyone is entitled to a diagnosis for prognosis and

management to be specific and precise.

The diagnostic label epilepsy is unsatisfactory for both

physician and patient because epilepsy is not a single disease
entity.
Conditions that Mimic Seizures

Breath-holding spells

Benign paroxysmal vertigo

Night terrors

Syncope

Shuddering attacks

Paroxysmal torticollis

Rage attacks

Masturbation

Hereditary chin trembling

Narcolepsy/cataplexy

Paroxysmal kinesigenic choreoathetosis

Pseudoseizures
Absence Seizures

Blank stare beginning and ending abruptly and lasting only a

few seconds

Rapid blinking

Chewing

Child is unaware of seizure

Learning difficulties are a possibility

What to do:
o No first aid required
o If first event, get medical evaluation
Infantile Spasms

Can occur between 6 months and 2 years of age

Appear in clusters of quick, sudden movements

Often mistaken for colic

Most often occur in relation to waking and sleeping times

What to do:
o No first aid is needed
o Observe duration of clusters
o Talk to doctor
Atonic Seizures

Sudden collapsing and falling down

Atonic seizures come in clusters

In less than one minute, child usually regains consciousness

and can stand and walk again

Often mistaken for clumsiness

What to do:
o Keep child safe during the event
o No first aid required
o Get medical evaluation
Uses of EEG

Differential diagnosis for other paroxysmal events

Differentiate partial from generalized seizures

Identification of certain epilepsy syndromes

Abnormal epileptiform activities

o Absent in 10-40% of epileptic patients
o Present in 1-5% of non-epileptic people

15 - Pediatrics 2

Bulk
Tone
DTRs
Fasciculations
Babinski
Sensory deficit

UMN
Minimal atrophy
Increased; spastic
Hyperreflexia
Absent
Present
May be present

LMN
Profound atrophy
Decreased; flaccid
Decreased/absent
Present/absent
Absent
May be present

Clinical Clues
1. Central Nervous System. UMN (spasticity, hyperreflexia);
may be accompanied by cerebral manifestations (seizures,
cognition, language and sensory problems)
2. Peripheral Nervous System. LMN (decreased to absent
reflexes, flaccid)
Guillain-Barre Syndrome
o Acute, autoimmune, polyradiculoneuropathy
affecting the PNS, usually triggered by an acute
infectious process
o Exhibits an ascending paralysis noted by weakness
in the legs that spreads to the upper limbs and the
face, along with complete loss of DTRs
Hypotonia
o Low neck muscle tone
o Child hangs upside down U with little or no
movement
o May be transient only child may become spastic
later
o More difficult to teach how to walk
o Rag doll sign
o Floppy
Disorders of the motor system may be:
1. Acute strokes/vascular, metabolic disorders, infections
o Seizures
2. Chronic cerebral palsy (static), congenital CNS lesion,
degenerative disorders (progressive)
Cerebral Palsy

2/1000

Most common cause of delay

Laymans term

Referred to a group of disorders characterized by motor

disorders (tone, posture, or movement), which are neither
progressive nor episodic
o Progressive degenerative disease
o Episodic seizures

The brain lesions are static and result from disorders of early
brain development, usually insults in the perinatal period
o Most consistent factor
anoxia, hypoxia of the newborn
o 40% (<10%? Not sure, sorry!) - perinatal asphyxia
o 80% - antenatal events causing abn. CNS deficit
o risk : LBW and <1000g risk for ICL and PVL

They are not progressive, but the symptoms may change in

time

Impairment in movement and posture leading to functional

deficits and the inability to perform activities of daily living

Caused by a broad group of developmental, genetic,

metabolic, ischemic, infectious and other etiologies that
produce a common neurologic phenotype
Epidemiology and Etiology

Most common and costly form of chronic motor disability with

a prevalence of 2/1000

<10% are due to perinatal asphyxia

80% pointed to antenatal events causing abnormal CNS

development

Intrauterine exposure to maternal infection (UTI and

chorioamnionitis)

LBW and those <1,000g increased risk for ICH and PVL

1st semester || AY 2012-2013

rainwater@mymelody.com

Axial hypotonia hypertonia

Appendicular hypertonia hypotonia
Traction test most sensitive test for hypotonia
(N) reversal of tone from:

Clinical Manifestations
1. Delay in development (i.e., poor head control, delays in gross
motor or fine motor development)
a. Poor head control (usually achieved by 4 months)
b. Delays in gross motor or fine motor development
2. Motor deficit depending on the area of the brain involved
and usually the risk factors present
3. Associated developmental disabilities mental retardation,
epilepsy, visual, hearing, speech and behavioral abnormalities
** 2, 3 severity is proportional

Clinical Manifestations

Movement disorders
o Spasticity

UE: flexor spasticity

LE: extensor spasticity

o Athetosis
o Dystonia abnormal posturing
o Rigidity
o Ataxia ataxia - incoordination
o Mixed motor problems

Associated with a spectrum of developmental disabilities:

mental retardation, epilepsy, hearing and visual problems,
speech, cognitive and behavioral
Physiological Classification

Motor Disorders in CP
Three main criteria in classification:
1. Type of motor disorder
2. Topographical distribution
3. Gross motor function
Types of Cerebral Palsy and the Major Causes
Physiologic
Topographic
Etiologic
Spastic
Monoplegia
Prenatal
Athetoid
Paraplegia
(e.g., infection,
Rigid
Hemiplegia
metabolic, anoxia,
Ataxic
Triplegia
toxic, genetic,
Tremor
Quadriplegia
infarction)
Atonic
Diplegia
Perinatal
Mixed
Double
(e.g., anoxia)
Unclassified
hemiplegia
Postnatal
(e.g. toxins,
trauma, infection)
Spastic Diplegia
Spastic
quadriplegia
Hemiplegia

Extrapyramidal/
Athetoid

Periventricular
leukomalacia
PVL/multicystic
encephalomalacia
Malformations
Stroke in utero or
neonatal

Pathology in the
basal ganglia,
putamen, globus
pallidus, thalamus

Functional
Class I no
limitation of activity
Class II slight to
moderate limitation
Class III moderate
to great limitation
Class IV
no useful physical
activity

Prematurity
Ischemia
Infection
Endocrine/metabolic/genetic
Thrombophilic disorders
Infection
Genetic
Hemorrhagic
Infarction
Asphyxia
Kernicterus
Mitochondrial
Genetic/metabolic

Paraplegia, Diplegia

Paraplegia both legs only

Diplegia with slight involvement elsewhere

Upper body usually normal or with very minor signs

Child may develop contractures of ankles and feet

Quadriplegia

Both arms and both legs

Arms, head, and mouth may twist strangely when walking

Often have severe brain damage, are never able to walk again

Knees press together

Legs and feet turned inward

Spastic: seesawing of the legs; increase in tone

Athetoid: too much involuntary movement
Rigid: all throughout movement
Monoplegia: uncommon
Diplegia: both lower extremities
Hemiplegia: Right or left half of body
Quadriplegia: Upper and lower extremities
Jitteriness: observe during movement
Child with spastic diplegia tip-toe always
*As long as insult happens in neonatal-perinatal period (4 months AOG
to 1 months of life) child with meningitis can have cerebral palsy.

16 - Pediatrics 2

Spastic Cerebral Palsy

Less commonly the head and shoulders may stiffen forward,

or the arms may stiffen straight across the body, with the
head pressed back
Spastic Quadriplegic Cerebral Palsy

Head may twist to one side; shoulders, head may press back

Fist grips thumbs; arm: may stiffen straight out, or stiffen bent

Legs: may stiffen with knees pressed together, or turn in

Body may stiffen like a board

Stiffness, with the knees bent or with legs separated, occurs

more commonly in the child with spasticity and athetosis
combined

Most severe form because of involvement of all four limbs

and the high association of mental retardation and seizures

Feeding problems (swallowing difficulty) are common due to

supranuclear bulbar palsies

Common neuropathologic findings

o PVL, multicystic encephalomalacia
Spastic Diplegic Cerebral Palsy

When you try to stand the child, the legs often stiffen

Bilateral spasticity of legs> arm

If severe, there is excessive adduction of the hips making

diaper change difficult

Scissoring posture of lower extremities

PVL: most common neuropathologic finding

Prognosis for normal intelligence is good

Minimal seizure

Hemiplegia

Arm and leg on one side

Arm bent; hand spastic or floppy, often of little use

Walks on tiptoe or outside of foot on affected side

Other side completely or almost normal

Notes:

Spastic Hemiplegia

spontaneous movements on the affected side

Arm > leg

Delayed walking until 18-24 months of age

Circumductive gait

Growth arrest in extremities especially if contralateral parietal

lobe is abnormal

Spasticity in the affected extremities

Equinovarus deformity (walks on tiptoes)

Ankle clonus + Babinski sign

CT: atrophic cerebral hemisphere with dilated lateral ventricle

contralateral to the side of the affected extremities

Athetoid Cerebral Palsy

Typical athetoid arm and hand movements may be as a

regular shake or as sudden spasms. Uncontrolled
movements are often worse when the child is excited or tries
to do something.

Poor balance, arm and head movement

Child who learns to walk may do so in a stiff, awkward position,

with the knees pulled together and bent. Feet often turn in.

Less common than the spastic type.

Hypotonic infants who do not have UMN signs but later on

develop increased variable tone (rigidity) and dystonia and
other dyskinesias

Intellect is preserved in many cases

Hypotonic with poor head control and marked head lag

Speech affected due to oropharyngeal muscle involvement

UMN signs (-), no seizures, preserved intellect

Most likely associated with birth asphyxia

Ataxic Cerebral Palsy

To keep balance, child walks bent forward with feet wide

apart, and takes irregular steps (like sailor on a rough sea, or
someone who is drunk.)

1st semester || AY 2012-2013

rainwater@mymelody.com

Diagnosis

Clinical diagnosis

Neuroimaging will document the extent of the structural

pathology, aid in diagnosis and prognostication, and rule out
treatable causes and slowly progressive neurological disorders

Thorough history to identify risk factors, developmental

assessment, physical and neurological examinations

Hearing and vision screening

EEG if with seizures

If no possible etiology or risk factors for CP, do diagnostic tests

o Neuroimaging CT/MRI

Document extent of structural pathology

o Metabolic screening
o Chromosomal studies
Differential Diagnosis
1. Motor delays from congenital structural malformations
2. Progressive disorders of the brain white matter diseases
3. Muscle disorders myopathies, dystrophies
4. Anterior horn cell disease spinal muscular atrophy (SMA)
Differentials
1. Dysmyelinating/demyelinating Disorders
o Abnormal myelin formation as in some metabolic
disorders
o Abnormal myelin secondary to brain insults from
infection, trauma, autoimmune
o Clinically: white matter involvement, with
progressive neurologic deficits (spasticity,
hyperreflexia, hearing and vision may be affected)
2. Spinal Muscular Atrophy
o Disorders of the anterior horn cell
o Usually progressive
o Of three varieties depending on the age of onset of
symptoms

Infantile type Wednig-Hoffman disease

Intermediate

Juvenile Kugelberg Welander disease

o Presents with LMN signs: fasciculations, floppy,
areflexic
3. Muscle-Congenital Myopathy
4. Nerve disorders
o Manifestations of lower motor disease, decreased
reflexes, tone (e.g., hereditary motor-sensory
neuropathy)
Effective management requires:
1. Understanding of the pathophysiology of the disorder
2. Careful assessment of the patients capabilities and limitations
3. Knowledge of available treatment regimens, their applications
and limitations
Management (Multidisciplinary)
1. Pediatrician
2. Neurologist: management of seizures, botulinum toxin
injections
3. Rehabilition specialists
4. Physical and occuptational therapists
5. Developmental psychologists
6. Education specialists
7. Orthopedic surgeons
8. Social workers

Diagnosis

DSM-IV-criteria for autism

Modified checklist for autism in toddlers (M-CHAT)

Pervasive developmental disorder screening test (PDDST)

Treatment

Multidisciplinary

Developmental pediatrician, pediatric neurologist, child

psychiatrist

Psychologist

Occupational/speech therapist

Special education teacher (if necessary)

Medications depending on co-morbid conditions

Attention Deficit Hyperactivity Disorder

Most common neurobehavioral disorder in childhood

Characterized by (DSM IV)

o Inattention
o Poor impulse control
o Motor overactivity/restlessness

Symptoms should be present for more than 6 months in at

least 2 settings are significantly affects social, academic or
occupational functioning
Etiology

Multifactorial
Genetic susceptibility
Maternal complications during pregnancy
Maternal smoking and alcohol intake during pregnancy
Abnormal brain structures
Psychosocial family stressors exacerbate and/or contribute to
the symptoms

Pathogenesis

Smaller prefrontal cortex and basal ganglia with 5-10% less

blood flow in these areas.
o Rich in dopamine receptors dopamine
hypothesis (disturbances in dopamine system are
related to the onset of ADHD)
Diagnosis

Clinical interview and history

o Fulfills criteria
o Family history of ADHD
o Family discord, situational stress

Behavior rating scales (e.g., Conners rating scale) help

establish the magnitude and pervasiveness of symptoms and
can be used for monitoring improvement with intervention
Treatment

Psychosocial treatments

Behaviorally oriented treatments

Medications: methylphenidate and atomoxetine

Autism Spectrum Disorder

Autism is a neurodevelopmental disorder of unknown etiology

but with a strong genetic basis

Behavioral phenotype
o Qualitative impairment in language/communication
o Impaired social interactions and reciprocity
o Lack of imaginative play
Signs and Symptoms

No pathognomonic symptoms or behavior

Most will present with:

o Impairment in joint attention (use of eye contact
and pointing to share experiences with others),
which normally develops at 18 months
o Lack of protoimperative pointing (to get an object
of desire)
o Lack of protodeclarative pointing (to share an
object of interest/naming)
o Lack of imaginative play

17 - Pediatrics 2

Manifestations

Poor eye contact

Verbal abilities vary: non-verbal to advanced speech

Speech may have odd prosody or intonation, echolalia,

pronoun reversal, nonsense rhyming

IQ from MR to superior functioning

Stereotypical/ritualistic behaviors

Marked need for sameness

Prognosis

Persists throughout the life span

Reduction in hyperactive behavior with age

Other symptoms: impulsivity, disorganization and inattention

become prominent affecting relationships and occupational
functioning

High risk for risk-taking behaviors (substance abuse) and

psychiatric disorders
Notes in purple:
Transcribed by:
Fred Monteverde
Notes from: Emy Onishi
Cecile Ong
Denise Zaballero

Fred Monteverde
Emy Onishi
Cecile Ong
Mitzel Mata
Regina Luz
Section C 2009!

Notes in red: whoever the notes on my photocopy came from.

Thank you!

1st semester || AY 2012-2013

rainwater@mymelody.com