FEVER

WITHOUT A FOCUS (Dra. Morelos)

FEVER

Controlled increase in body temperature over normal values

T >38C rectal

Normal 36.6C 37.0C rectal

HYPERTHERMIA

T >40C
o Central
o Heat stroke
o Malignant hyperthermia
o Drug fever

REGULATION OF BODY TEMPERATURE

Preoptic and Anterior Hypothalamus

Thermosensitive neurons

Normal Body Temperature

36.6C 37.9C rectal

Diurnal variation (Circadian Rhythm)

PATHOGENESIS OF FEVER

3 Mechanisms of Fever

The bodys thermostat is reset at a higher temperature

o In response to Pyrogens
o Heat production > heat loss
o Defective mechanisms of heat loss

PYROGENS

Endogenous Pyrogens
o Cytokines IL1 and IL2
o TNF
o Interferon and
Lipid mediator PGE2
o

Exogenous Pyrogens

Infectious pathogens
o Microbes and toxins stimulate production of
endogenous pyrogens
o Endotoxins

Other substances that stimulate endogenous pyrogens

o Antigen-antibody complexes
o Complement
o Lymphocyte products
o Androgenic steroid metabolites
o Vancomycin, Amphotericin B, Allopurinol

Producers of endogenous pyrogens

o Malignancies
o Inflammatory Diseases

EFFECTS OF FEVER

O2 Consumption

CO2 Production

Cardiac Output

Risk for seizures

ETIOLOGY OF FEVER

Infections

Inflammatory disorders

Neoplasms

Miscellaneous

The most common cause of acute fever are self-limited viral

infections and uncomplicated bacterial infections

FEVER PATTERNS

Slow decline of fever over a week viral

Prompt resolution of fever after effective antimicrobial tx

bacterial

Intermittent fever - normalizes

Septic/hectic fever extremely wide fluctuations of fever

Sustained fever does not vary by >0.5C

Remittent fever varies by >0.5C (never normalize)

Relapsing fever with intervals of normal temperature

st
rd

Tertian fever 1 and 3 (P Vivax)

st
th

Quartan fever 1 and 4 (P malariae)

Biphasic fever camel back fever pattern in Dengue, polio,

leptospirosis

Periodic fever regular periodicity

Factitious fever self induced

Double quotidian fever peaks twice in 24 hours, with

arthritic fevers

Single isolated fever spike transfusion reaction, catheter

placement (foreign body reaction), colonization of infected
body surface

EVALUATION OF ACUTE FEVER

History

PE

Labs

TREATMENT OF ACUTE FEVER

Tx of self-limiting illness

Tx for certain conditions only

o Fever <39C in healthy
o High risk groups
o Tx of underlying etiology

Antipyretics

FEVER WITHOUT A FOCUS

Rectal temperature of 38C as the sole presentation

o Fever without localizing signs
o Fever of unknown origin

FEVER WITHOUT LOCALIZING SIGNS

etiology and evaluation of fever without localizing signs

depends on the age of the child
o neonates or infants - 1 mo of age
o infants >1 mo - 3 mo of age
o children >3 mo - 3 yr of age

Low risk vs High risk

Febrile patients at risk for serious bacterial infections

(immunocompetent)
o Neonates <28days
o Infants 1-3mos
o Children 3-36 mos
o Hyperpyrexia >40C
o Fever with petechiae

Febrile patients at risk for serious bacterial infections

(immunocompromised)
o Sickle cell disease
o Asplenia
o Complement/Properdin deficiency
o Agammaglobulinemia
o AIDS
o Congenital heart disease (infective endocarditis is
most feared, also brain abscess with left to right
shunting)
o Central venous line
PEDIATRICS2 LE6 Handout [by: msredlips

o Malignancy
Toxic
o Clinical picture consistent with sepsis syndrome:

lethargy

signs of poor perfusion

cyanosis

hypoventilation

hyperventilation
all febrile children less than 36 months of age who are toxic-
appearing should be hospitalized for evaluation and
treatment of possible sepsis or meningitis

NEONATES: FEVER W/O LOCALIZING SIGNS

All should be hospitalized

difficult to clinically distinguish between a serious bacterial

infection and self-limited viral illness

Blood, Urine, Stool, CSF cultures/GS

Empirical IV antiviral / combination antibiotics

1-3MOS: FEVER W/O LOCALIZING SIGNS

Etiology
o Viral
o Bacterial
o GBS
o L. monocytogenes
o Salmonella
o E. coli
o N.meningitidis
o S.pneumoniae
o Hib
o Staph aureus

low risk
o Normal physical examination
o Uncomplicated medical history
o Normal labs

Urine:
<10 WBC/HPF, (-)nitrite
(-)leukocyte esterase
o Stool studies if diarrhea (-) RBC and <5 WBC/HPF
o CSF cell count <8 WBC/mm3 (-) Gram stain
o Peripheral blood: 5,000-15,000 WBC/mm3 <1,500
bands or band:total neutrophil ratio <0.2
o Chest radiograph without infiltrate

If child fulfills all low-risk criteria administer no antibiotics

Ensure follow-up in 24 hr and access to emergency care if

child deteriorates.

Daily follow-up should occur until blood, urine, and CSF

cultures are final.

If any cultures are positive, child returns for further

evaluation and treatment.

If child does not fulfill all low-risk criteria: hospitalize.

Administer parenteral antibiotics until all cultures are final

until definitive diagnosis is determined and until child is
adequately treated.

3-36 MOS. FEVER WITHOUT LOCALIZING SIGNS

Approximately 30% of febrile children have no localizing signs

of infection

Etiology
o Viral
o Bacterial (occult bacteremia)

S. pneumoniae

H. influenzae type B
2
PEDIA

PEDIATRICS2 LE6 Handout [by: msredlips

N. meningitidis
Salmonella, S. aureus. S. pyogenes

3-36 mos. Fever 38-39C without localizing signs (low risk)
Reassure: diagnosis is most likely a self-limiting viral infection

no antibiotics

Acetaminophen 15mg/kg q 4hrs

advise return

with persistence of fever

o If temperatures >39C

With appearance of new signs and symptoms

Risk factors for occult bacteremia

o temperature 39C
o WBC count 15,000/L
o absolute neutrophil count
o band count
o C-reactive protein

3-36 mos. Fever 39C without localizing signs
Sequelae of occult bacteremia

meningitis,
cellulitis,
pneumonia,
pericarditis,
epiglotitis,jt.infections, osteomyelitis, suppurative arthritis,
otitis media, sinusitis, enteritis, urinary tract infection

SEPTIC WORKUP

Urine culture for Males <6 mo of age Females <2 y of age

Stool culture if Blood and mucus in stool or 5 WBCs/hpf in

stool

Chest radiograph if with Dyspnea, tachypnea, rales, or

decreased breath sounds

Blood culture
o Option 1: All children with temperature 39C
o Option 2: Temperature 39C and WBC count 15
000

Lumbar puncture
o Clinician determines LP based on hx, observational
assessment, and PE

Blood culture
o (+) Streptococcus pneumoniae,

Persistent fever: Admit for sepsis

evaluation and parenteral antibiotics
pending results.

All others: Admit for sepsis evaluation

and parenteral antibiotics pending
results.

Urinalysis (+) All organisms:

o Admit if febrile or ill-appearing

Outpatient antibiotics if afebrile and well.

Empiric antibiotic therapy

o Option 1: All children with temperature 39C
o Option 2: Temperature 39C and WBC count 15
000

Acetaminophen 15 mg/kg per dose every 4 h for

temperature 39C

FUO: FEVER OF UNKNOWN ORIGIN

fever documented by a health care provider and for which

the cause could not be identified after 3 wks of evaluation as
an outpatient or after 1 wk of evaluation in the hospital

FUO Etiology
o Infections 36%
o Neoplastic diseases 19%
o Collagen Vascular Diseases/Autoimmune Disorders

o
o

13%
No Diagnosis 7%
FUO is more likely an unusual presentation of a
common disease than an uncommon disease.

FUO: 4 SUBTYPES

Classic FUO

Health-Care associated FUO

Immunedeficient FUO

HIV-related FUO

FUO: DIAGNOSTIC CONSIDERATIONS

Abscesses

Bacterial disease

Localized infections

Fungal disease

Parasitic disease

Viral disease

Rheumatologic disease

Hypersensitivity disease

Neoplasms

Granulomatous disease

Familial/hereditary diseases

Drug Fever

Miscellaneous

DRUG FEVER

Onset : 7-10days after start of tx

Hectic fever with rash/eosinophilia but with a preserved

sense of well being (20%)

DX: resolution of fever in 48 hrs after d/c of drug, or 3 to 5

drug T/2, whichever is longer; recrudescent fever occurs
within a few hours after the drug is restarted

FUO : HISTORY

Age

Exposure to wild or domestic animals zoonotic diseases

Pica

Unusual dietary habits

Travel and prophylactic immunizations

FUO :PE

General appearance, including sweating during fever

Ophthalmic examination

Sinuses

Pharynx

Thyroid

Cervical lymph nodes

Murmur

Abdomen

muscles and bones should be palpated

Rectal exam

Skin and nails

FUO: LABORATORY EVALUATION

CBC

Peripheral blood smear

Urinalysis

ESR CRP ANA RF

Cultures

Tuberculin test

Radiographic examinations

Bone marrow examination

Serologic tests

Radionuclide scans

Echocardiogram

Ultrasonography

CT scan/ MRI

Biopsy

Bronchoscopy, Laparoscopy, Endoscopy

FUO: TREATMENT

Therapy should be withheld until the cause has been

determined.

The ultimate treatment of FUO is tailored to the underlying

diagnosis.

Avoid empirical trials.

After a complete evaluation antipyretics may be indicated to

control fever and relieve symptoms.

FUO: PROGNOSIS

The prognosis of FUO is determined by the cause of the fever

and by the nature of any underlying disease or diseases.

Children with FUO have a better prognosis than do adults.

Patients in whom FUO remains undiagnosed after extensive

evaluation generally have a favorable outcome,
characteristically with resolution of their fever in 4 or more
weeks without sequelae

CHRONIC ILLNESSES (Dra. Morada)

EPILEPSY

It is a disorder of the brain

Characterized by:
o enduring predisposition to generate seizures
o neurobiologic, cognitive, psychological, and social
consequences

Present when >2 unprovoked seizures occur in a time frame

of >24 hr.

The occurrence of 1 seizure or of a febrile seizure does not

necessarily imply dx of epilepsy

Clinical dx

At least 1 unprovoked epileptic seizure with either a second

such sizure

Seizure disorder

Any one of several disorders:

o Epilepsy
o Febrile seizure
o Single seizure
o Seizures due to metabolic, infectious, hypocalcemia

st
Evaluation of 1 seizure

Adequacy of aiway, ventilation and cardiac function

Temp, BP, glucose

Infection, head trauma, drugs/toxins

History

Focal or generalized?

Description of seizure

Tonic = increased rigidity

Atonic = flaccidity

Clonic = rhythmic muscle contraction and relaxation

Myoclonus = shocklike contraction of a muscle

Aura: epigastric pain

PEDIATRICS2 LE6 Handout [by: msredlips

Treatment of epilepsy

Ensure that a patient has a seizure disorder and not a

condition that mimics epilepsy (migraine, tuberous sclerosis,
movement disorders, encephalopathies)

If (-) EEG and neuro exam : watchful waiting

Recurrent seizure: start anticonvulsant

DOC: depends on classification of seizure

4
PEDIA

PEDIATRICS2 LE6 Handout [by: msredlips

CEREBRAL PALSY

Permanent disorders of movement and posture causing

activity limitation

Attributed to nonprogressive disturbances in the developing

fetal or infant brain

Static encephalopathy

EPIDEMIOLOGY & ETIOLOGY

Most common and costly form of chronic motor disability

3.6/1000 incidence

1.4/1 male/female ratio

Born term, uncomplicated

Genetic: interleukin 6

Premature: ICH and periventricular leukomalacia (PVL)

Infertility treatments

CLINICAL MANIFESTATIONS

Spastic hemiplegia decreased spontaneous movements on

the affected side

Spastic diplegia bilateral spasticity of the legs that is greater

than in the arms

Spastic quadriplegia marked motor impairment of all

extremities

Athetoid hypotonic with poor head control; marked rigidity

DIAGNOSIS

Hx and PE: progressive disorder of the CNS

MRI scan of the brain

Tests of hearing and visual function

Genetic evaluation

TREATMENT

Recent study: prenatal treatment of mothers with

magnesium

Prevent development of contractures

Multidisciplinary

Treat spasticity: benzodiazepines

DIABETES MELLITUS

Metabolic syndrome characterized by hyperglycemia

Type 1 DM = caused by deficiency of insulin secretion due to

pancreatic B-cell damage

Type 2 DM = caused by insulin resistance at skeletal muscle,

liver, adipose tissue

Long-term Complications

Retinopathy

Nephropathy

Neuropathy

Ischemic heart disease

Arterial obstruction with gangrene of the extremities

TYPE 1 DM (Immune Mediated)

Boys = girls

Peak: 5-7 yr of age & puberty

+ family history but 85% of newly diagnosed do not have

family history

Environmental factors: viral infections, mumps virus, etc

PATHOGENESIS

Autoimmunity

A genetically susceptible host develops autoimmunity against

his own B cells.

CLINICAL MANIFESTATIONS

Hyperglycemia

Intermittent polyuria and nocturia

Polydipsia

Monilial vaginitis

Weight loss

Abdominal discomfort, nausea, emesis

Dehydration

Polyuria

Kussmaul respirations, fruity breath color, diminished

neurocognitive function, coma

DIAGNOSIS

Inappropriate polyuria in any child with dehydration, poor

weight gain, or the flu

Hyperglycemia

Glycosuria, ketonuria

Nonfasting blood glucose >200 mg/dL (with or without

ketonuria

Electrolyte abnormalities

Baseline HbA1c

DIABETIC KETOACIDOSIS

Occurs in 20-40% with new onset DM

Mild: oriented, alert but fatigued

Moderate: Kussmaul respirations; oriented but sleepy;

arousable

Severe: Kussmaul or depressed respirations; sleepy to

depressed sensorium to coma

TREATMENT

Insulin therapy

Diabetes education monitoring of blood glucose, etc

th

DKA protocol see Table 583-4, 19 ed Nelson

Cerebral edema the major cause of morbidity and mortality

Nutritional management

Monitoring

BRONCHIAL ASTHMA

Airways hyperresponsiveness to provocative exposures

Inflammatory condition

ETIOLOGY

Genetics
o Interleukin-4 gene
o ADAM 33

Environment
o Allergens, infections, microbes, pollutants, stress

EPIDEMIOLOGY

Boys

Children in poor families

Ethnic minorities, urban living

TYPES OF CHILDHOOD ASTHMA
1. Recurrent wheezing
2. Chronic asthma
3. Females who experience obesity and early-onset puberty

PATHOGENESIS

Airflow obstruction

Small airways: airflow is regulated by smooth muscle

encircling the lumens; bronchoconstriction of muscular bands

Cellular inflammatory infiltrate and exudates

Breach in normal immune regulation

Mucus hypersecretion

CLINICAL MANIFESTATIONS

Intermittent dry coughing

Expiratory wheezing

Older: shortness of breath/chest tightness

Younger: chest pain

Lack of improvement with bronchodilator inconsistent with

asthma

Other findings

Decreased breath sounds (R lower posterior lobe)

Crackles and rhonchi

Labored breathing

Insp and exp wheezing, poor air entry, suprasternal and

intercostal retractions, nasal flaring, accessory respiratory
muscle use

ASTHMA TRIGGERS

Viral infections of the respiratory tract

Aeroallergens: animal dander, indoor allergens, dust mites,

cockroaches, molds

Seasonal aeroallergens: pollens and molds

Tobacco smoke

Air pollutants: dust, etc

Strong or noxious odors or fumes

Occupational exposures: paint, etc

Cold air, dry air

Exercise

Crying, laughter, hyperventilation

Co-morbid conditions: rhinitis , sinusitis, GER

DIAGNOSIS

History

PE

Improvement with bronchodilator

Asthma triggers

Environmental history


PEDIATRICS2 LE6 Handout [by: msredlips

DIFFERENTIAL DIAGNOSIS:
Upper Respiratory Tract Conditions

Allergic rhinitis

Chronic rhinitis

Sinusitis

Middle Respiratory Tract Conditions

Laryngotracheobonchomalacia

Pertussis

Vocal cord dysfunction

Foreign body aspiration

Chronic bronchitis (tobacco smoke)

Lower Respiratory Tract Infections

Viral bronchiolitis

Gastroesophageal reflux

Tuberculosis

Pneumonia

Pulmonary edema (e.g. congestive heart failure)

LABORATORY

Pulmonary Function Testing

o Spirometry
o Bronchoprovocation challenges
o Exercise challenges
o Peak expiratory flow (PEF) monitoring

Radiology

TREATMENT
1: Regular Assessment and Monitoring

Severity
o Age group: 0-4 yr, 5-11 yr, >12 yr
1. Intermittent Asthma - <2 days/wk sx
2. Persistent Asthma
a. Mild - >2 days/wk but not daily
b. Moderate - daily
c. Severe throughout the day

Control
o Well-controlled: sx <2 days/wk but not more than
once on each day
o Not well-controlled: sx >2 days/wk or multiple
times on <2 days/wk
o Very poorly controlled: sx throughout the day

Responsiveness to therapy
o The ease with which asthma control is attained by
treatment
o Can encompass monitoring for adverse effects
related to medication use

2: Patient Education

Written asthma management plan

o Daily routine management plan
o Action plan for asthma exacerbations

Regular follow-up visits:

o 2x yearly (more often if asthma not well controlled
o Monitor lung function annually
o CAMP = Childhood Asthma Management Program

3: Control of Factors Contributing to Asthma Severity

Eliminating and reducing problematic environmental

exposures

Treat co-morbid conditions

6
PEDIA

PEDIATRICS2 LE6 Handout [by: msredlips

o
o
o

Rhinitis
Sinusitis
GER

4: Pharmacotherapy

Long-Term Controller Medications

Quick-Reliever Medications

Step-Up, Step-Down Approach

Long-Term Controller Medications
1. Inhaled corticosteroids (Fluticasone)
2. Systemic corticosteroids
3. Long-acting inhaled B-agonists (LABAs) (Salmeterol)
4. Leukotriene-modifying agents (Montelukast)
5. Nonsteroidal anti-inflammatory agents (Cromolyn)
6. Theophylline
7. Anti-immunoglobulin E (Omalizumab)

Quick-Reliever Medications
1. Short-acting inhaled B-agonists (SABA): Albuterol,
Terbutaline
2. Anticholinergic agents: Ipratropium bromide
3. Short-course systemic corticosteroids (Prednisone)

Delivery Devices

Metered-dose inhaler (MDI)

o Dry powder inhaler (DPI): Diskus, Twisthaler
o Suspension/solution via nebulizer

Spacer devices
o For preschool-aged children

Inhalation Technique

For each puff of MDI-delivered medication = slow (5-sec)

inhalation, then a 5- to 10-sec breath-hold

Spacer/mask: each puff for about 30 sec with regular

breathing

PROGNOSIS

35% of preschool-aged children have recurrent wheezing

1/3 persistent asthma

2/3 improve

Asthma severity by 7-10 y/o is predictive of asthma

persistence in adults

PREVENTION

Cornerstone of asthma control = anti-inflammatory

interventions

Avoidance of tobacco smoke

Prolonged breastfeeding (>4 mo)

Active lifestyle

Healthy diet

CHRONIC ILLNESSES in CHILDHOOD (Dra. SG Aro)

DEFINITION

Chronic: of long duration

Special: distinctive, exceptional,

Disability: incapacity, handicap

CHRONIC ILLNESS - defined by its duration and nature; health

condition that persists longer than 3 months

FUNCTIONAL LIMITATION specific impact on function

DISABILITY social impact of a condition on a childs daily

life; assessed by measuring limitations (participate in daily
activities, school performance, attendance,community
functions)

CHRONIC ILLNESS

Complex and dynamic

Rare and heterogenous

In infancy, affects both growth and development

Failure to thrive common manifestation affecting feeding

and metabolic demands

Boys have higher rates of chronic illness than do girls

Contributes to social disparities in child health

Differences Between Acute & Chronic Illness


Acute
Chronic
Onset
abrupt
usually graduated
Duration
limited
lengthy, indefinite
Cause
single
multiple, changes
Diagnosis
usually accurate often uncertain
Prognosis
usually accurate often uncertain
Intervention
usually effective often indecisive
Outcome
cure

no cure
Uncertainty
minimal
pervasive

The Impact of Chronic Illness The Individual

Initial Impact
o Shock
o Denial
o Loss and grief
o Anxiety and depression

20-25% experience psychological symptoms

If these reactions last too long, they can have an negative

effect on the illness

Must adjust to:

o Symptoms of the disease
o Stress of Treatment
o Feelings of vulnerability
o Loss of Control
o Threat to self-esteem
o Financial Concerns
o Changes in family structure

Chronic Illness as a Crisis

Illness is a crisis because it is a turning point in an individuals

life.

Disruption to established patterns of personal and social

functioning produces a state of psychological, social, and
physical disequilibrium

Adaptation = finding new ways of coping with drastically

altered circumstances. Restore equilibrium.

Crisis Theory (Moos, 1982)

A model describing the factors that affect peoples

adjustment to having serious illness.

Coping process (3 stages) is influenced by 3 factors

o Illness-Related Factors
o Background and personal Factors
o Physical and Social Environment Factors

Coping process influences outcome of crisis

Crisis Theory of Chronic Illness A Model

Contributing Factors

Illness-Related Factors
o Degree of illness acceptance
o Degree of lifestyle/functional impairment

Background and Personal Factors

o Demographic - Age, Gender, SES
o Personality - Negative affectivity vs. Hardiness

Physical and Social Environment Factors

o Social support Instrumental & Emotional

In the long run emotional is better

The Coping Process

Cognitive appraisal
o Meaning or significance of the illness
o Threat and coping ability

Adaptive tasks
o Formulation of tasks to help cope with illness

Illness-related Impairment, treatment,

hospital

General psychosocial functioning Self-

perception, self-esteem

Coping skills
o Denial, information seeking, goal setting, recruiting
support, catharsis

Outcome of Crisis

Adaptation and Adjustment

o Physical, vocational, self-concept, social, emotional,
compliance

Quality of Life
o Degree of quality people appraise their lives to
contain

Quality = fulfillment or purpose

o Health-related quality of life (physical status and
functioning, psychological status, social functioning,
disease or treatment-related symptomatology)

The Impact of Chronic Illness - The Family

Must adjust to:

o Increased stress
o Change in the nature of the relationship
o Change in family structure/roles
o Lost income all have impact

Parental Responses to Illness or Disability

PEDIATRICS2 LE6 Handout [by: msredlips


Family Centered Approach & Developmental Approach

Infancy

Toddlerhood

Preschool

SchoolAge

Adolescence

Trust

Autonomy

Initiative

Industry/Accomplishment

Identity

Assessing Family Strengths

Available Support Systems

Perception of the illness/disability

Coping Mechanisms

Available Resources

Concurrent Stresses

Tasks of Parents of Children with Chronic Conditions

1.
2.

3.
4.

5.

6.
7.

Accepting the Childs Condition

Its not the hand youre dealt, but how you play your cards
Managing Day-to-Day

Constant Attention

Details/preplanning

Rxns of other children

Social Relationships

Effects on Siblings

Marital Relationships
Meeting the Childs Normal Developmental Needs
Meeting Developmental needs of others in the Family
Sibling issues
Parental roles
Single parenting
Normalcy
Extended family
Coping with ongoing stress and Periodic Crises
How is the family affected with this ongoing stress?
How do they react when there is an exacerbation?
How do families endure this?
What are their coping mechanisms?
Assisting Family Members in Managing their Feelings
Establishing a Support System

Examples of Chronic Illnesses

Cancer

Neurologic (CP, Epilepsy)

Connective Tissue Diseases (Arthritis)

Asthma

Congenital anomalies (CHD)

Muscular dystrophy

Sickle cell anemia

8
PEDIA

PEDIATRICS2 LE6 Handout [by: msredlips

Diabetes
HIV
CKD

NEUROLOGIC: Cerebral Palsy
Definition

A group of non progressive disorders of movement and

posture due to non- progressive brain dysfunction

Static encephalopathy

The full extent of motor disability may not be evident until 3

or 4 years of age.

Intellectual, behavioral, and/or sensory difficulties may

accompany, but not a part of the diagnostic criteria.

Prevalence: 1.5 - 2.5/1,000 live births

o Does not reflect the large reduction in neonatal
mortality that has taken place over the past 20
years.

5-15% of surviving low birth weight infants

When to Suspect?

Term infants who are ill in the neonatal period: HIE, low
st
APGAR score( <5), seizures in 1 day of life, continuing
neurologic abnormality : 55% risk for chronic motor disability

Approx 80% - no substantive asphyxia

Presence of malformations and dysmorphic features

About 1/3 of CP in term infants occurred in association with

cortical dysgenesis

Low birth weight infants: low birth weights and abnormally

short gestation are significant risk factors for CP

Preterm infants who are SGA are at special high risk

Congenital malformations located outside of CNS inc the risk

for CP

Chorionitis is a risk factor for CP, regardless of birth weight

Twin births contribute to 10% of CP in the US

Intrauterine and neonatal infections such as TORCH and

other infections

Maternal conditions such as unusual menstrual period,

thyroid d., estrogen adm have been asso with CP

Hyperbilirubinemia : kernicterus

Motor milestones are the most commonly used features to

clinically monitor CP: developmental quotient for motor skills
(MQ)

MQ = motor milestones / chronologic age x 100% (half

correction for prematurity)

MQ of 50% - 70% is borderline; <50% is associated with

significant pathology

Hand preference prior to the first birthday

Unexplained assymmetry after 3 months

Persistence of primitive reflexes > 6mos:

o prominent fisting
o obligate positive support reflex
o ATNR
o Moro reflex
o Hypotonia/ hypertonia
o Hypereflexia and ankle clonus

Classification according to area of brain involved:
1. Spastic most common, motor part of cerebral cortex

Hemiplegia: Arm and leg on one side is involved

Diplegia: Both legs weak and spastic, arms less weak.

Associated with premature birth

Quadriplegia: All extremities are severely involved;

prominent bulbar signs
2. Dyskinetic (Extrapyramidal) - basal ganglia affected

Choreoathetoid

Dystonic
3. Ataxic cerebellum and adjacent brainstem involved
4. Mixed type large areas of cortex and subcortical area including
basal ganglia involved

CP hemiplegic type

7 year old boy with left hemiplegia predominating markedly

in upper limb.
o Abduction of the arm, flexion at the wrist.
o No pincer grasp

CP diplegic type

Increased muscle tone in the lower extremities.

When the child is held vertically, the legs extend and assume
a scissored position.

Legs are often internally rotated.

CP quadriplegic

Bilateral spasticity predominating in the upper limbs with

involvement of bulbar muscles

Almost always in association with severe subnormality and

microcephaly

Totally dependent ADL

CP dyskinetic

The general appearance of the child is striking with grimacing

face and bizarre contractions at each attempted movement.

Swallowing difficulties

Drooling

CP ataxic

Ataxia affecting both lower and upper limbs with dysmetria

and intention tremor.

Able to walk by 3-4 years of age although they may fall

frequently.

Wide-based stance

Etiologies

Unknown

Prenatal factors

Perinatal factors

Postnatal factors

DIAGNOSTICS

Cranial ultrasound

CT scan if suspecting TORCH

MRI for malformations, i.e. cortical dysplasia

Metabolic work up as needed

EEG

Associated conditions

Cognitive/behavioral
o Mental retardation (65%)
o Learning disabilities
o ADHD and other behavior problems

Epilepsy (33%)

GI
o Dysphagia
o GE-reflux

o Failure to thrive
Orthopedic
o Hip dislocation
o Scoliosis
o Joint contractures
o Arthritis
Hearing and visual loss
Respiratory problems
o Obstructive sleep apnea

Factors affecting prognosis

Type of cerebral palsy

Degree of delay in meeting milestones

Pathologic reflexes

Degree of associated deficits in intelligence

Emotional adjustment

Treatment

Physiotherapy
o manipulation of or exercising affected muscles can
help contain contractures
o Night splints to ankles stretching of achilles tendon.
o Soft splinting lessens knee contractures
o Serial plastering may restore range of movement
o Ankle-foot orthoses

Pharmacologic
o Diazepam
o Baclofen

Oral not effective

Intrathecal (continuous infusion or boluses)

o Botulinum toxin

Surgery
o Lengthening of muscles (achilles tendon)
o Soft tissue surgery around the hips and knee
o Correction of dislocations (hip)
o Transferring a tendon

Ex. With an overflexed wrist, the surgeon may

transplant a wrist flexor onto the dorsum of
the hand to increase extensor.

General principles of treatment

Define long term objectives not only in terms of motor

condition
o Cognitive skills
o Social skills
o Emotional status
o Vocational potentials
o Availability of family support

Consider patients age and growth and development

Consider alternative approaches: family based and culture

competent

Prevention

Avoiding alcohol and smoking during pregnancy

Preventive work in Rh (-) mothers

Regular antenatal care

Immunization program for rubella

Newborn screening
o Early detection of amino acid disorders,
hypothyroidism and galactosemia



PEDIATRICS2 LE6 Handout [by: msredlips

PULMONARY: CHRONIC COUGH

CAUSES OF CHRONIC COUGH

Allergic Rhinitis

Classic Asthma

Cough-variant Asthma

Respiratory Infections, with or without asthma

Immunodeficiency Syndromes

Sinus Infections especially those caused by: Streptococcus

pneumoniae, Moraxella
catarrhalis,
Nontypable
H. influenzae

Cystic Fibrosis

Ciliary Dyskinesia

Foreign body aspiration

Irritation: Air pollution, tobacco smoke, wood smoke, glue

sniffing, volatile chemicals

Swallowing Dysfunction

Gastroesophageal reflux

Habit cough

Anatomic abnormalities: TEF, Laryngeal cleft, Vocal cord

paralysis, Tracheobronchomalacia

Neurodevelopmental delays leading to frequent aspiration

Pulmonary sequestration

Bronchogenic cyst

Mediastinal tumors

Congestive heart failure

Interstitial lung disease

Differential Diagnosis of Chronic Cough (in descending order of
likelihood)

MOST COMMON CAUSES OF CHRONIC COUGH
Asthma

Chronic inflammatory disease of the airway with variable

airway obstruction and airway hyperresponsiveness

Clinical Manifestations

cough

chest tightness

wheezing

Breathlessness

Gurgly chest (halak)

Trigger Factors of Asthma in Various Age Groups

10

PEDIATRICS2 LE6 Handout [by: msredlips

In past 12 months, 4 wheezing episodes (>24h), with at least 1 physician-

confirmed, PLUS
1 Major Criterion OR
2 Minor Criteria
Parent with asthma Wheezing apart from colds
Atopic dermatitis Eosinophilia ( 4%)

Allergic sensitization Allergic sensitization to

to 1 aeroallergen* milk, egg, or peanuts

DIAGNOSIS OF ASTHMA

Modified Asthma Predictive Index

PHARMACOLOGIC APPROACH FOR INITIATING THERAPY

Classification of Asthma by Severity Before Initiation of Treatment

Clinical Control of Asthma

Determine the initial level of control to implement treatment

(assess patient impairment)

Maintain control once treatment has been implemented

(assess patient risk)

LEVELS OF ASTHMA CONTROL

PND, throat clearing, lacrimation, allergic shiners, allergic

salute, facial grimace
Comorbidities:

asthma

sinusitis

otitis media

conjunctivitis

Differentials

Vasomotor rhinitis

NARES

Infectious rhinitis

Rhinitis medicamentosa

CSF rhinorrhea

Foreign body

Classification of allergic rhinitis

Monitoring to maintain control

Control should be monitored to maintain control and

establish lowest step and dose

After the initial visit: 1-3 months and every 3 months

thereafter

After an exacerbation follow-up: within 2 weeks to 1 month

Allergic Rhinitis

nasal hypersensitivity symptoms induced by an

immunologically mediated (most often IgE-dependent)
inflammation after the exposure of the nasal mucous
membranes to an offending allergen.

Symptoms
o Rhinorrhea
o nasal obstruction or blockage
o nasal itching
o Sneezing,
o postnasal drip
o Allergic conjunctivitis

Asthma is found in as many as 15% to 38% of patients with

allergic rhinitis

a symptomatic disorder of the nose induced by an IgE

mediated inflammation after allergen exposure of the
membranes of the nose

sneezing, rhinorrhea, nasal pruritus

PEDIATRICS2 LE6 Handout [by: msredlips

11

IMMUNOLOGY
ATOPIC DERMATITIS

Itch that rash

INFANT PHASE
o birth-2yo
o cheeks, abdomen, extensor

CHILDHOOD PHASE
o 2-12 yo
o
Flexural

ADOLESCENT/ADULT PHASE
o diffuse lesions with increased scaling & decreased
excoriations

(3 major, 3 minor)

MAJOR

MINOR

family hx of atopy
xerosis (dry skin)

area of distribution
nipple eczema

relapsing course
pityriasis alba

pruritus

dermatographism




keratosis pilaris (chicken skin)




food intolerance

palmar hyperlinearity

dennie morgan fold


DIFFERENTIALS

Seborrheic Dermatitis

Diaper Dermatitis

Scabies

Psoriasis

Dishydritic Eczema

Management

Hydration

Eliminate Triggers

Antihistamines

Emollients

Steroids

UV light

Antibiotics

IMMUNODEFICIENCY

8 or more EAR infections within 1 year

2 or more serious sinus infections within 1 yr

2 or more mos on antibiotics with little effect

2 or more pneumonias within 1 year

Failure to thrive

Recurrent deep skin or organ abscess

Persistent thrush in mouth/skin after age 1

12

PEDIATRICS2 LE6 Handout [by: msredlips

Need for IV antibiotics to clear infections

2 or more deep seated infxs (meningitis, osteomyelitis,
sepsis, cellulitis)
Family history of immunodeficiency

HIV/AIDS

HIV is a virus (a retrovirus)

o HIV-1 Primarily in US
o HIV-2 Primarily in Africa & Asia

AIDS is a disease
o Virus attacks immune system
o Utilizes CD4 T-cell to reproduce its genome
o T-cells die leading to increased vulnerability to rare
opportunistic diseases
o Complications and death result from these diseases

Epidemiology

Routes of Infection

Sexual activity involving the exchange of body fluids.

Sharing contaminated needles.

Birth by infected mother.

From HIV Infection to AIDS: Four Stages of Progression

Mild symptoms like those of other diseases (e.g., soar throat,

fever, rash, headache). Lasts 1-8 weeks.

Latent period for as long as 10 years with no or few

symptoms.

AIDS related complex cluster of symptoms (e.g., swollen

glands, loss of appetite, fever, fatigue, night sweats,
persistent diarrhea).

Severe immune impairment multiple opportunist infections

(e.g., lungs, gastrointestinal tract).

AIDS Diagnosis

AIDS diagnosis after development of:

o Pneumocystis carinii pneumonia
o Kaposis sarcoma
o CD4 levels < 200/microleter.

Viral load test: determines level of HIV in body.

AIDS Treatment Options

Hope for eventual vaccine

Anti-retroviral drugs (Nevirapine, Zidovudine)

Role of Psychology

Helping people with HIV

o Psychological impact of HIV
o Compliance with medical regimes
o Palliative care
o Increasing family support

Prevention
o Behavioral Measures
o Personality/Coping

Psychosocial Impact

Stigma - Fear, blame & rejection from others.

Concerned about who in their social network they can tell.

Increased anxiety, depression and coping problems

Adverse Psychosocial Factors and AIDS Progression

Yoichi & Vedhara (2009)

Meta-analysis examining psychosocial factors on

immunological and clinical indicators of disease progression
o Social isolation, life events, depression, anger,
distress, neuroticism, lifetime traumas, avoidant
coping
o Mortality, symptoms, CD4 decline, AIDS stage

AIDS Prevention

Education is not enough continue high levels of risk

behaviors.

Abstinence is not enough

Need new intervention strategies.

o Condom use
o Needle Exchange

Risk may be linked to certain personality characteristics.

ENDOCRINE
Diabetes Mellitus
Criteria for the diagnosis of diabetes mellitus

Symptoms (polyuria, polydipsia, weight loss) of diabetes plus

1. RBS11.1 mmol/L (200 mg/dl)


or
2. FBS7.0 mmol/l (126 mg/dl).

Fasting is defined as no caloric intake for at least 8 h.

or
3. 2-hour postload glucose 11.1 mmol/l (200 mg/dl) during
an OGTT.
The test should be performed as described by WHO (86), using a
glucose load containing the equivalent of 75 g anhydrous glucose
dissolved in water or 1.75 g/kg of body weight to a maximum of 75 g
(65).

Pathogenesis of type 1 diabetes

Individuals have an absolute deficiency of insulin secretion

and are prone to ketoacidosis

Most cases are primarily due to T-cell mediated pancreatic

islet -cell destruction, which occurs at a variable rate, and
becomes clinically symptomatic when approximately 90% of
pancreatic beta cells are destroyed.

Serological markers of an autoimmune pathologic process,

including islet cell, GAD, IA-2, IA- 2, or insulin
autoantibodies, are present in 85-90% of individuals when
fasting hyperglycemia is detected.

Management of Diabetes Mellitus

Diet

Medication
o Insulin injections
o Meds to control glucose in other ways

Compliance ranges from 67% to 85%

o Hypertension

30% to 90% do not take as

prescribed
o Cholesterol control

50% stop taking after 6 months

Exercise

Stress management

Adherence to Diabetic Regimen

80% of patients administer insulin in an unhygienic manner.

58% administer the wrong dose of insulin.

77% test or interpret the glucose levels incorrectly.

75% dont eat the prescribed foods.

75% dont eat with sufficient regularity.

Psychosocial Factors

Social support: Increases adherence

Self-efficacy: Increases self-management and optimism

Self-image: Adolescents

Stress: Causes less insulin and more glucose production

PEDIATRICS2 LE6 Handout [by: msredlips

13

Congenital Adrenal Hyperplasia

Measured by 17-OHP in NBS

Prevalence 1:10,000

Definition of Terms

A disorder in adrenal steroidogenesis arising from a

deficiency in enzymes essential to cortisol, aldosterone and
androgen production

Metabolic Syndrome

21-Hydroxylase Deficiency

>90% of CAH

Required for synthesis of Cortisol & Aldosterone

Types:
o Classical

Salt wasting most severe

Simple Virilizing
o Non-Classical mildly elevated androgens

Epidemiology: common in Philippines 1:10,000

Genetics: chromosome 6

Symptoms:
o Progressive wt loss, anorexia
o Vomiting, dehydration
o Weakness, hypotension
o Hypoglycemia, hyponatremia, hyperkalemia

May appear 2 wks age

If untreated: shock, arrythmia, death

Diagnostics

11-deoxycortisol, deoxycorticosterone: elevated

Plasma renin: suppressed

Aldosterone low

Hypokalemic alkalosis

Treatment

Hydrocortisone 10-15mg/BSA/day

Fludrocortisone 0.1mg per day

Congenital Hypothyroidism

Positive NBS if TSH is elevated

Confirmatory: Elevated TSH and Low FT4

Treatment: Levothyroxine 10-15mcg/k/day

PEDIATRICS2 LE6 Handout [by: msredlips

85% of congenital hypothyroidism is due to thyroid

dysgenesis
10-15% due to dyshormonogenesis

Steroidogenesis

14

ONCOLOGY
Leukemia

Etiology is unknown and multifactorial

Genetics and environmental factors play important roles

Affects about 40/1M children under 15 yrs

ALL (acute lymphoblastic leukemia) accounts for ~ 75% of

cases

CML (chronic myelogenous leukemia) ~ <5%

Signs and symptoms

o Bone marrow failure (anemia, neutropenia,
thrombocytopenia)
o Specific tissue infiltration (lymph nodes, liver,
spleen, brain, skin, bone)

Presents with: pallor, petechiae, ecchymose,lethargy, bone

or joint pains

PE
o Lymphadenopathy
o Hepatosplenomegaly
o CNS involvement

Laboratory and Imaging Studies

o CBC, PBS
o Bone marrow aspirate
o CXR
o Ctogenetic analysis

Treatment
o Chemotherapy
o Cell transplantation

Tumors
AGE is important

Most frequently encountered malignant abdominal masses

Neuroblastoma

Wilms tumor

Hepatoblastoma

Lymphoma

Neuroblastoma

Occurs anywhere along sympathetic chain or adrenal medulla

o But abdominal in 65% of cases

Most common extracranial tumor in infants

36% < 1 year old

75% < 4 years old

Metastatic at dx: 75%

S/Sx highly associated with Neuroblastoma

Anorexia, wt loss, pallor, abd pain, irritability, weakness

Exophthalmos

Periorbital hemorrhage(raccoon eyes)

Horners syndrome

Meiosis, ptosis, enophthalmos, anhydrosis (2 cervical

sympathetic involvement)

Massive hepatomegaly

Constipation, abdominal pan

Localized back pain, weakness

Scoliosis, bladder dysfunction

Palpable nontender subQ nodules (neonatal)

Elevated urine VMA

Wilms Tumor

Arises from embryonic renal precursor cells

Most common pediatric malignancy of the kidney

Peak age at diagnosis: 2-3 years (80% diagnosed before 5

years of age)

Rare in infants

Asymptomatic mass in flank

25% with associated systemic S/Sx

o Malaise
o Pain
o Hematuria (usually microscopic)
o Hypertension (inc renin)
o Hemorrhage into tumor (10% of cases)

HEPATOBLASTOMA

Most common liver tumor of childhood (liver tumors = only

1-2% of childhood cancers)

Mean age at dx 1 year (80% diagnosed before 3 yrs old)

Advanced disease at presentation 40%

Signs and Symptoms

Asymptomatic abdominal mass

Anorexia, pain, weight loss (15%)
Jaundice rare

Laboratory Findings

Thrombocytosis (as high as 1,500,000)

AFP elevated in almost all

Lymphoma

Diffuse aggressive malignancy in children

Can present at 1-5 years old, but more common in older

children and adolescents

60% NHL; 40% Hodgkins

1/3 of NHL present with abdominal disease

Lymphoma s/sx

Abdominal pain

Vomiting

Diarrhea

Abdominal distention

Intussusception

Peritonitis

Ascites

Intussusception in child > 1 year old strong warning to look

for lymphoma

Physical Findings associated with abdominal masses

Many asymptomatic and diagnosed accidentally take a

few seconds to palpate abdomen in all patients

Location , size, consistency of mass

Bruit , ascites, distended superficial abdominal veins

Routine lab and imaging studies needed

CBC

Coagulation studies

Urinalysis

Tumor markers

Plain abdominal x-ray / UTZ / CT scan

CARDIAC
Approach to Heart Diseases in Children
Congenital vs. Acquired?

History

Physical Examination

Chest X-Ray

EKG

2DEchocardiography

Maternal History
st
Infections: 1 trimester of pregnancy
1. German measles - Congenital Rubella Syndrome; PS; PDA
2. Cytomegalovirus - teratogenic
Herpes - myocarditis last trimester

Coxsackie B
Illness
1. DM - cardiomyopathy (HOCM)

- structural (VSD, TGA,PDA)
2. SLE - Heart Blocks
3. CHD - 15% incidence of CHD
(vs 1% general pop.)



PEDIATRICS2 LE6 Handout [by: msredlips

15

Medications
1. Amphetamines (uppers) VSD, PDA, ASD, TGA
2. Anticonvulsants
a) Diphenylhydantoins PS, AS, COA
b) Trimethadione TGA, TOF, HLHS
3. Progesterone/Estrogen VSD, TGA, TOF

Alcohol - Fetal Alcohol Syndrome


- VSD, PDA, ASD, TOF

Past History
1. Cyanosis including spells

Cyanosis - deep & fast breathing

vs
Breath holding spell - holding breath

Cyanosis birth (or 2 wks of life) emergency

2. CHF
3. Weight gain/feeding
4. Heart murmur
5. Frequent Respiratory Infections (lower)

Weight affected more than the height

Weight severely affected dysmorphic conditions

Others:
o Chest pains
o Joint swellings
o Neurologic symptoms

Family History

Incidence in general population 8 to 12/1000 live births

Recurrence Risk related to recurrence risk of the syndrome or

H.D.

One child affected risk recurrence in sibling 3% (VSD)

2.5 % (TOF)

Inspection & Palpation: Abdomen

Distension ascites

Pulsatile abdominal aorta aortic run-off

Liver
o Infants : soft palpable 2 3 cm BRCM 1 year old : 2 cm &
4 5 years old : 1 cm
o Hepatomegaly : hallmark of systemic venous
congestion in infants
o Pulsatile liver : TR or inc. RA pressure

Palpation: Pulses

Rate

Regularity

Quality :
o Rate of rise
o Pulse volume

Fast & brisk : VSD, MR

Fast & large: PDA, AR, severe anemia

Simultaneous palpation of peripheral pulses delay in lower
extremities is suggestive of coarctation

HEART MURMURS Location

PEDIATRICS2 LE6 Handout [by: msredlips

16

Inspection & Palpation: Extremities

Hands & feet

o Cyanosis : clubbing of fingers & toes

Inspection & Observation: Genetic Abnormalities

Inspection & Palpation: Chest

Apex beat most lateral cardiac impulse

Point of maximal impulse

QUESTION #1: Does the patient have a MURMUR?

NO The absence of a murmur does not rule out heart disease in the
presence of other cardiac signs and symptoms.
Correlate with clinical history and ask the other questions below.

YES

PATHOLOGIC vs. PHYSIOLOGIC (innocent/functional)

TIMING
PATHOLOGIC
PHYSIOLOGIC
SYSTOLE

Ejection
All >Gr.3/6 Gr.3/6 or less


<Gr.3/6 but with
Normal heart sounds


click or abnormal
No clicks


heart sounds
Regurgitant
All regurgitant and Never


late systolic
DIASTOLIC All diastolic
Never
CONTINUOUS
All except venous
Only venous hum


hum

Does the patient have congenital heart disease?
Cyanotic Congenital Heart Disease

Truncus Arteriosus

Transposition of Great Vessels

Tricuspid Atresia

Tetralogy of Fallot

Total Anomalous Pulmonary Venous Return

Ebsteins Disease

Eisenmengers Syndrome

COMMON CXR OF CHD
Ventricular Septal Defect

Increased vascularity

Normal or enlarged cardiac size

Chamber prominence:
o either or both ventricles
o left atrium

Enlarged main and central

pulmonary arteries

Normal or small aorta

Tetralogy of Fallot

Decreased vascularity

Normal or enlarged cardiac size

right ventricular prominence

Concave main pulmonary artery

segment

Prominent aorta

BOOT SHAPED HEART

right aortic arch (in 20-25%)

Cyanotic Congenital Heart Disease
Transposition of Great Arteries: CXR

Egg on its side
RV cardiomegaly; narrow pedicle; hypervascular markings

Total Anomalous Pulmonary Venous Return

Increased vascularity

Cardiomegaly

Chamber prominence:
o right atrium
o right ventricle

Enlarged systemic vein into which

drainage occurs

Type I (Supracardiac)
o left-sided vertical vein connects pulmonary venous
confluence to the left innominate vein, right SVC or
azygos vein
o SNOWMAN APPEARANCE

EBSTEINS ANOMALY

Cardiomegaly, decrease pulmonary vascular markings;
WALL TO WALL HEART

Rheumatic Heart Disease

Chronic valvar heart disease as a sequelae of rheumatic fever

& its recurrences

Most common cause of acquired heart disease in children &

young adults worldwide

Most common cause of heart failure among school-aged

children & young adults

RENAL
Chronic Kidney Disease

Congenital and obstructive abnormalities are the most common

causes

Present between birth to 10 yo (FSGS, chronic GN)

Signs and Symptoms

o
Growth failure
o
Renal osteodystrophy
o
Anemia
o
Hormonal abnormallities

Treatment
o
Multidisciplinary
o
Symptomatic treatment eg. Acidosis NaHC03; ROD
phosphate binders; anemia erythropoietin
o
dialysis
o
Optimal: renal transplantation
--END J--
PEDIATRICS2 LE6 Handout [by: msredlips

17