PEDIATRICS REVIEWER

Outline
I. Respiratory Diseases
A. Community Acquired Pneumonia
B. URTI
C. Asthma
D. Allergic rhinitis
II. GI Diseases
A. AGE
B. Intestinal parasitism
III. Infectious Diseases
A. Dengue
IV. Skin infections
A. HFMD
B. Impetigo
C. Head lice

RESPIRATORY DISEASES

Community Acquired Pneumonia (Nelson)

- Definition - inflammation of lung parenchyma
- Leading cause of infectious death globally among children < 5 y/o
- Etiology

-
- Most common: Microorganisms
- Non-infectious causes: aspiration, foreign bodies, hydrocarbons, hypersensitivity reactions, drug or radiation induced pneumonitis
- Difficult to determine etiology
- S. pneumoniae (pneumococcus) is the most common bacterial pathogen in children 3 weeks to 4 years of age
- Mycoplasma pneumoniae and Chlamydophila pneumoniae are most frequent bacterial pathogens in children 5 years and
older
- S. aureus pneumonia often complicates illness caused by influenza viruses
- Viral pathogens are the most common causes of lower respiratory tract infections in infants and children older than 1 month, but younger than
5 yrs of age
- Respiratory syncytial virus (RSV) and rhinoviruses are the most commonly identified pathogens, esp in children younger than 2 yr of
age
- Pathogenesis
- Normal defense mechanisms: mucociliary clearance, macrophages, secretory IgA, coughing
- Viral pneumonia - spread of infection along airways accompanied by direct injury of respiratory epithelium —> swelling, abnormal secretions,
cellular debris —> airway obstruction (small airways of infants make them susceptible) —> atelectasis, interstitial edema, hypoxemia (VP
mismatch) —> secondary bacterial infection
- Bacterial pneumonia - colonization of trachea —> gain access to lungs OR direct seeding of lung tissue after bacteremia
- M pneumoniae —> attach to respi epithelium —> inhibit ciliary action —> cellular destruction and inflammatory response in
submucosa —> airway obstruction —> spread of infection along bronchial tree
- S pneumoniae —> local edema —> aid in the proliferation of organisms, spread to adjacent portions of lung —> focal lobar
involvement
- GAS —> results in more diffuse lung involvement —> necrosis of tracheobronchial mucosa, formation of large amounts of exudate,
edema, local hemorrhage with extension to interalveolar space
- S. Aureus - confluent bronchopneumonia, unilateral
- Recurrent pneumonia - 2 or more episodes in a single year or 3 or more episodes ever with radiographic clearing between occurrences
- Clinical Manifestations
- Preceded by rhinitis and cough, usually several days prior
- Tachypnea - most consistent clinical manifestation
- Increased work of breathing accompanied by: Intercostal, subcostal and suprasternal retractions, Nasal flaring, Use of accessory muscles
- Crackles and wheezing - difficult to localize esp in children with hyperresonant chest
- Cyanosis and lethargy - in infants mark severe infection
- Fever - lower in viral < bacterial
 - Difficult to distinguish

-
- Abdominal distention (due to swallowed air and ileus) and pain (common in lower lobe pneumonia)
- Liver may seem enlarged due to downward displacement
- Differential Diagnosis
- Hereditary disorers
- Disorders of immunity
- DIsorders of Cilia
- Anatomic disorders
- Diagnosis
- Chest X-ray - PA and L show infiltrates
-

Viral Bacterial

hyperinflation with bilateral interstitial infiltrates and peribronchial large pleural effusion, lobar consolidation
cuffing,

normal or not elevated High Fever

> 20,000/mm3, lymphocyte predominance 15- 40k/mm3

- Pneumococcal - confluent lobar consolidation

- Definitive - PCR assay, isolation of organism from blood, pleural fluid or lung
- Need for hospitalization:
- Age <6, toxic appearance, immunocompromised, mod to severe respiratory state, vomiting, dehydration, no response to therapy,
social factors
- TREATMENT
- Antibiotics (5-7 days, <10 days or 5 days if azithromycin)
- Amoxicillin (90 mg/kd/day orally BID)
- Alternative: cefuroxime and co-amoxiclav
- Macrolide (Azithromycin) - School age or adolescent with M or C pneumoniae
- Alterntive clarithromycin or doxycycline
- Fluoroquinolones - adolescents
- Viral - don’t give antibiotics
- Hospitalized - receive supportive care and may require intravenous fluids; respiratory support, including supplemental oxygen, continuous
positive airway pressure (CPAP), or mechanical ventilation; or vasoactive medications for hypotension or sepsis physiology
- Additional: oral zinc - 10 mg/day for <12 mos
- COMPLICATIONS
- Pleural effusion - blunting of posterior and lateral costophrenic angle
- Pneumothorax - CXR as pleural lines
- direct spread of pneumonia within the thoracic cavity (pleural effusion, empyema, and pericarditis)
- bacteremia and hematologic spread
- meningitis, endocarditis, suppurative arthritis, osteomyelitis
- Parapneumonic effusions and empyema (differentiate transudative from exudative)
- PREVENTION
- PCV and influenza vaccines
- PROGNOSIS
- slow response to therapy
- improvement in clinical symptoms (fever, cough, tachypnea, chest pain) within 48-72 hours
- CXR if there is lack of response to initial treatment
- mortality is rare

URTI
- Definition
- Acute viral infection of URT
- Can be common cold, sinusitis, pharyngitis, retropharyngeal and lateral pharyngeal abscess, tonislitis, croup, acute epiglottitis, bacterial
tracheitis
- Common cold
- Pathogenesis
- Mechanism
- Direct hand to hand contact
- Inhalation of small-particle aerosols - Usually airborne from coughing
- Deposition of large-particle aerosols - Expelled during a sneeze and land on nasal or conjunctival mucosa
 - Causative agents - Rhinovirus and coronavirus
- Clinical Manifestation
- Onset occurs 1-3 days after viral infection
- The usual cold persists for 1 week
- Symptoms vary according to age
- Infants: fever and nasal discharge may predominate
- Older children and adults: fever is uncommon
- First symptom: sore or scratchy throat followed by nasal obstruction and rhinorrhea
- Cough is associated with 2/3 of colds
- Begins after onset of nasal symptoms and may persist for an additional 1-2 weeks after resolution of other symptoms
- Other systemic symptoms: fever, headache, hoarseness, body malaise, difficulty in sleeping, and decreased appetite
- Physical findings are limited to the upper respiratory tract
- Increased nasal secretion
- Change in color or consistency of mucus
- Swollen nasal cavity, erythematous nasal turbinates
- Anterior cervical lymphadenopathy (a form of defense mechanism) and conjunctivitis
- Abnormal middle ear pressure is common
- Differential Diagnosis
- Allergic rhinitis
- Vasomotor rhinitis
- Rhinitis medicamentosa
- Foreign body
- Sinusitis
- Streptococcosis
- Pertussis
- Congenital syphilis
- Diagnosis
- Clinically
- Viral - culture, antigen detection, PCR, serology
- Bacterial - cultures, antigen detection
- Allergic rhinitis - nasal smear
- Treatment and Prevention
- Supportive
- Antiviral - ribavirin
- Antihistamine - not usually given, 1st gen can help reduce rhinorrhea (anticholinergic)
- Antipyretics and NSAIDS as needed
- Nasal decongestants
- Vit C prophylaxis - prevent
- Antitussives - non productive cough only
- Vaccines and handwashing
- Complications
- Acute otitis media
- Sinusitis
- Asthma exacerbation
SINUSITIS
ASTHMA
- Definition: Chronic inflammatory disorder
- Associated with airway hyperresponsiveness → recurrent episodes of wheezing, breathlessness, chest tightness and coughing, particularly at night or in
the early morning
- Pathogenesis
- Airway hyperreactivity
- Inherent tendency of the trachea and bronchi to narrow in response to a variety of stimuli
- Airway inflammation
- Exposure to allergens → cells, interleukins, prostaglandins will be released → producing asthma symptoms
- Classification
-

Severity Daytime/Nighttime PEF or FEV1

PEF Variability

Intermittent <2 days/week >90%

<2 nights/month <20%

Mild Persistent > 2 days/week but not daily >80%

> 2 nights/month 20-30%

Moderate Persistent Daily 60-80%

> 1 night/week but not nightly 30%

Severe Persistent Throughout the day <60%

 Often 7x/week 30%
- Types
- Recurrent wheezing in early childhood
- Triggered by common respiratory viral infections
- Resolves in preschool/lower years
- Chronic asthma associated with allergy
- Persists into childhood and adulthood
- Triggers
- Allergens
- Animal allergens
- Mold spores
- Pollens
- Insects
- Drugs
- Food
- Irritants
- Paint odors
- Hair spray
- Perfumes
- Chemicals
- Air pollutants
- Tobacco smoke
- Weather changes
- Viral infections
- Rhinovirus
- Clinical Manifestations
- Intermittent dry cough
- Expiratory wheezing
- Shortness of breath
- Chest tightness
- Barrel-chested
- Symptoms are severe at night or in the early morning, and improve through the day
- Sometimes triggered by hyperventilation, laughing, cold or dry air and airway irritants
- Risk factors:
- Family history of allergy
- History of other allergic conditions
- Parental asthma
- Symptoms apart from colds

ALLERGIC RHINITIS
- Definition
- Common chronic disease affecting 20-30$ of children
- Inflammatory disorder of the nasal mucosa marked by nasal congestion, rhinorrhea, and itching, often accompanied by sneezing and
conjunctival inflammation
- Epidemiology
- Associated with a 3-fold increase in risk for asthma at an older age
- Incidence rates approaching 40%
- Genetic factors, changes in environment, diet, and the microbiome
- Symptom may appear in infancy; diagnosis generally established by the time the child reaches age 6 year
- Prevalence peaks late in childhood
- Risk factors
- Family history of atopy
- Serum IgE higher than 100 IU/mL before 6 year
- Mothers smoke heavily: even before delivery and above all before the infants reach 1 yr
- Heavy exposure to indoor allergens
- Delivery by cesarean section with a parental history of asthma or allergies
- Lack of exposure to the maternal microbiota through fecal/vaginal flora during delivery
- Children between 2-3 yr old who have elevated anticockroach and antimouse IgE: inc risk of wheezing, AR and atopic dermtitis
- Occurence of 3 or more episodes of rhinorrhea in the 1st year of life: AR at age of 7 yr
- Protective risk factors
- Exposure to dogs, cats, and endotoxin early in childhood protects against the development of atopy
- Prolonged breastfeeding, not necessarily
- Early introduction to wheat, rye, oats, barley, fish and eggs
- Reduced diversity of the intestinal microbiota during infancy is associated with increased risk of allergic disease at school
age
- Etiology and Classification
- Ethnopathogenesis:
- Characterized by a constellation of symptoms (sneezing; rhinorrhea; obstruction of the nasal passages; conjunctival, nasal and
pharyngeal itching; and lacrimation) all occurring in a temporal relationship to allergen exposure
- Manifestations caused by sensitization of IgE-rich intraepithelial mast cells with allergens
 - 2 factors necessary for expression
- Sensitivity to an allergen
- Presence of the allergen in the environment
- Inhalant allergen: cause of all forms of AR irrespective of terminology
- Classification

-
- Pathogenesis
- Exposure of an atopic host to an allergen leads to the production of sIgE (allergen-specific IgE) which is strongly associated associated with
eczema throughout childhood and with asthma and rhinitis after age 4 yr
- Early-phase allergic responses
- Initiated by bridging of the IgE molecules on the surface of mast cells by allergen
- Characterized by degranulation of mast cells and release of preformed and newly generated inflammatory mediators, including
histamine, prostaglandin 2, and the cysteinyl leukotrienes
- Late-phase
- Appears 4-8 hr following allergen exposure
- Inflammatory cells, including cysteinyl leukotrienes, cationic proteins, eosinophil peroxidase, major basic protein and serve as a
source of IL-3, IL-5, granulocyte-macrophage colony-stimulating factor and IL-13
- Priming
- Due to repeated intranasal introduction of allergens
- A more brisk response even with a lesser provocation
- Over the course of an allergy season: multifold increase in submucosal mast cells takes place
- Clinical Manifestations
- Older children blow their noses, but younger children tend to sniff and snort
- Nasal itching → grimacing, twitching, picking of the nose → epistaxis
- Allergic salute
- Upward rubbing of the nose with an open palm or extended index finger
- To relieve itching and briefly unblock the nasal airway
- Gives rise to nasal crease (hortizontal skin fold over the bridge of the nose)
- Diagnosis based on symptoms in the absence of an upper respiratory tract infection and structural abnormalities
- Intermittent nasal congestion
- Itching
- Sneezing
- Clear rhinorrhea
- Conjunctival irritation
- May lose their sense of smell and taste;others may experience headaches, wheezing and coughing
- Nasal congestion severe at night → mouth brething and snoring, interfering with sleep and rousing irritability
- Signs on PE
- Abnormalities of facial devleopment
- Dental malocclusion
- Allergic gape (continuous open-mouth breathing)
- Chapped lips
- Allergic shiners (dark circles under the eyes)
- Transverse nasal crease
- Conjunctival edema, itching, tearing, and hyperemia
- Nasal exam
- Clear nasal secretions
- Edematous, boggy and bluish mucus membranes with little or no erythema
- Swollen turbinates → block the nasal airway
- Thick, purulent nasal secretions → infection
- Differential diagnosis
- Evaluation entails:
- Thorough history
- Environment
- Diet
- Family history of allergic conditions (eczema, asthma, AR)
- PE
- Sneezing
 - Rhinorrhea
- Nasal itching
- Congestion
- Laboratory evaluation
- Elevated IgE, sIgE antibodies
- Positive allergy skin test
- Nonallergic rhinitides
- Sporadic symptoms
- Causes are often unknown
- Nonallergic inflammatory rhinitis with eosinophils
- Imitates AR in presentation and response to treatment
- Without elevated IgE antibodies
- Vasomotor rhinitis
- Excessive responsiveness of the nasal mucosa to physical stimuli
- Infectious rhinitis, structural problems (nasal polyps, septal deviation), rhinitis medicamentosa (caused by overuse of
topical vasoconstrictors), hormonal rhinitis associated with pregnancy or hypothyroidism, neoplasms, vasculitides, and
granulomatous disorders

-
- Complications
- Undertreated AR → detracts from the quality of life, aggravates asthma and enhances its progression
- Allergic conjunctivitis
- Characterized by itching, redness, swelling of the conjunctivae
- Present in at least 20% of the population and >70% of patients with AR
- Chronic sinusitis
- Common complication of AR
- Sometimes associated with purulent infection, but most patients have negative bacterial cultures despite marked mucosal
thickening, and sinus opacification
- Marked eosinophilia
- Sinusitis of triad asthma
- Asthma, sinusitis with nasal polyposis, aspirin sensitivity
- Often responds poorly to therapy
- Coexists with asthma may be taken too lightly or completely overlooked
- Up to 78% of patients with asthma have AR, 38% with AR have asthma
- Aggravation of AR consicides with exacerbation of asthma and treatment of nasal inflammation reduces bronchospasm, asthma-
related emergency department visits and hospitalizations
- Postnasal drip associated with AR → persistent or recurrent cough
- Eustachian tube obstruction and middle ear effusion are frequent complications
- Chronic allergic inflammation causes hypertrophy of adenoids and tonsils → eustachian tube obstruction, serous effusion, otitis media, and
obstructive sleep apnea
- Linked to snoring in children
- Children with rhinitis: anxiety and physical, social, emotional issues that affect learning and ability to integrate with peers
- Contributes to headaches and fatigue, limits daily activities, interferes with sleep
- Laboratory findings
- Epicutaneous skin tests
- Best method for detection of sIgE, with a positive predictive value of 48.7% for epidemiologic diagnosis of AR
- Inexpensive and sensitive, risks of discomfort are minimal
- Prior to exam, montelukast should be withheld for 1 day, most sedating antihistamine preparations for 3-4 days, and nonsedating
antihistamines for 5-7 days
- Serum immunoassays for sIgE
- For patients with dermatographism or extensive dermatitis, those taking medications taht interfere with mast cell degranulation,
others at high risk for anaphylaxis, and some who cannot cooperate with the procedure
- Presence of eosinophils in the nasal smear supports the diagnosis of AR, and neutrophils suggest infectious rhinitis
- Eosinophilia and measurements of total serum IgE concentrations → low sensitiity
- Treatment
- ARIA:

-
- Goals: safe effective prevention and relief of symptoms
- Specific measures to limit indoor allergen exposure may reduce the risk of sensitization and symptoms of allergic respiratory
disease
- Allergen-specific immunotherapy is a well-defined treatment for IgE-mediated allergic disease
- Allergy immunotherapy: effective treatment for AR and allergic conjunctivitis
- Change the course of allergic disease and induce allergen-specific immune tolerance

Oral histamines Reduces sneezing, rhinorrhea, and ocular symptoms

Second-generation antihistamines are preferred → sedation

Pseudophedrine Nasal and sinus congestion and pressure and other symptoms e.g. rhinorrhea, sneezing,
lacrimation, itching eyes, oronasopharyngeal itching and cough
Oral vasoconstrictor distrusted for causing irritability and insomnia for its association with
infant mortality

Nasal spray ipatropium bromide Treatment of serous rhinorrhea

Intranasal decongestants Should be used for <5 days and should not be repeated more than once a month to avoid
(oxymetazoline and phenylephrine) rebound nasal congestion

Leukotriene-modifying agents Modest effect on rhinorrhea and nasal blockage

Nasal saline irrigation Good adjunctive option with all other treatments of AR

Intranasal corticosteroids For patients with more persistent, severe symptoms

Most effective therapy for AR, may also be beneficial for concomitant allergic conjunctivitis
- Prognosis
- Therapy with nonsedating antihistamines and topical corticosteroids → improves health-related quality-of-life measures
- Remission rate is between 10-23%
- Pharmacotherapy that will target cells and cytokines involved in inflammation and treat allergy as a systemic process
AGE
- Definition: infection of the gastrointestinal tract cause by bacterial, viral or parasitic pathogens
- Common manifestations are: diarrhea and vomiting
- Epidemiology
- Second most common cause of child deaths worldwide
- Interventions that have contributed to decline in mortality
- Rotavirus vaccination
- Improved case management of diarrhea
- Improved nutrition of infants and children
- Etiology
- Infection acquired through the fecal-oral route or by ingestion of contaminated food or water
- Associated with poverty, poor environmental hygiene and development indices
- Enteropathogens that are infectious in a small inoculum can be transmitted person-to-person, or cholera, which is passed as a consequence
of contamination of food or water supply
A. Non-infectious

B. Bacterial
C. Viral
 D. Parasitic

- Pathogenesis
- Noninflammatory diarrhea
- Enterotoxin produced by some bacteria
- Destruction of villus cells by viruses
- Adherence by parasites
- Adherence and/or translocation by bacteria
- Usually seen in the colon
- Clinical presentation dysentery/bloody stools
- Inflammatory diarrhea
- Caused by bacteria that directly invade the intestine
- Produce cytotoxins with consequent fluid, protein and cells that enter the intestinal lumen
- Usually seen in the proximal small bowel
- Clinical presentation: watery diarrhea
- No fecal leukocytes in stool exam
- Penetrating
- Involves the distal small bowel
- E.g. salmonella typhi
- Risk factors
- Environmental contamination
- Increased exposure to enteropathogens
- Young age
- Immunodeficiency
- Measles
- Malnutrition
- Lack of exclusive or predominant breastfeeding
- Clinical Evaluation of Diarrhea
- Most common manifestations: diarrhea, abdominal cramps and vomiting
- Nausea and vomiting : upper intestinal infection
- Fever: suggests an inflammatory process
- Severe abdominal pain and tenesmus: involvement of the large intestine and rectum
- Assess the degree of dehydration and acidosis and provide rapid resuscitation and rehydration with oral or intravenous fluids
 - Obtain appropriate contact, travel or exposure history. Include information on exposure to contact with similar symptoms, intake of
contaminated food or water, child-care center attendance, recent travel of patient or contact with a person who traveled to a diarrhea-endemic
area, and use of antimicrobial agents
- Clinically determine the etiology of diarrhea for prompt management
- IMCI
 -
- Management
- Oral rehydration therapy
- Oral rehydration salts
- Na/Glucose transporter
- Main driver of the therapeutic effect of ORS
- Na and Glucose will go in which water will follow
- Enteral Feeding and Diet selection
- Aids in recovery from the episode
- Once rehydration is complete, food should be reintroduced
- Breastfeeding or nondiluted regular formula should be resumed as soons as possible
- Zinc Supplementation
- Oral zinc (20mg/day) for 10-14 days
- Prevention
- Promotion of exclusive breastfeeding
- Improved complementary feeding practices
- Rotavirus immunization
- Improve water and sanitary facilities and promotion of personal and domestic hygiene
INFECTIOUS DISEASES
1) Dengue
a) Definition
i) Dengue infection is a systemic disease caused by arthropod borne viruses
ii) It has a wide clinical spectrum that includes severe and non-severe forms
iii) Course includes 3 phases, namely:
(1) Febrile
(2) Critical
(3) Recovery
b) Course of Dengue Illness
i) Febrile phase
(1) Lasts 2-7 days
(2) Clinical signs and symptoms may include the following:
(a) Fever
(b) Headache
(c) Body malaise
(d) Myalgia
(e) Arthralgia
(f) Retro-orbital pain
(g) Anorexia
(h) Nausea / vomiting
(i) Diarrhea
(j) FLushed skin
(k) Rash (petechial, Hermann’s sign)
(3) Laboratory tests
(a) CBC → leukopenia with or without thrombocytopenia
(b) Dengue NS1 antigen test
(c) Dengue IgM antibody test (optional)
ii) Critical phase
(1) Defervescence occurs on the 3rd to 7th day of illness and patients may improve or deteriorate
(2) Warning signs:
(a) Abdominal pain or tenderness
(b) Persistent vomiting
(c) Clinical signs of fluid accumulation
(d) Mucosal bleeding
(e) Lethargy
(f) Restlessness
(g) Liver enlargement > 2 cm
(h) Laboratory → increase in hematocrit > 20% from baseline, and/or thrombocytopenia
(3) Further deterioration may lead to shock, with or without respiratory distress, severe bleeding, and/or severe organ
impairment
(4) Period of significant plasma leakage usually lasts from 24-48 hours
iii) Recovery phase
(1) Patients general well-being improves, hemodynamic status stabilizes and diuresis ensues
(2) Classical rash of “isles of white in the sea of red”
c) Etiology
i) Caused by 4 closely related but antigenically distinct serotypes 1, 2, 3, 4 of the genus Flavivirus
ii) Infection provides life-long immunity against infecting viral serotype but not against other serotypes
iii) Principal vector is Aedes aegypti
d) Epidemiology
i) Peak months for dengue are July to August
ii) Majority of cases were male and belonged to 1 - 10 years old age group

2) Hand, Foot, Mouth Disease (HFMD)

● Common viral illness usually affecting infants and children less than 5 years old
● Characterized by: oral enanthem + macular/maculopapular/vesicular rash of the hands and feet
● Usually starts with:
○ Fever
○ Reduced appetite
○ Sore throat
○ Malaise
● Virology: Coxsackie A16 and Enterovirus A71: most frequently associated with HFMD, responsible for majority of large outbreaks
● Incubation period: 3-5 days, 2-7 days
● Pathogenesis:
○ Mode of transmission
■ Oral ingestion of virus shed from gastrointestinal or URT of infected individuals
■ Contact with vesicle fluid or oral and respiratory secretions
■ Fecal shedding: up to 10 weeks after onset of infection
■ Respiratory shedding: up to 30 days after onset of infection
○ Once ingested, enterovirus replicate in the submucosal lymphoid tissues of the lower intestine and pharynx
 ○ Enterovuirus then spread to regional lymph nodes → viremia → infection of reticuloendothelial tissues and multiple organs → death
of infected cells + inflammation + necrosis
● Biopsies of HFMD vesicular lesions:
○ Vesicular fluid: Loose strands of fibrin, lymphocytes, monocytes and neutrophils
○ Overlying Epidermis: extensive acantholysis + reticular degeneration with perivascular foci of lymphocytic, monocytic, and
neutrophilic leukocytes in upper dermis
○ Upper epidermis: shadow cells, follicles and sweat glands contain necrotic cells
○ Light microscopy of biopsies of skin lesions or scrapings of the base of vesicles does not demonstrate nuclear inclusion
bodies and multinucleated giant cells, which helps to distinguish HFMD from varicella-zoster virus and herpes simplex
virus
● Clinical features
○ Presentation
■ Mouth or throat pain (verbal children) or refusal to eat (nonverbal children)
■ Fever generally < 38.3C
■ No prodromal symptoms (but if present, usually, fever, fusiness, abdominal pain, emesis, diarrhea)
○ Examination findings:
■ Oral enanthem + exanthem (but one may occur without the other)
■ Oral enanthem:
● Anterior to faucial pillars: tongue & buccal mucosa >> gingivolabial groove and soft and hard palates > uvula,
lips, tonsils
● Erythematous macules → vesicles surrounded by thin halo of erythema → vesicles rupture → superficial ulcers
with greyish-yellow base and erythematous rim
○ Vesicles: 1-5 mm or greater
○ Ulcers: 1-10mm or greater
■ Exanthem:
● Macular, maculopapular, or vesicular (1-10mm)
○ Vesicles: thin-walled, contains clear/turbid fluid, with thin halo of erythema
● non-pruritic , usually not painful (painful if due to Coxsackie A6), resolve in 3-4 days
● Typical locations: hands (dorsum of fingers, interdigital area, palms), feet (dorsum of toes, lateral border of feet,
soles, heels), buttocks, legs (upper thighs), and arms
● Less common locations: torso, face
○ Enterovirus A71 HFMD: associated with severe illness, complicated by CNS disease (rhomboencephalitis, acute flaccid paralysis,
aseptic meningitis), pulmonary edema, and hemorrhage, and heart failure
○ Coxsackie A6 HFMD: associated with more severe disease than typical HFMD
■ Higher fever
■ Wider distribution
■ More extensive skin involvement
■ Longer duration
■ Palmar and plantar desquamation 1-3 wks after HFMD
■ Nail dystrophy
● Complications
○
○
3) CCCC