Pediatric 2 Flashcards
Measles
Etiology
Transmission
Pathogenesis
Measles
Etiology:
Measles is a highly contagious viral illness caused by measles virus which is a single-stranded, lipid-enveloped RNA virus in the family Paramyxoviridae and genus Morbillivirus.
Transmission:
The portal of entry of measles virus is through the respiratory tract or conjunctivae following contact with large droplets or small-droplet aerosols in which the virus is suspended. Patients are infectious from 3days before to up to 4-6 days after the onset of rash. Approximately 90% of exposed susceptible individuals experience measles. Face-to-face contact is not necessary, because viable virus may be suspended in air for as long as 1hr after the patient with the source case leaves a room. Secondary cases from spread of aerosolized virus have been reported in airplanes, physicians’offices, and hospitals.
Pathogenesis:
Measles infection consists of 4 phases: incubation period, prodromal illness, exanthematous phase, and recovery. During incubation, measles virus migrates to regional lymph nodes. A primary viremia ensues that disseminates the virus to the reticuloendothelial system. A secondary viremia spreads virus to body surfaces. The prodromal illness begins after the secondary viremia and is associated with epithelial necrosis and giant cell formation in body tissues. Virus shedding begins in the prodromal phase. With onset of the rash, antibody production begins, and viral replication and symptoms begin to subside.
Measles
Cf
Lab tests
Dx
Ddx
Clinical Manifestations:
Measles is a serious infection characterized by high fever, an enanthem, cough, coryza, conjunctivitis, and a prominent exanthem. After an incubation period of 812 days, the prodromal phase begins with a mild fever followed by the onset of conjunctivitis with photophobia, coryza, a prominent cough, and increasing fever. Koplik spots represent the enanthem and are the pathognomonic sign of measles, appearing 1-4 days prior to the onset of the rash. They first appear as discrete red lesions with bluish white spots in the center on the inner aspects of the cheeks at the level of the premolars. They may spread to involve the lips, hard palate, and gingiva. They also may occur in conjunctival folds and in the vaginal mucosa. Koplik spots have been reported in 50–70% of measles cases but probably occur in the great majority.
Symptoms increase in intensity for 2-4 days until the 1st day of the rash. The rash begins on the forehead (around the hairline),behind the ears, and on the upper neck as a red maculopapular eruption. It then spreads downward to the torso and extremities, reaching the palms and soles in up to 50% of cases. The exanthema frequently becomes confluent on the face and upper trunk. With the onset of the rash, symptoms begin to subside. The rash fades over about 7 days in the same progression as it evolved, often leaving a fine desquamation of skin in its wake. Of the major symptoms of measles, the cough lasts the longest, often up to 10 days. In more severe cases, generalized lymphadenopathy may be present, with cervical and occipital lymph nodes especially prominent.
Modified Measles Infection:
In individuals with passively acquired antibody, such as infants and recipients of blood products, a subclinical form of measles may occur. The rash may be indistinct, brief, or, rarely, entirely absent. Likewise, some individuals who have received a vaccine, when exposed to measles, may have a rash but few other symptoms. Persons with modified measles are not considered highly contagious.
Laboratory Findings:
- The diagnosis of measles is almost always based on clinical and epidemiologic findings.
- In the acute phase reduction in the total white blood cell count, with lymphocytes decreased more than neutrophils. However, absolute neutropenia has been known to occur.
- In measles not complicated by bacterial infection, the ESR and CRP levels are usually normal.
Diagnosis:
In the absence of a recognized measles outbreak, confirmation of the clinical diagnosis is often recommended.
- IgM antibody in serum: IgM antibody appears 1-2 days after the onset of the rash and remains detectable for about 1 mo.
- Viral isolation from blood, urine, or respiratory secretions can be accomplished by culture.
- Molecular detection by polymerase chain reaction is available.
Differential Diagnoses:
Typical measles is unlikely to be confused with other illnesses, especially if Koplik spots are observed.
*Measles in the later stages or modified or atypical infections may be confused with a number of other exanthematous immune mediated illnesses and infections, including rubella, adenovirus infection, enterovirus infection, and Epstein-Barr virus infection. *Exanthem subitum (in infants) and erythema infectiosum (in older children) may also be confused with measles.
*Mycoplasma pneumoniae and group A Streptococcus may also produce rashes similar to that of measles.
*Kawasaki syndrome can cause many of the same findings as measles but lacks discrete intraoral lesions (Koplik spots) and a severe prodromal cough and typically leads to elevations of neutrophils and acute-phase reactants. In addition, the characteristic thrombocytosis of Kawasaki syndrome is absent in measles.
*Drug eruptions may occasionally be mistaken for measles.
Measles
Complications
Complications:
Morbidity and mortality from measles are greatest in:
= younger than 5 yr of age(especially <1 yr of age) and older than 20 yr of age. = crowding =severe malnutrition =low serum retinol =immunocompromised persons The complications of measles include:
- Pneumonia: is the most common cause of death in measles(manifests as giant cell pneumonia caused directly by the viral infection or as superimposed bacterial infection”Streptococcus pneumoniae, Haemophilus influenzae, and Staphylococcus aureus”.
- Bronchiolitis obliterans.
- Croup, tracheitis, and bronchiolitis.
- Acute otitis media.
- Sinusitis and mastoiditis.
- Retropharyngeal abscess.
- Diarrhea and vomiting, with dehydration as a consequence.
- Febrile sizures occur in < 3%.
- Appendicitis or abdominal pain my occur from obstruction of the appendiceal lumen by lymphoid hyperplasia.
- Encephalitis (a postinfectious, immunologically mediated process and is not the result of a direct effect by the virus. Clinical onset begins during the exanthema and manifests as seizures(56%), lethargy(46%), coma(28%), and irritability(26%). Findings in CSF include lymphocytic pleocytosis in 85% of cases and elevated protein concentrations. Approximately 15% of patients with measles encephalitis die. Another 20–40% of patients suffer long-term sequelae, including cognitive impairment, motor disabilities, and deafness. Measles encephalitis in immunocompromised patients results from direct damage to the brain by the virus. Subacute measles encephalitis manifests 1-10 mo after measles in immunocompromised patients, particularly those with AIDS, lymphoreticular malignancies, and immunosuppression. Signs and symptoms include seizures, myoclonus, stupor, and coma.
11.Hemorrhagic measles(black measles)”manifested as a hemorrhagic skin eruption and often fatal”
12.Thrombocytopenia, myocarditis, cellulitis, and toxic shock syndrome are other rare complications.
13.Measles during pregnancy is associated with high rates of maternal morbidity, fetal wastage, and stillbirths, with congenital malformations in 3% of liveborn infants.
14.Subacute sclerosing panencephalitis (SSPE) is a chronic complication of measles with a delayed onset and an outcome that is nearly always fatal. After 7-10 yr the virus apparently regains virulence and attacks the cells in the central nervous system. Measles at an early age favors the development of SSPE. Subtle changes in behaviour or school performance appear, including irritability, reduced attention span, and temper outbursts.
Measles
Ttt
Postexposure Prophylaxis:
Management of measles is supportive because there is no specific antiviral therapy. # Maintenance of hydration, oxygenation, and comfort are goals of therapy. # Antipyretics for comfort and fever control are useful.
Treatment:
infants younger than 6 mo of age. In children with signs and symptoms of vitamin A deficiency, a 3 rd age appropriate dose is recommended 2-4 wk after the 2 nd dose.
Postexposure Prophylaxis:
Susceptible individuals exposed to measles may be protected from infection by either vaccine administration or with Ig. The vaccine is effective in prevention or modification of measles if given within 72hr of exposure. Ig may be given up to 6 days after exposure to prevent or modify infection.
Ig is indicated for susceptible household contacts of measles patients, especially infants younger than 6mo of age, pregnant women, and immunocompromised persons.
Mumps
Definition & Etiology
Spread
Cf
Mumps
Mumps is an acute self-limited infection. It is characterized by fever, bilateral or unilateral parotid swelling and tenderness, and the frequent occurrence of meningoencephalitis and orchitis.
Etiology:
Mumps virus is in the family Paramyxoviridae and the genus Rubulavirus. It is a single-stranded pleomorphic RNA virus. Humans are the only natural host.
Spread:
Mumps is spread from person to person by respiratory droplets. Virus appears in the saliva from up to 7days before to as long as 7days after onset of parotid swelling. The period of maximum infectiousness is 1-2days before to 5days after onset of parotid swelling.
Clinical Manifestations:
The incubation period for mumps ranges from 12 to 25days but is usually 16-18 days. Mumps virus infection may result in clinical presentation ranging from asymptomatic or nonspecific symptoms to the typical illness associated with parotitis with or without complications involving several body systems.
The typical patient presents with a prodrome lasting 1-2days consisting of fever, headache, vomiting, and achiness. Parotitis follows and may be unilateral initially but becomes bilateral in approximately 70% of cases. The parotid gland is tender, and parotitis may be preceded or accompanied by ear pain on the ipsilateral side. Ingestion of sour or acidic foods or liquids may enhance pain in the parotid area. As swelling progresses, the angle of the jaw is obscured and the ear lobe may be lifted upward and outward. The opening of the Stensen duct may be red and edematous. The parotid swelling peaks in approximately 3days and then gradually subsides over 7days. Fever and the other systemic symptoms resolve in 3-5days.
Submandibular salivary glands may also be involved or may be enlarged without parotid swelling. Symptoms in immunized individuals are the same but tend to be less severe, and parotitis may be absent.
Mumps
Ddx
Complications
Differential Diagnoses:
-Parainfluenza1 and parainfluenza 3 viruses,
-Influenza A virus,
-Cytomegalovirus,
-Epstein-Barr virus,
-Enteroviruses,
-Lymphocytic choriomeningitis virus,
-HIV
-Purulent parotitis (caused by Staphylococcus aureus, unilateral, extremely tender, associated with an elevated white blood cell count and may involve purulent drainage from the Stensen duct),
-Submandibular or anterior cervical adenitis,
-Obstruction of the Stensen duct, -Collagen vascular diseases (Sjögren syndrome, systemic lupus erythematosus)
-Tumor, and Drugs.
Complications:
The most common complications of mumps are meningitis, with or without encephalitis, and gonadal (orchitis, oophoritis) involvement.
Uncommon complications include conjunctivitis, optic neuritis, pneumonia, nephritis, pancreatitis, mastitis, and thrombocytopenia.
Complications can occur in the absence of parotitis especially in immunized individuals.
Mumps
Ttt
Prognosis
Prevention
Treatment:
No specific antiviral therapy is available for mumps. Management should be aimed at reducing the pain associated with meningitis or orchitis and maintaining adequate hydration. Antipyretics may be given for fever.
Prognosis:
The outcome of mumps is nearly always excellent, even when the disease is complicated by encephalitis, although fatal cases from CNS involvement or myocarditis have been reported.
Prevention:
Immunization with the live mumps vaccine is the primary mode of prevention. It is given as part of the MMR 2-dose vaccine schedule, at 12-15mo of age for the 1 st dose and 4-6yr of age for the 2 nd dose. If not given at 4-6yr, the 2 nd dose should be given before children enter puberty.
Rubella
Definition & Etiology
Pathology
Rubella
Rubella (German measles or 3-day measles) is a mild, often exanthematous disease of infants and children that is typically more severe and associated with more complications in adults. Its major clinical significance is transplacental infection and fetal damage as part of the congenital rubella syndrome(CRS).
Etiology:
Rubella virus is a single-stranded RNA virus with a lipid envelope and 3 structural proteins. The virus is sensitive to heat, ultraviolet light, and extremes of pH but is relatively stable at cold temperatures. Humans are the only known host.
Pathogenesis:
Following infection, the virus replicates in the respiratory epithelium and then spreads to regional lymph nodes. Viremia ensues and is most intense from 10 to 17 days after infection. Viral shedding from the nasopharynx begins approximately 10 days after infection and may be detected up to 2 wk following onset of the rash. The period of highest communicability is from 5 days before to 6 days after the appearance of the rash.
Rubella
Cf
Laboratory findings
Dx
Clinical Manifestations:
Postnatal infection with rubella is a mild disease not easily discernible from other viral infections, especially in children. Following an incubation period of 14-21 days, a prodrome consisting of low-grade fever, sore throat, red eyes with or without eye pain, headache, malaise, anorexia, and lymphadenopathy begins.
Suboccipital, postauricular, and anterior cervical lymph nodes are most prominent. In children, the 1 st manifestation of rubella is usually the rash, which is variable and not distinctive. It begins on the face and neck as small, irregular pink macules that coalesce, and it spreads centrifugally to involve the torso and extremities, where it tends to occur as discrete macules.
About the time of onset of the rash, examination of the oropharynx may reveal tiny, rose-colored lesions (Forchheimer spots) or petechial hemorrhages on the soft palate.
The rash fades from the face as it extends to the rest of the body so that the whole body may not be involved at any one time.
The duration of the rash is generally 3days, and it usually resolves without desquamation.
Subclinical infections are common, and 25–40% of children may not have a rash. Teenagers and adults tend to be more symptomatic and have systemic manifestations, with up to 70% of females demonstrating arthralgias and arthritis.
Laboratory findings:
Leukopenia, neutropenia, and thrombocytopenia have been described during postnatal rubella.
Diagnosis:
The most common diagnostic test is rubella immunoglobulin(Ig) M enzyme immunosorbent assay, which is typically present about 4 days after the appearance of the rash.
Rubella
Ddx
Complications
Ttt & supportive care
Prognosis
Prevention
Vaccination
Differential Diagnoses:
- Measles(in severe cases it may resemble measles but absence of Koplick spots, absence of severe prodrome, and the shorter course allow differentiation).
- Adenovirus.
- Parvovirus B19 (erythema infectiosum).
- Epstein-Barr virus.
- Enterovirus.
- Roseola infantum.
- Mycoplasma pneumoniae.
Complications: are infrequent and generally not life threatening. + Postinfectious thrombocytopenia: manifests about 2wk following the onset of the rash as petechiae, epistaxis, gastrointestinal bleeding, and hematuria. It is usually self-limited.
+ Arthritis: especially in adult women, begins within1wk of onset of the exanthema and classically involves the small joints of the hands. It is self-limited and resolves within weeks without sequelae.
+ Encephalitis is the most serious complication of postnatal rubella. It occurs in 2forms: a postinfectious syndrome following acute rubella and a rare progressive panencephalitis manifesting as a neurodegenerative disorder years following rubella. + GuillainBarré syndrome, peripheral neuritis, myocarditis.
Treatment:
There is no specific treatment available.
Supportive Care:
Postnatal rubella is generally a mild illness that requires no care beyond antipyretics and analgesics. Intravenous immunoglobulin or corticosteroids can be considered for severe, nonremitting thrombocytopenia.
Prognosis:
Postnatal infection with rubella has an excellent prognosis. Reinfection with wild virus occurs postnatally in both individuals who were previously infected with wildvirus rubella and vaccinated individuals. Reinfection with serious adverse outcomes to adults or children is rare and of unknown significance.
Prevention: Patients with postnatal infection should be isolated from susceptible individuals for 7days after onset of the rash. Standard plus droplet precautions are recommended for hospitalized patients.
Vaccination:
Rubella vaccine is usually administered in combination with measles and mumps (MMR) or also with varicella(MMRV) in a 2-dose regimen at 12-15mo and 4-6 yr of age. It theoretically may be effective as postexposure prophylaxis if administered within 3days of exposure.
Roseola
Definition
Cf
Human herpesvirus 6 (HHV-6A and HHV-6B)
and human herpesvirus 7 (HHV7) cause
infection in infancy and early childhood.
HHV-6B is responsible for the majority of
cases of roseola infantum (exanthema
subitum or sixth disease) and is associated
with other diseases, including encephalitis,
especially in immunocompromised hosts.
A small percentage of children with roseola
have primary infection with HHV-7.
The peak age of primary
HHV-6B infection is 6-9 mo of life
Clinical Manifestation:
Roseola infantum is an acute, self-limited disease of infancy and early
childhood. It is characterized by the abrupt onset of high fever, which
may be accompanied by fussiness. The fever usually resolves acutely
after 72 hr (“crisis”) but may gradually fade over a day (“lysis”)
coincident with the appearance of a faint pink or rose-colored,
nonpruritic, 2-3 mm morbilliform rash on the trunk. The rash usually
lasts 1-3 days but is often described as evanescent and may be visible
only for hours, spreading from the trunk to the face and extremities.
Because the rash is variable in appearance, location, and duration, it is
not distinctive.
Associated signs are few but can include mild injection of the
pharynx, palpebral conjunctivae, or tympanic membranes and
enlarged suboccipital nodes. In Asian countries, ulcers at the
uvulopalatoglossal junction (Nagayama spots) are commonly
reported in infants with roseola.
High fever (mean: 39.7°C [103.5°F]) is the most consistent
finding associated with primary HHV-6B infection.
Additional symptoms and signs include irritability, inflamed
tympanic membranes, rhinorrhea and congestion,
gastrointestinal complaints, and encephalopathy. The mean
duration of illness caused by primary HHV-6B infection is
6days, with 15% of children having fever for 6 or more
days. Much less is known about the clinical manifestations
of HHV-7 infection. Primary infection with HHV-7 has
been identified in a small number of children with roseola in
whom the illness is indistinguishable from that caused by
HHV-6B.
Roseola
Dx
Lab findings
Diagnosis:
1.A history of 3 days of high fever in an otherwise nontoxic 10 mo old
infant with a blanching maculopapular rash on the trunk suggests a
diagnosis of roseola.
2.Viral culture is the gold standard method to document active viral
replication(expensive, time-consuming, and available only in research
lab.).
3. Detection of viral DNA by PCR on acellular fluids such as plasma
or reverse transcriptase PCR on peripheral blood mononuclear cell
samples.
Laboratory Findings:
*Low mean WBC count.
*Thrombocytopenia, elevated serum transaminase values, and atypical
lymphocytes.
*CSF: normal or only minimal CSF pleocytosis with mildly elevated
protein.
Rosella
Complications
Ttt
Prognosis
Prevention
Complications:
1.Convulsions (the most common, 1/3 of patients)
2.Partial seizures, prolonged seizures, postictal
paralysis, and repeated seizures.
3.Encephalitis, acute disseminated demyelination,
autoimmune encephalitis, cerebellitis.
4.Hepatitis, and myocarditis
Reactivation esp. in imunocompromised.
Treatment:
Supportive care is usually all that is needed for
infants with roseola.( hydration and may use
antipyretics if the child is especially uncomfortable
with the fever).
Specific antiviral therapy is not recommended for
routine cases of primary HHV-6B or HHV-7 infection.
Unusual or severe manifestations of primary or
presumed reactivated HHV-6B infection such as
encephalitis, especially in immunocompromised
patients, may benefit from treatment (Ganciclovir,
foscarnet, and cidofovir).
Prognosis:
Roseola is generally a self-limited illness
associated with complete recovery.
Although seizures are a common complication of
primary infection with HHV-6B and HHV-7, the risk
of recurrent seizures does not appear to be higher
than that associated with other causes of simple
febrile seizures.
Prevention:
Primary infections with HHV-6 and HHV-7 are
widespread throughout the human population with no
current means of interrupting transmission.
Scarlet fever
Scarlet fever is an upper respiratory tract infection
associated with a characteristic rash, which is caused by an
infection with pyrogenic exotoxin (erythrogenic toxin)–
producing in individuals who do not have antitoxin
antibodies. GAS can produce up to 12 different pyrogenic
exotoxins, and repeat attacks of scarlet fever are possible.
It is most common in children 5-15 yr old. The incubation
period ranges from 1-7 days, with an average of 3 days. The
onset is acute and is characterized by fever, vomiting,
headache, toxicity, pharyngitis, LAP, and chills. Abdominal
pain may be present; when this is associated with vomiting
before the appearance of the rash, an abdominal surgical
condition may be suggested.
The rash appears within 24-48 hr after onset of
symptoms, although it may appear with the
first signs of illness. It often begins around the
neck and spreads over the trunk and
extremities.
The rash is a diffuse, finely papular,
erythematous eruption producing bright red
discoloration of the skin, which blanches on
pressure. It is often accentuated in the creases
of the elbows, axillae, and groin. The skin has
a goose-pimple appearance and feels rough.
The cheeks are often erythematous with pallor
around the mouth( circumoral pallor).
Generally, temperature increases abruptly, may peak at 39.6-40°C
(103-104°F) on the 2nd day, and gradually returns to normal
within 5-7 days in untreated patients; it is usually normal within
12-24 hr after initiation of penicillin therapy. The tonsils are
hyperemic and edematous and may be covered with a gray-white
exudate. The pharynx is inflamed and covered by a membrane in
severe cases. The tongue may be edematous and reddened.
After 3-4 days, the rash begins to fade and is followed by
desquamation, initially on the face, progressing downward, and
often resembling a mild sunburn. Occasionally, sheet-like
desquamation may occur around the free margins of the
fingernails, the palms, and the soles.
The tongue is usually coated and the papillae are swollen. After
desquamation, the reddened papillae are prominent, giving the
tongue a strawberry appearance.
Diagnosis:
The presentation of scarlet fever can be diagnosed
clinically, further testing can be used to confirm the
diagnosis:
1.Culture of throat swab on sheep blood agar plate.
2.Rapid antigen detection test.
Treatment:
GAS is exquisitely sensitive to penicillin and
cephalosporins, and resistant strains have never been
encountered. Penicillin or amoxicillin is therefore the
drug of choice (except in patients who are allergic to
penicillins) for pharyngeal infections as well as for
suppurative complications.
[Oral penicillin V for 10 days, or a single i.m
benzathine penicillin G, or amoxicillin for 10 days,
or cephalosporin for 10 days is the treatment].
For penicillin-allergic petients: oral clindamycin for 10
days, erythromycin or clarithromycin for 10 days, or
azithromycin for 5 days.
Complications:
Cervical lymphadenitis, peritonsillar abscess,
retropharyngeal abscess, otitis media, mastoiditis, and
sinusitis still occur in children in whom the primary illness
has gone unnoticed or in whom treatment of the
pharyngitis has been inadequate. GAS pneumonia can also
occur.
Acute rheumatic fever and acute poststreptococcal
glomerulonephritis are both nonsuppurative sequelae of
infections with GAS that occur after an asymptomatic
latent period.
Epstein-Barr virus(EPV) [Infectious Mononucleosis]
Definition
Oncogenesis
Cf
It is characterized by systemic somatic complaints
consisting primarily of fatigue, malaise, fever, sore
throat, and generalized lymphadenopathy. Originally
described as glandular fever, it derives its name
from the mononuclear lymphocytosis with atypical-
appearing lymphocytes that accompany the illness.
Oncogenesis:
Benign EBV-associated proliferations include:
oral hairy leukoplakia, primarily in adults with
AIDS,
lymphoid interstitial pneumonitis, primarily in
children with AIDS.
Malignant EBVassociated proliferations include:
nasopharyngeal carcinoma,
Burkitt lymphoma,
Hodgkin disease,
lymphoproliferative disorders,
leiomyosarcoma in immunodeficient states,
including AIDS.
Clinical Manifestations:
The incubation period of IMN in adolescents is 30-50
days. In children, it may be shorter. The majority of
cases of primary EBV infection in infants and young
children are clinically silent. Patients may complain of
malaise, fatigue, acute or prolonged (>1 wk) fever,
headache, sore throat, nausea, abdominal pain, and
myalgia. This prodromal period may last 1-2 wk.
The complaints of sore throat and fever gradually
increase until patients seek medical care. Splenic
enlargement may be rapid enough to cause left
upper quadrant abdominal discomfort and
tenderness, which may be the presenting complaint
The classic physical examination findings are
generalized lymphadenopathy (90% of cases),
splenomegaly (50% of cases), and hepatomegaly (10%
of cases). LAP occurs most commonly in the anterior
and posterior cervical nodes and the submandibular
lymph
nodes and less commonly in the axillary and inguinal
lymph nodes. Epitrochlear lymphadenopathy is
particularly suggestive of IMN. Symptomatic hepatitis or
jaundice is uncommon, but elevated liver enzymes are
very common.
Splenomegaly to 2-3 cm below the costal margin is
typical (15-65% of cases) and is seen in most cases by
ultrasonography; massive enlargement is uncommon.
The sore throat is often accompanied by moderate to
severe pharyngitis with marked tonsillar enlargement,
occasionally with exudates. Palatal petechiae at the
junction of the hard and soft palate are frequently
seen. The pharyngitis resembles that caused by
streptococcal infection. Other clinical findings may
include rashes and edema of the eyelids.
Rashes are usually maculopapular and have been
reported in 3-15% of patients. Patients with IMN
treated with ampicillin or amoxicillin may experience
“ampicillin rash,” which may occur with other β-
lactam antibiotics.
Infants coinfected with HIV acquire EBV infection
Infants coinfected with HIV acquire EBV infection at
an earlier age, have higher EBV plasma loads that
are slower to resolve, and more frequently develop
pneumonia and hepatosplenomegaly and require
hospitalization compared to HIV-negative infants.
EBV
DX
DDX
LAB findings
Diagnosis:
The diagnosis of IMN implies primary EBV infection. A
presumptive diagnosis may be made by the presence
of typical clinical symptoms with atypical
lymphocytosis in the peripheral blood. The diagnosis
is usually confirmed by serologic testing, either for
heterophile antibody or specific EBV antibodies.
Culture of EBV is tedious and requires 4-6 wk.
Differential Diagnosis:
Infectious mononucleosis-like illnesses may be
caused by primary infection with cytomegalovirus, T.
gondii, adenovirus, hepatitis virus, HIV, or possibly
rubella virus.
Streptococcal pharyngitis may cause sore throat
and cervical lymphadenopathy indistinguishable
from that of infectious mononucleosis but is not
associated with hepatosplenomegaly.
Leukemia(esp. if extremely high or low white blood
cell counts, moderate thrombocytopenia, and even
hemolytic anemia).
Laboratory Tests:
In >90% of cases there is leukocytosis of 10,000-20,000 cells/µL, of
which at least two thirds are lymphocytes; atypical lymphocytes
usually account for 20-40% of the total number (mature T lymphocytes
that are larger overall, with larger, eccentrically placed indented and
folded nuclei with a lower nuclear-to-cytoplasm ratio).
Atypical lymphocytosis may be seen with many infections usually
causing lymphocytosis other than EBV including: acquired
cytomegalovirus infection (in contrast to congenital cytomegalovirus
infection), toxoplasmosis, viral hepatitis, rubella, roseola, mumps,
tuberculosis, typhoid, Mycoplasma infection, and malaria, as well as
some drug reactions.
Mild thrombocytopenia to 50,000-200,000 platelets/µL occurs in more
than 50% of patients, but only rarely is associated with purpura.
Mild elevation of hepatic transaminases occurs in approximately 50%
of uncomplicated cases, but is usually asymptomatic without jaundice.
EBV
HeterophileAntibodyTest
Specific Epstein-Barr Virus Antibodies:
Ttt
Complications
Prognosis
HeterophileAntibodyTest:
Heterophile antibodies agglutinate cells from species
different from those in the source serum. The transient
heterophile antibodies seen in infectious mononucleosis,
also known as Paul-Bunnell antibodies, are IgM antibodies
detected by the Paul-Bunnell Davidsohn test for sheep red
cell agglutination. The heterophile antibodies of infectious
mononucleosis agglutinate sheep or, for greater sensitivity,
horse red cells.
Heterophile antibody tests are positive in 75% of cases in
the 1st wk and 90-95% of cases in the 2nd wk. The most
widely used method is the qualitative rapid slide test using
horse erythrocytes.
If the heterophile test result is negative and an EBV infection
is suspected, EBV-specific antibody testing is indicated.
Specific Epstein-Barr Virus Antibodies:
EBV-specific antibody testing is useful to confirm
acute EBV infection, especially in heterophile-
negative cases, or to confirm past infection and
determine susceptibility to future infection. The
EBNA, EA, and VCA antigen systems are most
useful for diagnostic purposes.
The detection of IgM antibody to VCA is the most
valuable and specific serologic test for the
diagnosis of acute EBV infection and is generally
sufficient to confirm the diagnosis.
Treatment:
There is no specific treatment for infectious
mononucleosis.
The mainstays of management are rest, encouraging
adequate fluid and nutrition intake, and symptomatic
treatment with acetaminophen or nonsteroidal
antiinflammatory agents to manage fever, throat
discomfort, and malaise.
Bed rest is necessary only when the patient has
debilitating fatigue.
Advise against participation in contact sports and
strenuous athletic activities during the 1st 2-3 wk of illness
or while splenomegaly is present because blunt
abdominal trauma may predispose patients to splenic
rupture.
Corticosteroids: short course(<2wk)
prednisolone 1 mg/kg/day or equivalent for
7 days and tapered over another 7 days,
indicated in:
o airway obstruction,
o thrombocytopenia with hemorrhaging,
o autoimmune hemolytic anemia,
o seizures, and meningitis.
Antiviral therapy is not recommended
Complications:
1. Subcapsular splenic haemorrhage or splenic rupture.
2. 2. Airway obstruction.
3. Neurological manifestations ( headache, seizures,
ataxia, meningitis, facial nerve palsy, transverse
myelitis, and encephalitis).
4. Alice-inWonderland syndrome
(metamorphopsia)(perceptual distortions of sizes,
shapes, and spatial relationships).
5. Guillain-Barre or Reye syndrome.
6. Hemolytic anemia, aplastic anemia, mild
thrombocytopenia, or severe neutropenia.
7. Myocarditis, interstitial pneumonia, pancreatitis,
parotitis, and orchitis.
Prognosis:
The prognosis for complete recovery is
excellent. The major symptoms typically last 2-
4 wk followed by gradual recovery within 2 mo
of onset of symptoms.
Cervical lymphadenopathy and fatigue may
resolve more slowly. Prolonged and
debilitating fatigue, malaise, and some
disability that may wax and wane for several
weeks to 6 mo are common complaints even
in otherwise unremarkable cases.
Definition of congenital heart disease
Classification of congenital heart disease
Definition of congenital heart disease
Congenital heart disease(CHD) is defined as the structural ,functional or positional abnormality of the heart, in isolation or in combination, present from birth, but may manifest any time after birth or may not manifest at all
Classification of congenital heart disease
Acynotic CHD-1
A- LV or RV volume overload as: VSD, PDA and ASD
b- LV or RV pressure overload as: AS, COA and PS
Cynotic CHD-2
A- With decrease of pulmonary blood flow as: TOF, DORV+PS and single ventricle +PS
B- With increase of pulmonary blood flow as: DTGA, TAPVD and truncus arteriosus
VSD
Ventricular Septal Defects:
Ventricular septal defects (VSDs) are the most common form of congenital heart disease(30%) if bicuspid aortic valve is excluded, slightly more common in females approximately 56% female, 44% male
Type of VSD 1-perimembranous VSD =70% 2-Outlet (infundibular or conal or supracristal) defects account for 5% to 7% of all VSDs in the Western world and about 30% in Far Eastern countries 3-Inlet (or AV canal) defects account for 5% to 8% 4-Trabecular (or muscular) defects account for 5% to 20% of all VSDs
Clinical Manifestations
Small VSD:
In infants with small VSDs, a murmur usually is detected at 1 to 6 weeks of age when the infant returns for the initial checkup after discharge from the newborn nursery.
With small defects, the clinical course is benign throughout infancy and childhood.
There are normal patterns of feeding, growth, and development.
The only risk is that of endocarditis, which is rare before the age of 2 years.
By palpation, the precordial activity is normal. A thrill may be palpable along the lower left sternal border and is associated with a grade IV to VI holosystolic murmur
Moderate and Large size VSD:
may develop symptoms as early as 2 weeks of age. The initial symptoms consist of tachypnea with increased respiratory effort, excessive sweating owing to increased sympathetic tone, and fatigue when feeding. The infant progressively tiers with feeding; this symptom begins during the first month and increases in severity as pulmonary vascular resistance decreases. Symptoms occur earlier in the premature than in the full-term infant, it is not unusual for symptoms to be preceded by respiratory infection. In the absence of infection, the cardiovascular basis for the respiratory symptoms probably is pulmonary edema of mild to moderate degree with elevated pulmonary venous pressure and decreased lung compliance
In children with large shunts for 4 to 6 months, the left anterior thorax bulges outward the pulmonary component of the second sound is usually loud.
Cyanosis during the early weeks of life is often transient and frequently presents only with superimposed stress or illness. Persistent cyanosis from birth indicates a more complicated lesion than isolated VSD. However, the occurrence of cyanosis after infancy suggests reversal of the shunt to right to left because of progressive pulmonary vascular disease or the development of significant infundibular pulmonary stenosis(pulmonary stenosis)
Palpation reveals a prominent right ventricular lift that is usually maximal in the xiphoid region. There may be a very short or no systolic murmur from the VSD
Investigation:
1) ECG
A. With a small VSD, the ECG is normal.
B- moderate and large size VSD with LVH and RVH and sign of PHT 2) CXR
A-Small VSD may be Normal CXR
B- Cardiomegaly of varying degrees is present and involves the LA, left ventricle (LV), and sometimes RV. Pulmonary vascular markings increase. The degree of cardiomegaly and the increase in pulmonary vascular markings directly relate to the magnitude of the left-to-right shunt
3) Echocardiography
4) Magnatic resonance imaging 5) Cardiac catheterization
Treatment
Medical Therapy
Children with small VSDs are asymptomatic and have excellent long-term prognosis. Neither medical therapy nor surgery is indicated. If children with moderate or large VSDs develop symptomatic congestive heart, a trial of medical therapy is indicated. Furosemide is used in a dosage of 1 to 3 mg/kg/day divided into two or three doses. Chronic furosemide can result in hypocalcaemia, hypokalemia, metabolic alkalosis and renal damage. Addition of spironolactone can be helpful to minimize potassium loss. Potassium supplementation is difficult to achieve in most infants because of the unpalatable taste of the supplements.
Additional to initial therapy includes increasing the caloric density of the feedings by using milk with 24-30 Kcl/once Systemic afterload reduction with enalapril (initial dosage of 0.1 mg/kg/24 hours divided into twice daily, gradually increasing to 0.5 mg/kg/24 hours divided into twice daily dose. A traditional approach has been to administer digoxin to infants with congestive heart failure associated with moderate or large VSD and increased pulmonary blood flow. Several studies have shown that the contractile function of the left ventricle is normal or increased, casting doubt on the usefulness of digoxin. Digoxin may be indicated if diuresis and afterload reduction do not provide adequate symptom relief and surgery is not advisable. The usual dose of digoxin is 10 μg/kg/day that can be given once daily or in divided doses twice a day
Clinical Course and Prognosis
1-Patients with small defects have an excellent prognosis, albeit with a small risk of endocarditis, aortic valve insufficiency, and late cardiac arrhythmia
2-A large number of these defects close spontaneously; this number approaches 75% to 80%, with most closing in the first year of life
3- with moderate-sized defects may develop large left-to-right shunts in infancy, and their main risk is heart failure between 1 and 6 months of age.
4-Moderate and large defects, occasionally develop significant infundibular pulmonary stenosis
5-Patients with large defects are the most difficult to manage because of the dangers of mortality in the first year of life owing to heart failure and associated pulmonary infections as well as the problem of development of elevated pulmonary vascular resistance
General examination of skin in new born
Plethora is seen in polycythemia, cold and hot weather
The skin of the N.B.B. is covered by a greasy material secreted by epithelial cells called vernix caseosa (more in the preterm)which protects the skin from the effect of amniotic fluid.
Occasionally, one half of the body may appear red and the other half is pale (Harlequin color change) which is usually transient and of unknown significance.
Cyanosis :Central cyanosis is pathological ,while peripheral or acrocyanosis is benign( more in the preterm babies).
Milia: Small sebaceous cysts, pinpoint in size, whitish spots seen on the nose, cheeks and forehead, it disappears in a few weeks spontaneously. It is a normal finding.
Erythema toxicum neonatorum : red blotchy, macular patches with a white
center seen all over the body, sparing the soles and palms.
It affects 50% of full term infants, less common in preterm infants. Pustules may be seen in the center containing eosinophils.
They usually appear on the first few days and disappear spontaneously.
Mongolian spots: blue, gray, flat, macular lesions seen normally over the sacrum, sometimes on the upper back, legs, hands and rarely on the face. They may be solitary, numerous or patchy. They are seen in colored children much more than whites. They usually fade during the first few years of life. They may be misdiagnosed as bruises
PREMATURITY
PREMATURITY:
The problems of prematurity are due to poor adaptation to extra uterine life due to immaturity of body organs:
Respiratory problems:
1. R.D.S.(Respiratory Distress Syndrome).
2. Chronic lung disease: B.P.D. (bronchopulmonary dysplasia).
3. Apnea.
Neurologic problems:
1. Hypoxic-ischemic encephalopathy(H.I.E.).
2. Intraventricular hemorrhage(I.V.H.).
3. Convulsions.
Cardiovascular complications:
1. Hypotension.
2. P.D.A.(patent ductus arteriosus).
Hematologic:
1. Anemia.
2. Hyperbilirubinemia.
3. Organ hemorrhage.
4. D.I.C.
Nutritional problems (especially in those born before 32 weeks of gestation). G.I. problems (N.E.C. : necrotizing enterocolitis).
Metabolic:
Hypoglycemia, Hypocalcemia.
Renal problems :low G.F.R.
Temperature regulation e.g. hypothermia. Ophthalmologic e.g. R.O.P.(retinopathy of prematurity).
MANAGEMENT OF THE PREMATURE INFANT :
1. Delivery: should be in a hospital well equipped with resuscitation tools and highly experienced staff.
2. Neonatal management:
a. Thermal regulation either by overhead radiant warmer or an incubator. The accepted skin temperature is 36-36.5c.
b. Oxygen therapy and assisted ventilation.
c. Fluid and electrolytes therapy.
d. Nutrition: enteral, N.G. tube or parenteral.
e. Management of hyperbilirubinemia and infections.
LONG TERM PROBLEMS OF PREMATURITY:
1. Poor growth and development.
2. R.O.P.
3. B.P.D.
4. Increased rate of post neonatal illnesses.
5. Increased frequency of congenital anomalies.
Immunizations:
The timing of immunizations of premature babies is based on the infant’s chronologic age, not on the gestational age.
It may be advisable to delay administration of hepatitis B vaccine until the infant weighs 2000 g. or more.
The full doses of all immunizations should be given.
NEONATAL(PRIMITIVE)REFLEXES
NEONATAL(PRIMITIVE)REFLEXES:
1.Moro response:
The baby is put supine, his head is lifted
a little off table and then dropped suddenly supported by the examiner’s hand. There is abduction and extension of arms with opening of hands followed by adduction.
It should disappear by the age of 3-4 months.
Causes of asymmetrical Moro reflex:
-Hemiplegia.
-Fractured humerus or clavicle. -Shoulder dislocation.
-Erbs palsy. -Klumpke’s palsy.
2.Rooting reflex:
When the corner of the mouth is touched, the lower lip is
lowered and the head or tongue moves toward the stimulus.
3.Sucking reflex:
The baby should actively suck his finger or the examiners clean finger.
Causes of absent rooting and sucking reflexes:
-Septicemia. -Perinatal asphyxia. -Birth trauma. -Cold injury.
Rooting and sucking reflexes normally persist for 4 months while awake, and for 7 months while asleep.
4.Doll’s eye response:
There is a delay of eye movement if the head is turned to one side. It disappears by 2-3 weeks.
5.Stepping reflex:
The contact of the sole of the foot on the table causes stepping. It disappears by 5-6 weeks.
6.Grasp Reflex (Palmar & Plantar):
The insertion of an object or finger in the palm or sole of the baby causes reflex flexion of the fingers.
Palmar grasp disappears by 2 months, while .plantar grasp disappears by 10 months
7.Asymmetrical tonic neck reflex:
The turning of the head to one side causes extension of the arm and leg on the same side and flexion on the other side. It disappears by 2-3 months, and it persists in cerebral palsy.
SIGNIFICANCE OF PRIMITIVE REFLEXES:
Absence, persistence, or asymmetry of neonatal reflexes may indicate serious neurological or systemic problems.
