كورس الاطفال 2022
Open in Telegram
Show more
The country is not specifiedThe category is not specified
344
Subscribers
No data24 hours
No data7 days
No data30 days
Posts Archive
لسهوله الحفظ : developmental history
1month=raise head from prone position
2month=smile
3month=coos يناغي,support with forarm
4month=laugh,roll from supine to prone
6month=sit without support,move the object يحرك الاشياء
9month=crawl,catching bottle
1year=walk alon,catch pencil
15month=creep up stairs يسلق درج
18month=run and throw objects from standing without fall
2year=walk up and down steps without help,play
3year=يكدر يرسم دائره ويصعد درج ويلعب ويه اصدقائه
4year=يرسم مربع وينزل درج ويلبس ملابسه بشكل طبيعي
5year=يربط حذائه ويرسم مثلث ويقفز على الاشياء
📎 Treatment of neonatal sepsis: Supportive care and antibiotics because antibiotics take at least 12-24 hours. -warmth👉 Start intravenous line and Correct hypoglycemia👉 Vitamin K👉 oxygen👉 gentle stimulation👉 Avoid enteral feeding if very sick👉 Dopamine if the perfusion is poor👉 antibiotic in EOS👉 Ampicillin (100–150 mg/kg/d divided every 12 hr), plus Aminoglycoside (gentamicin 3–4 mg/kg/dose every 24 hr) or third-generation cephalosporin (cefotaxime 100 mg/kg/d divided every 12 hr)👉 antibiotic in LOS 👉 vancomycin (10–15mg/kg every 8–24 hr), third-generation cephalosporin (cefotaxime or ceftazidime, if Pseudomonas aeruginosa is strongly suspected) or an aminoglycoside.
🐝 duration of antibiotic therapy:
🕸Proven sepsis;Pneumonia is 10–14 days.
🕸 Proven meningitis due to GBS requires a minimum of 14 days.
🕸Proven gram-negative meningitis is treated for minimum of 21 days or 14 days after obtaining a negative culture.
🕸Osteomyelitis, septic arthritis, cerebritis & endocarditis is up to 6 wk.
🕸UTI requires 7- 14 days.
ملخص ال sepsis
———————————————————————————————-
📎Neonatal Sepsis :systemic illness induced by septicemia occurring in the first 4 weeks of life.
📎Neonates more susceptible: Immature immune response(neutrophils deficient ability to adhere to vessel walls and decreased ability deform & migrate
into tissues, have decreased chemotaxis, Decreased amount of opsonins ,Deficient monocytes). Genetic(Polymorphisms over expression or under expression of proteins /genes)
📎Classification neonatal :
-Early Onset(Onset of symptoms before 72 hours of birth): often presents fulminant, multi-systemic illness due to bacteria acquired before and during delivery. manifests frequently pneumonia/less commonly as septicemia or meningitis.Caused by GBS, Gram-negative enteric pathogens, Listeria monocytogenes, Staph, Enterococcus.
-Risk factors EOS:
🕸Maternal factors :-fever, chorioamnionitis(risk 1 / 10), PROM >18 hrs, UTI, genital colonization with GBS and diarrhea, Foul smelling amniotic fluid, Multiple per vaginum examinations, Difficult or prolonged labor, Poor socio-economic status, poor nutrition.
🕸Neonatal factors: Preterm(deficiency of Immune globulin, complement function & phagocytic activity)and low birth weight,Perinatal asphyxia(depressed immune functio),Vigorous resuscitation,Invasive procedures,Aspiration of meconium,Congenital malformations e.g. meningomyelocele,Male neonate.
-Late onset(Onset of symptoms after 72 hours of birth):cause by organisms from home or hospital,present either fulminant or localized infection.often associated with meningitis or other localized infections. Mortality rate : 2- 6 %.
caused by:Coagulase-negative staphylococci (most common in infants with CVL),S. aureus, GBS, enterococcus, and gram-negative,candida.
🕸Risk factors of LOS include:Prematurity & LBW,Prolonged hospitalization & previous antibiotics use,Presence of foreign like ET tube & catheters,Invasive procedures ,Lack of breast feeding,Superficial infections,Aspiration of feeds).
🕸Sepsis Syndrome: septicemia is associated with altered organ perfusion (hypoxia, increased blood lactate, oliguria & altered mental state). If untreated, this condition leads to early septic shock and progresses quickly into refractory shock & multi organ dysfunction and death.
📎Clinical manifestations of neonatal sepsis :demand a high index of suspicion for early diagnosis.The most common manifestation is respiratory distress appear most commonly on day 1 of life, the majority by 12 hours of age in EOS and an
alteration in feeding behavior in LOS.
So these manifestations are: Lethargy, jaundice and temperature instability, Respiratory (Distress after a period of normality and apnea), Arrhythmia, hypotension and shock, Poor feeding, vomiting, abdominal distention and bilious aspirates, irritability, seizure and bulging fontanelle, Petechial rashes, bleeding from puncture sites and sclerema,unexplained metabolic acidosis, hyperglycemia or hypoglycemia.
-Pneumonia(tachypnea, chest retraction, grunting, early cyanosis, apneic spell , cough is unusual Findings on auscultation of the chest are non-specific and non- contributory)
-Meningitis(often silent, highly suggestive manifestations of meningitis are high-pitched crying, fever, seizures, neck retraction and bulging anterior fontanelle).
📎Diagnosis: Specific(Blood culture,CSF examination and culture,Urine culture,Tracheal aspirate culture,
Body surface cultures,PCR,Latex agglutination test).
🕸Indications to do CSF exam & culture:positive blood culture,when clinical course or laboratory data strongly suggest bacterial sepsis,Infants who initially worsen with antimicrobial therapy.
👉Normal parameters of CSF in neonates :
Leukocytes(30 cells /μl, more than 60% of them are polymorphs),Glucose(about 50% of blood glucose),Protein(up to 150 mg /dl in term babies and up to 180 mg /dl in preterms)
-Diagnosis is suggested by :
■ CSF protein level > 150 mg/dl.
■ Glucose < 30 mg/dl.
■ Leukocytes > 30/μl and positive Gram stain.
■The diagnosis is confirmed by CULTURE.
Hypoxic-Ischemic Encephalopathy (HIE)
🫂🫂🫂🫂🫂🫂🫂🫂🫂🫂🫂🫂🫂🫂🫂🫂🫂🫂🫂🫂
👏 HIE is an important cause of permanent damage to CNS that may lead to neonatal death or manifested later as cerebral palsy or developmental delay.
👏 Brain Damage:
-Term Newborn: Necrosis of cerebral cortex (later, cortical atrophy) and parasagittal ischemic injury, so they often have focal cortical infarcts that manifested as focal seizures and hemiplegia.
-Preterm Newborn: Periventricular leukomalcia of white matter (later, spastic diplegia), status marmoratus of basal ganglia and IVH.
👏 Brain Regions vulnerable for damage: Basal Ganglia, Hippocampus, Purkinje Neurons in Cerebellum, Brain-stem, Periventricular white matter tracts.
👏Treatment: Hypothermia(decreases the rate of apoptosis and reduces the energy reqirements so preserves the antioxidants)👉 cerebral cooling or systemic hypothermia to a core temprature of 33.5°C within the 1 st6hrs of life and lasting to 72hrs👉 Rewarming is gradual over 6-8 hrs👉 To control seizures(Phenobarbitone 20 mg/kg, Phenytoin 20 mg/kg, Lorazepam 0.05-0.1 mg/kg/dose)👉 Supportive care👉 Prevent hyperthermia👉 Adequate oxygenation👉maintain BP 👉 hemodynamic status 👉 acid-base balance 👉 control possible infection is important.
👏 Bad Prognosis: initial blood pH < 6.7, Low Apgar Score (0-3) at 5 min, Decerebrate posture, Lack of spontaneous activity, High Base deficit ( > 20 -25 mmol/l)
👏Long Term Handicaps: Developmental Delay, Microcephaly Cerebral Palsy ,Deafness ,Seizures ,Blindness ,Problems with cognition, memory, fine motor skills and behavior
ملخص محاضره Asphyxia
————————————————————————————————
👾Asphyxia: no spontaneous breathing or represented irregular breathing movement after birth. severe enough to cause metabolic acidosis, neonatal encephalopathy, and multi-organ system dysfunction.
-Anoxia : Complete lack of oxygen in the cells.
-Hypoxia : Decreased availability of oxygen in the cells.
-Hypoxemia : Decreased arterial concentration of oxygen.
-Ischemia : Insufficient blood flow to the cells.
👾 Prenatal Risk Factors: Extreme maternal age (<20 or >35 yr), Placenta previa and abruption, Preterm gestation, Meconium stained amniotic fluid, Malpresentation and abnormal lie, PROM, Post term gestation, Pre-eclampsia, Fetal bradycardia, Multiple pregnancy,DM,Drug use
👾Causes: -Antenatal factors: Placental insufficiency:Low maternal o2[anemia, pulmonary or cardiac or neurologic disease],low maternal blood flow (Infection, shock, dehydration),low blood from placental(cord prolapse, cord entanglement, true knot, cord compression), Impaired gas exchange across placenta or fetal tissues ( maternal hypertension, vascular disease, Diabetes Mellitus, drug abuse, postmaturity, placental calcification, infarct or fibrosis), Increased fetal oxygen requirement (fetal anemia, fetal infection, or intra uterine growth retardation).
-Intranatal factors: Inadequate oxygenation of maternal blood (hypoventilation during anesthesia, CHD, RF or CO poisoning), Low maternal BP (acute blood loss, spinal anesthesia, great vessels compression by gravid uterus), Uterine tetany (oxytocin induced), Premature separation of placenta,Compression or knotting of umbilical cord,Placental insufficiency due to toxemia or postmaturity.
-Postnatal factors: severe respiratory distress ,fetal cyanotic congenital heart disease, Severe anemia, Shock, failure of breathing adequately after birth because of a cerebral defect or narcosis or injury.
👾 Effects of Birth Asphyxia: Adrenal hemorrhage, DIC, Subcutaneous fat necrosis, hyponatremia, hypoglycemia, hypocalcemia or myoglobinuria,GIT(Perforation, ulceration with hemorrhage and necrosis), Acute tubular or cortical necrosis, Pulmonary hypertension, pulmonary hemorrhage, RDS,MI, hypotension, tricuspid insufficiency,CNS(Hypoxic-ischemic encephalopathy, infarction, intracranial hemorrhage, seizures, cerebral edema, hypotonia or hypertonia).
👾 Shunting of blood to brain, heart and adrenals and away from lungs, gut, kidneys, liver, spleen and skin, in an attempt to maintain perfusion to more vital organs.
👾 Biochemical Changes: Increase in lactate👉 acidosis👉 Myocardial Depression 👉Reduced Cardiac Output👉 Respiratory acidosis👉 free radicals and nitric oxide in damaged tissues.
👾 Circulatory Response of Fetus👉 ↑ shunting through Ductus Venosus, Ductus Arteriosus and Foramen Ovale👉 Transient maintenance of perfusion of the brain, heart, and adrenals👉 periventricular leukomalacia👉 Hypotension(myocardial dysfunction, capillary leak syndrome and hypovolemia)
👾Clinical: -Before delivery(Abnormal HR,IUGR, Increased movements of fetus)
-At delivery(No spontaneous breathing, meconium stained amniotic fluid)
-After delivery(hypotonic or hypertonic, Pallor, cyanosis, apnea, bradycardia and no response to stimulation,Crebral edema lead to brainstem depression, Seizures)
👾 American criteria for Birth Asphyxia:(pH <7 in an umbilical artery blood sample, Persistance of Apgar Score < 3 at 5 minutes, Neonatal Encephalopathy manifesting as seizures, hypotonia or coma in the immediate neonatal period, multi-organ dysfunction).
ملخص محاضره Lymphoma احمد عبد الله من احد الزملاء👏
————————————————————————————
Hodgkin lymphoma affected B lymphocytes
***R S (Reed Sternburgen ) Cell is pathognomic +hall mark of Hodgkin lymphoma مهمة
Peak age of HL is 15 _35 (Adolescents +young adult )
لكن في developing conteries
Peak age before Adolescents
** HL Lymphom is most common cancer in Adolescents + young adult
2 nd most common malignancy is Non hodgkin lymphoma
( HL )3 rd most common in children younger than 15 yrs
**Most predominant HL classification is Nodular lymphocytes HL
Clinical featur (HL )
Painless , Nontender , firm , rubbery, cervical or suprclavicular LAP
Usually medistinal
Clinically hepatosplenomegaly rarely
ممكن يجي المريض sing and symptom of airway obstruction
Hepatocellular dysfunction
Bone marrow infliteration
Below diaphragm rare (3%)
System symptoms important in staging
1 unexplained fever >38 c
2weight loss >10% over 6 months
3 drenching night sweats.
Dignosis ( HL)
جدا مهمة **
Any pt with persistent unexplained lymphomadenopathy +unassociated with obvious underlying inflammatory or infectious process _ لازم اسويله
Chest radiography [CT or PET scan ](to see if there is large medistinal mass)
قبل ما نسوي اله
Lymph node biopsy
CT scan particularly important in
Size of medistinal mass
Extent of medistinal mass
Most relapse occur 1st 3 years after diagnosis
Poor prognosis of HL
Tumor bulk
Stage at dignosis
Extra lymphatic disease
Presence B sptoms (systemic)
If pt relapse (less than 12 mnth from dignosis )
Indication __ myleablative chemotherapy and autologous stem cell transplantation with or without radiation
NHL
IN adult ___indolent بطيء
IN Pediateric ___ high grade +aggressive
NHL
Survival rate 90_95 % localized
70_90% advanced
Small number NHL due specific etiology :
HIV , EBV
Bloom syndrome , ataxia _telangtesia
Severe combined immunodeficiency syndrome , without _ALdrich syndrome
4 subtype of NHL
LBL from immature B or T lymphocytes
٣الباقي يجن من mature 👇
BL
DLBCL
ALCL
Surgery in NHL is used for dignosis
Radiation therapy indication :
1_CNS involved in LBL
2_presence of acute superior medistinal syndrome
3_paraplegia
Treatment of NHL is multiple agent systemic chemotherapy with intact tracheal chemotherapy
-Erb pulsy: Most common, 5th and 6th cervical nerves injury, absence of Biceps reflex and Moro reflex, arm retains a position of adduction and internal rotation, fully extended at the elbow, with pronation of the forearm and flexion of the wrist and fingers; “Waiter Tip position”. Most of them resolve spontaneously. may also be associated with injury to the phrenic nerve.
-KLUMPKE PALSY: Involves the C8 and T1 nerves, resulting in weakness of the intrinsic hand muscles and long flexors of the wrist and fingers, The grasp reflex is absent but the biceps reflex is present. may be associated with ipsilateral Horner syndrome (ptosis, miosis and and enophthalmos).
-Total arm paralysis:all nerve roots are involved.
-treatment: pain management and holding the affected arm in comfortable position, passive range-of motion exercises should be started and continued weekly for at least 3 months.
Infants without recovery by 3 to 6 months of age may be considered for surgical exploration.
🐝phrenic nerve injury: 3rd – 5th cervical nerve roots, paralysis of the ipsilateral diaphragm. It can be associated with brachial plexus injury. Respiratory distress, recurrent episodes of cyanosis with diminished breath sounds on the affected side.Bulging of the abdomen does not occur with inspiration.
-treatment: supportive in hopes of recovery for 30 days. Surgical plication or diaphragmatic pacing may be needed.
—-——————————————————————————-
🐝 CLAVICULAR FRACTURE: most frequently fractured bone during birth.
-risk factors: HBW ,Prolonged second stage of labor ,Shoulder dystocia ,Instrumented deliveries ,Increased maternal age,treatment: Pain relief for 5 - 7 days until the callus formed.
🐝 LONG BONE FRACTURES: Breech presentation, CS,LBW,treatment: Immobilization and splinting. Closed reduction and casting, Proximal femoral fractures may require a spica cast.
🐝 INTRA-ABDOMINAL INJURY: Liver injury is more common than spleen.
-clinical: sudden pallor, shock, abdominal distention, and abdominal discoloration,anemia, poor feeding, tachypnea, and tachycardia.
-treatment: Volume replacement and correction of any coagulopathy, rupture or hemodynamic instability, a laparotomy is required to control the bleeding.
ملخص birth trauma ج٢
————————————————————————————————
🐝 INTRACRANIAL INJURIES Risk factor:Forceps delivery,Vacuum extraction,Prolonged second stage of labor,Precipitous delivery,Macrosomia.
👾 EPIDURAL HEMORRHAGE :is very rare in neonates.It primarily arises from injury to the middle meningeal artery.Frequently associated with a cephalohematoma or linear skull fracture.It’s lentiform lesion in the temporo-parietal region.
-Clinical: Hypotonia ,Seizures ,Bulging fontanelles ,Change in the level of consciousness
-Treatment: If such signs are found, surgical evacuation is necessary.
👾 SUBDURAL HEMORRHAGE: most common intracranial hemorrhage in term newborns. It is caused by rupture of bridging veins.The most common location for SDH is interhemispheric or tentorial.
-clinical: Respiratory symptoms such as apnea,Seizures,Focal neurologic deficits,Irritability and an altered level of consciousness.
-treatment: Mostly closely observation without surgical intervention.Surgical evacuation is necessary when increased intracranial pressure.
👾 SUBARACHNOID HEMORRHAGE: second most common, caused by rupture of the bridging veins or small leptomeningeal vessels.
-clinical: Respiratory symptoms such as apnea,Seizures,Focal neurologic deficits,Irritability and an altered level of consciousness.
-treatment: Close monitoring may be all that is necessary.but if signs of herniation are encountered, surgical evacuation is warranted.
👾 INTRAPARENCHYMAL HAEMORRHAGE:
-Intracerebral hemorrhage:causes(Rupture of an arteriovenous malformation or aneurysm.Coagulation disturbances. Secondary to a large ICH in any other compartment)
-Intracerebellar hemorrhage :causes(More common in preterm, primary hemorrhage or may result from venous hemorrhagic infarction or from extension of intraventricular hemorrhage)
-Clinical: clinically silent in preterm, term infant(Seizures ,Hemiparesis ,Irritability ,Depressed level of consciousness)
-treatment: Symptomatic treatment and support.
Neurosurgical intervention.
👾 GERMINAL MATRIX HEMORRHAGE (Intraventricular Hemorrhage):causes(Trauma,Perinatal asphyxia,Secondary to venous hemorrhagic infarction in the thalamus)
-Factors involved in pathogenesis:(Ischemia / reperfusion,Fluctuating cerebral blood flow,Increase in cerebral venous pressure,Platelet dysfunction,Coagulation disturbances)
-clinical: preterm newborn(usually silent or presented with decreased levels of consciousness and spontaneous movement, hypotonia , abnormal eye movement), term newborns(seizures, irritability, apnea, lethargy, vomiting with dehydration and full fontanels)
-treatment: Supportive care,Careful monitoring,Surgical intervention.
—————————————————————————————
🐝 Retinal Hemorrhage: 75% of vacuum deliveries, 33% of spontaneous vaginal deliveries, and 6.7% of cesarean deliveries. Associated optic nerve injury.can be seen up to 3 to 4 weeks after birth.
🐝 Congenital Muscular Torticollis: unilateral shortening of the sternocleidomastoid muscle,Occur in breech delivery, right side is affected more often than the left.usually discovered in the first 6 - 8 weeks of life.head is tilted toward the side of lesion & rotated to the contralateral side. The chin is slightly elevated.Treatment: Gentle stretching,Surgery
🐝 FACIAL NERVE PALSY: Forceps delivery, Prolonged second stage of labor.Traumatic facial palsies resolve in 2 - 3 weeks.
-clinical: Weakness of the affected side. At rest, the nasolabial fold is flat,mouth and the eye remains persistently open on the affected side, During crying, there is inability to wrinkle the forehead or close the eye.Lacerations and bruising. Neurologic findings.
-treatment: artificial tears and taping to prevent corneal injury. Neurosurgical repair only after lack of resolution during 1 year of observation.
🐝 BRACHIAL PLEXUS INJURY: paralysis of upper arm muscles following trauma to spinal roots C5 -T1.
-risk factors (Macrosomia, Shoulder dystocia,Breech presentation, Difficult & instrumented deliveries)
ملخص Birth trauma ج١
————————————————————————————————
🐝 RISK FACTORS: macrosomia, Instrumental deliveries, breech presentation, Versions and extractions, precipitous delivery, extreme prematurity, Fetal anomalies, short maternal stature, pelvic anomalies Oligohydramnios, Primiparity.
——————————————-
🐝 Erythema and Abrasions: Mainly due to forceps, are self-limited and no require treatment.
🐝 Petechiae: Due to tight nuchal cord, a precipitous delivery, or a breech presentation. No specific treatment , they usually disappear within the 1 st few days after birth.
🐝 Ecchymosis & Bruising:traumatic and breech. deliveries,increased risk of hyperbilirubinemia.More in preterm newborns than in term. Most of them resolve spontaneously within 1 week.
🐝 Subcutaneous Fat Necrosis: most commonly in term and post-term newborns, focal pressure and ischemia to adipose tissue, Resolution:spontaneously by 6 - 8 weeks of age. hard & well-circumscribed, surrounded by erythema, Require long-term follow-up for the development of hypercalcemia.
🐝 Lacerations: Usually occur from scalpel use, Most commonly are mild lacerations that are restricted to the skin, most common sites are the scalp, the gluteal region, and the thigh. Adhesive tape across the laceration is usually sufficient.
🐝 caput saccedaneum: serosanguineous fluid collection above the periosteum, soft tissue swelling with purpura and ecchymosis, may extend across the midline, edema disappears within the 1st few days of life, Molding of the head disappear during the 1st weeks of life. Rarely result in shock. No specific treatment is needed,In cases of shock, blood transfusion is needed.
🐝 cephalohematoma: subperiosteal blood collection by rupture of vessels beneath the periosteum, Swelling usually over a parietal or occipital bone, not cross a suture line and is often not associated with discoloration of the overlying scalp, not apparent for several hours to days because the bleeding is slow, resolve over the course of 3 to 4 weeks. If infection is suspected (aspiration of the mass).If sepsis is developed (antibiotics are used ). hyperbilirubinemia(treated by phototherapy).
🐝 subgaleal haemorrhage : bleeding between the galea aponeurosis of the scalp and the periosteum. firm-to-fluctuant mass that crosses suture lines.The mass is typically noted within 4 hours of birth. sequestration of 40% or more of blood volume of the newborn and cause hemorrhagic shock.clinical findings for SGH includes tachycardia, a falling hematocrit and increasing OFC in the first 24 to 48 hours after birth.
-Diagnosis:Use either CT scan or MRI,blood test, Bilirubin levels, Coagulation profile.
-Treatment: Supportive, Transfusions if blood loss is significant, severe cases surgical evacuation and cauterize the bleeding vessels. lesions typically resolve over a 2–3 week period.
———————————————————————-
🐝LINEAR SKULL FRACTURES : Usually affect the parietal bones.May occur due to compression from forceps or from the skull pushing against the maternal symphysis or ischial spines.Usually need only close follow-up evaluation and monitoring.
🐝 DEPRESSED SKULL FRACTURES: Forceps delivery is one of the major risk factors. fracture is > 1 cm increase possibility of an intracranial process, fracture is < 1 cm, depressed, and with no neurodeficit, it can be managed with close monitoring.
-Indications for surgical managemen: bone fragments in the cerebrum, neurologic deficits, increased intracranial pressure,
cerebrospinal fluid beneath the galea, Failure to closed manipulation.
-Intrauterine infection : may be presented with the scarring or active lesions of the skin and CNS findings ; microphthalmia, retinal dysplasia, chorioretinitis, microcephaly, hydranencephaly and intracranial calcifications.
🕸Diagnosis: Definitive diagnosis is by positive viral culture from vesicles in 24–72 hours. PCR can assist in diagnosis but may be falsely negative in the CSF, Electroencephalography and brain imaging.
🕸treatment: Acyclovir (60 mg/kg/d divided q8h),Localized disease:14 days,Disseminated & CNS disease:21 days.Topical ophthalmic drugs are helpful for eye lesions.
🕸prevention: by cesarean section within 6 hours after rupture of the membranes in the presence of known infection
ملخص ال TORCH ج٢
————————————————————————————————
🦋Rubella: highly contagious illness, single stranded RNA, In non-immunized populations(10 - 20% susceptible), Reinfection occurs in 2% but is generally subclinical, transmitted to the fetus through the placenta and is capable of causing serious congenital defects, abortions, and stillbirths. The risk of fetal infection and congenital defects is 80 - 85% in 1st trimester, bu 12-20weeks, the risk of congenital defects decreases to 10-20%. After 20 weeks is 0- 10 %
🕸 Congenital Rubella Syndrome : Cardiac defects, Microcephaly and encephalitis, Cataracts, salt & pepper retinopathy and microphthalmia, Sensorineural deafness, (Blueberry Muffin) rash due to extramedullary hematopoiesis, Radiolucency of long bones, Hepatosplenomegaly, IUGR, Adenopathy, Thrombocytopenia and purpura.
🕸Diagnosis: characteristic clinical illness in the mother (rash, adenopathy, and arthritis). Cord blood rubella specific IgM and PCR of amniotic fluid. Postnatally, the confirmation of diagnosis is by :culture of pharyngeal secretions, blood, urine, CSF in the infant. Increase of rubella-specific IgM antibodies, rubella-specific IgG antibodies that persist at a higher levels,RT-PCR.
🕸treatment: no specific treatment for congenital rubella infection. Close monitoring within the first 6-12 months of life is recommended; particularly for the evaluation of hearing impairment.Preventive measures include recommended immunizations.
🕸prognosis: heart defects often can be corrected surgically, but damage to the nervous system is permanent.
————————————————————————————————
👾 Cytomegalovirus Infection: human herpesvirus 5, HHV-5, the most common virus transmitted in utero, Transplacental( It can occur during either primary or reactivated infection but it is more common in primary infection which results in fetal infection in 30% to 40% of cases),Acquired Infection around the time of delivery (via contact with infected genital tract secretions) & postnatally (via blood transfusion or ingestion of CMV-infected breast milk or direct contact with other body fluids such as urine and saliva).
🕸 Clinical: Intracranial calcifications,Chorioretinitis, Growth restriction,Microcephaly, Direct (cholestatic) jaundice, Hepatosplenomegaly,Petechiae and blueberry muffin spots, sensorineural deafness in 20%–30%. Human CMV is the most common cause of nonhereditary sensorineural hearing loss in children.
🕸Diagnosis: Amniocentesis, Culture, PCR
🕸Treatment: Supportive,Ganciclovir therapy ((6 mg/kg IV q12h for 6 weeks) recommended for neonates with symptomatic congenital infection affecting the central nervous system and may prevent progression of hearing loss and neuronal damage and promote head circumference growth in the first 6 - 12 months of life.
————————————————————————————————
💐 Herpes Simplex: HHV-2 & HHV -1: dsDNA, Intranatal infection (acquired through an infected birth canal, it is about 88% - 93% of the cases), Postnatal infection (via direct contact with affected areas, it is about 5% - 10%), Antenatal infection(intrauterine:via contact after rupture of membranes, <2 %). 70% of mothers with primary infection at the time of delivery are asymptomatic.
🕸 The risk of neonatal infection with primary maternal infection is 25%–60%.While risk is <2% in recurrent HSV infection.
🕸clinical: localized and disseminated infection is usually 5–14 days of age, while CNS disease usually presents later, at 14–28 days.
-Localized to skin, eyes and mouth (45%) disease : Vesicular lesions on an erythematous base or zoster-like eruptions. Keratoconjunctivitis, ulcerative lesions of the mouth, palate, and tongue.
-Disseminated disease(25%): poor feeding, fever/ hypothermia, lethargy, apnea, convulsion, respiratory distress, hepatomegaly, jaundice and DIC.
-CNS disease(30%): Seizures, lethargy, irritability, tremor, poor feeding, temperature instability and a bulging fontanelle.
