راس طفلي صغير-مثال آخر للتوضيح

[ONE]

استشاره وصلتني بايميلي من منتدى آخر وحبيت اعرضها لكم للفائده:

السلام عليكم د.طارق ورحمه الله وبركاته.

انا سيده ابلغ من العمر 23 عام ورزقت بطفلين و طفلي الثاني ولد وحجم راسه صغير جدا.

طبعا مع اسالتي سوف ختصر لكم الاجوبه:

-وزنه صغير عند الولاده 2300 كم, اكمل 38 اسبوع في الحمل.
-نعم اصبت بحمى في الشهر الخامس وازلت الحمى بعد 5 ايام بدون اي مضاعفات.
-لايوجد احد مصاب باي مرض وراثي بالاسره وانا متزوجه من رجل لايقربني بالنسب.
-لااخذ اي ادويه.
نعم اخبروني مع فحص لطفل انيوجد في راسه تكلسات ولم افهم ماذا يعنون.
-نعم يوجد لدينا قطط في البيت .
-نعم تاخر بالنمو الذهني والجسماني والان عمره عامان.
نرجو الفائده.

الجواب:
وعليكم السلام ورحمه الله وبركاته:

وصفج بحاله الطفل لها علاقه بامراض وراثيه سببها مايسمه مجموعه TORCH وهي عباره عن اصابه فيروسات او طفيليات اثناء الحمل ومجموعه TORCH اختصار لعده اسماء
TORCH = Toxo, Other (HIV, syphilis), Rubella, CMV, Herpes (HSV, VZV)يشترك صغر راس الطفل ووجود تكلسات مخيه بمرضين هم toxoplasmosis or CMV (cytomegalo virus)
وتكون الاصابه عادته في الاشهر الاخيره من الحمل لمرض توكسو لكن ضررها اقل اذا مااصيب في اول اشهر الحمل.
اما اذا اصيب بفيروس CMV فتكون الاصابه شدده في الاشهر الاولى منها في الاخيره.

الامراض السابقه مثل الايدز او الهربز او الزهري او الحصبه الالمانيه ايضا تصاب بها المرأه الحامل وتسبب تلف دماغي او عصبي للطفل لكن وصفج لاينطبق عليها.

عدما سالتج هل يوجد حيوانات في البيت اجبتي بنعم يوجد لديكم قطط, نعلم ان القطط او الثعالب وبعض الثديات تحمل Toxoplasmosis في امعائها وتتم الاصابه بملامسه فضلات القطط.

ننصح المرأه الحامل بعدم تربيه الحيوانات اثناء الحمل واذا اصيبت بحمى في هذه الفتره فيجب عليها مراجعه طبيب الحمل لاجراء الفحوص واعطاءها الادويه المناسبه لتخفيف وطأت الاصابه.

للاسف اصابه طفلك متاخره والان يجب اعطائه الادويه في حاله نشط جرثومه توكسو واصبه العين اما بالنسبه لتحسن حالته الهنيه فصعب التوقع بها حيث منهم من يعدي هذه المرحله ومهم من يصاب بالصرع مستقبلا.

لذا علاج المشاكل المترتبه لمرض توكسو مهمه.
هناء سوف اضع بعض الصور لجميع الحالات لشكل الاطفال والبالغين المصابين بمجموعه تورش اثناء الحمل مع توضيح كامل لطرق وتشخيص وعلاج مجموعه تورش لتكون مرجع للاطباء او طلاب الطب ف هذا المنتدى.

وشكرا اختنا الفاضله على المشاركه.

انتهت الاستشاره
+++++++++++

طفل مصاب بضمور الراس كما في مرض TOXO or CMV

http://upload.farsuae.com/thumbnail/42784544/cm1.jpg (http://upload.farsuae.com/preview/42784544/cm1.jpg.html)

طفل مصاب بالتهاب شبكيه العين كما في مرض TOXO or CMV

http://www.neuae.com/up/get-1214155449.jpg (http://www.neuae.com/up)
تكلسات دماغيه ما في مرض TOXO or CMV

http://upload.farsuae.com/thumbnail/55832522/tx2.jpg (http://upload.farsuae.com/preview/55832522/tx2.jpg.html)

اصابه جلديه لمرض الزهري في مرحله متقدمه

http://upload.farsuae.com/thumbnail/98954358/sy2.jpg (http://upload.farsuae.com/preview/98954358/sy2.jpg.html)

اصابه في العضو الذكري لمرض الزهري يسى chancer وهو غير مؤلم وفي اول مراحله مما يهمل ويصيب زوجته بالزهري

http://upload.farsuae.com/thumbnail/91724547/sy6.gif (http://upload.farsuae.com/preview/91724547/sy6.gif.html)

طفل مصاب بالزهري الوراثي

http://upload.farsuae.com/thumbnail/19128988/sy1.jpg (http://upload.farsuae.com/preview/19128988/sy1.jpg.html)



حساسيه لمرض الزهري في اول مراحله يتم اهماله

http://upload.farsuae.com/thumbnail/93996139/sy5.gif (http://upload.farsuae.com/preview/93996139/sy5.gif.html)

شكل الاسنان في مرض الزهري الوراثي

http://upload.farsuae.com/thumbnail/13798227/sy3.gif (http://upload.farsuae.com/preview/13798227/sy3.gif.html)

شكل الانف في مرض الزهري اوراثي
http://upload.farsuae.com/thumbnail/97274716/sy4.jpg (http://upload.farsuae.com/preview/97274716/sy4.jpg.html)

سرطان الجلد لمرض الايدز ويسمى kaposi sarcoma

http://upload.farsuae.com/thumbnail/88864273/hiv.jpg (http://upload.farsuae.com/preview/88864273/hiv.jpg.html)
التالي مرجع مهم قمت بتلخيصه من كتاب برادلي المعروف لدى الاطباء:

Congenital Infections

TORCH = Toxo, Other (HIV, syphilis), Rubella, CMV, Herpes (HSV, VZV)

HIV
• Infection is perinatal in most (3rd trimester or at delivery); directly related to maternal viral levels:
o 0% transmission with viral load <1000 copies
o 63% with >100,000 copies and NO AZT
• Transmission in breast milk occurs
• Features:
o ALL are symptomatic (wrt HIV) at birth
o Four clinical stages: Not symptomatic; mild; moderate; severe symptomatic
 Mild sym – lymphadenopathy, hepatosplenomegaly, dermatitis, parotitis
 Moder – anemia, bacterial mening, candidiasis, chronic diarrhea and much more
 Severe – AIDs defining illness (just like the adults)
o Early progressors – early encephalopathy and OIs
o Late progressors – remain asymptomatic until school age
o Neurologic complications
 HIV encephalopathy MOST common (OIs of CNS rare)
• Developmental regression
• Neurological dysfunction (spasticity, hyperreflexia, weak, EPS)
• Acquired microcephaly (if onset < 2yrs) and brain atrophy
• May be fulminant, progressive or stepwise
• 20-30% without HAART; 5-7% with HAART
• MRI – Atrophy, demyelination, basal ganglia calcification (when rapid)
 DSPN – occurs; neuropathy and myopathy rare
 PCNSL – 3-4% - most common cause focal deficit in kids with HIV (rarely Toxo)
 Stroke – inflammatory vasculopathy – 1.3% / yr risk; hemorrhagic 2nd to ITP
• Diagnosis – usual viral PCR studies
• Treatment
o Prenatal AZT during last trimester reduces transmission to 8% risk; 2-4% rate with HAART
o HAART therapy for infected kids

CMV
• Most common (1-2%) – 1 infection in mom acquired via contact with others infected body fluids
o RFs – low socioeconomic class; work in childcare
• Transmission to fetus transplacental – 50% risk in maternal 1 infection; 1% risk during reactivation
• 1st trimester infection is associated with devastating neurological complications (active organogenesis)
• IF symptomatic at birth or abnormal MRI – HIGH chance of CP & MR
• Features (% are of those that are symptomatic at birth):
o Asymptomatic in utero in MAJORITY – 10% manifest symptoms – 30% fatal
o Systemic
 IUGR
 Hepatosplenomegaly (70%)
 Thrombocytopenia; Jaundice
o Ocular – chorioretinitis (20%)
o Neurological
 SN Hearing loss (60%) – also occurs in 15% of initially asymptomatic by age 3-4
 Microcephaly at birth (50%) or at 1 year or age (34%)
 Mental retardation (50%) and developmental delay
 Cerebral palsy (50%)
 Seizures (10%)
o Imaging
 Intracerebral calcifications - periventricular (80%)
 Migrational disorders (lissencephaly, polymicrogyria etc…) – unique to CMV
 Ventricular dilation; WM abnormalities
• Diagnosis
o Viral culture (urine, blood, CSF)
o Serology (IgM in neonate OR 4 fold elevation in specific IgG)
o PCR
o In infants with DD and microcephaly – establish Dx with serology and imaging (calcification)
• Treatment – Ganciclovir (but NO need unless ACTIVE infection of some type e.g. retinitis)

Toxoplasmosis
• 1/1000 live births; transplacental infection during 1 maternal infection and chronic infection in immunocompromised mom
• Highest risk of congenital infection during 3rd trimester (60-65%) BUT lowest risk of sequelae
• Lowest risk of congenital infection during 1st trimester (15-25%) BUT highest risk of sequelae
• Features (Triad – hydrocephalus, chorioretinitis and intracranial calcifications):
o 75-90% newborns are Asymptomatic BUT may appear later in infancy or childhood
o Systemic
 Lyphadenopathy (common)
 Hepatosplenomegaly, jaundice, rash, pneumonitis (less common)
 Blueberry muffin lesions – dermal erythropoiesis (also seen in CMV)
o Ocular – Chorioretinitis (76% of symptomatic i.e. very common)
o Neurological
 Microcephaly (25%)
 Hydrocephalus (40%)
 CP (20-50%)
 MR (40%)
 Seizures (50%)
o Imaging
 Ventricular dilation (60%)
 Calcification (80%) – basal ganglia and periventricular
 Hydrocephalus – most common cause of the congenital infections
• Diagnosis
o Newborns - IgM titres in neonates or 4 fold sera elevation
o Older child with MR – Positive serology (IgG) with compatible clinical features
• Treatment
o Infected Newborns – Pyrimethamine + Sulfadiazine + Folic acid x 1yr
 Improves outcomes, reduces neuron morbidity, decreases calcifications
o Infected moms during pregnancy - ??>12 weeks same regimen reduces congenital infection

Syphilis
• Transplacental passage - most infectious during 1 or 2 stages
• 30-50% fetal transmission rates
• CDC criteria: any child born stillborn or alive to untreated mom with syphilis has congenital syphilis
• Features:
o Early features in 30% (mainly systemic) – i.e. 70% are asymptomatic – serology positive
 Periostitis and osteochondritis affecting long bones (most common)
 RASH on soles and palms
 Hepatosplenomegaly
 Syphilitic rhinitis persistent (“snuffles”)
 Lymphadenopathy
 Meningoencephalitis (variable)
o Late features (untreated > 2yrs)
 Hutchinson’s teeth (pear shaped upper incisors)
 Saddle nose
 Saber shins
 Syphilitic rhagades (perioral fissures)
 Neuro: Mental retardation; CP; SN; Hearing loss; Hydrocephalus
• Diagnosis
o Long Bone radiographs
o Serology (VDRL and FTA-ABS)
• Treatment – All CDC defined – Penicillin G 10-14 days

Herpes Simplex (85% type 2)
• Transmission occurs via:
o During DELIVERY through contact with infected secretions – MOST
 50% infection rate with lesions; 33% with asymptomatic sheading
 CS – prevents infection usually BUT 20-30% of cases occur after CS
o Transplacental (during viremia or 1 infection);
o Ascending > prolonged rupture of membranes
o Post-nataly via infected oral secretions
• Neonatal infection highest during 1; lower during reactivation
• Features:
o Intrauterine infection – resemble other congenital infections + cutaneous lesions
 Cutaneous – bullae, scarring, vesicle (>90%)
 Systemic – choriretinitis, hepatosplenomegaly
 Neurologic – microcephaly, hydranencephaly
o Neonatal HSV (acquired at birth) – Three forms recognized
1. Mucocutaneous (42%)
• Eye, skin and mucosal involvement (vesicles etc)
• 94% normal development; 0% mortality
2. Disseminated (23%)
• Resembles ordinary bacterial sepsis
• 60% Normal development (of survivors); 60% mortality
3. Encephalitis (35%)
• Lethargy, poor feeding, stupor & coma, seizures
• 40% Normal development; 15% mortality
• Imaging – NOT temporal lobes – is diffuse encephalitis
• Sequelae – seizures, MR, visual and motor impairment
o 8% Recurrence in survivors
• Diagnosis
o EEG – Periodic phenomena sensitive and specific
o Imaging – may be normal
o CSF HSV PCR
• Treatment – Any suspicion (fever, altered LOC) in infants, start treatment until investigations done
o Acyclovir 30mg/kg/d divided tid

Rubella
• Respiratory transmission – cause of German measles – winter/spring rash, fever, coryza
• Maternal infection asymptomatic often – 1st trimester 90% fetal infection; 3rd trimester 30% rate
• Rates declined 99% with immunization program – now seen in the non-immunized only
• May be asymptomatic at birth with later development of clinical manifestations
• Features (devastating disease) -
o Systemic – fetal death, premature birth, cardiac malformations (50%)
o Ocular (70%) – microphthalmia, cataracts, pigmentary retinopathy
o Neurologic
 SN deafness (70%); Microcephaly ; MR & Behavior problems
o Delayed progressive panencephalitis – 10-14 yrs > acquired or congenital – like SSPE
o Imaging – calcifications, WM abnormal
• Diagonsis – serology
• Treatment - NONE

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