Dr Rithwik Sunil, Dr Praveena N Bhaskaran, Dr C Jayakumar
Four month old male ba presented with abnormal shape of head and distended abdomen. Vitals and PICCLE were normal
ANTENATAL HISTORY: 3RD child of NCM after a failed
Copper T device application
There is H/o fever with lymphadenopathy in 3rd month for which supportive treatment was received
History of spotting 2nd and 3rd month.
Antenatal Scan showed cardiac defect ventriculomegaly and hepatosplenomegaly.
Last trimester also she had Bleeding at 7 months
Growth scan showed fetal ventricle dilated. Corpus callosal agenesis
Bilateral hydrocoele
No history of GDM/PIH/hypothyroidism for the mother
LSCS was done due to abruptio placenta and delivered a ba weighing 1.35kg 3 weeks prior to the the EDC
Ba has asphyxia and hence – Intubated and child shifted to NICU
Extubated to HFNC 24 Hours of life .
(at 13 Days of Life)
Ba had NEC and received IV Piptaz, IV Amikacin
Sepsis Screen done was negative
USG Abdomen showed mild splenomegaly, minimal ascitis, gall gladder sludge.
NSG done showed b/l caudothalamic groove hemorrhage, SAH and intraparenchymal hemorrhage, dilated b/l lateral ventricle
On Day 27 ba has late onset sepsis for which Meropenam and Amikacin was given LP was done TC-60(all lymphocytes CSF sugar-27 CSF Protein=477 CSF Culture was sterile. MRI brain showed No obvious IVH. Ischemic type punctate white matter lesion in bilateral frontoparital lobe. Mild to moderate HIE changes in brain. repeat tap done day 36 and day 40 was dry
Repeat CSF analysis: 30 cells, protien-375, sugar-29,culture was sterile.
USG abdomen showed Umbilical hernia present.
In view of stormy antenatal and post natal history, a TORCH panel was sent
Torch Panel showed Toxoplasma IgM +(32.8), Toxoplasma IgG +(291), CMV IgG +ve (34) . Urine CMV negative. Child was then started on Septran at 12mg/kg/day .
Septran was continued for 1 1/2 months
Child was then referred to AIMS for further management
DEVELOPMENTAL HISTORY: Cooing partial neck control attained
Immunization History. No vaccines taken
CLINICAL EXAMINATION : At admission, Child afebrile and alert Vitals: Temp: 97F, PR- 130/min, RR- 38/min, BP-90/60 mmHg, SpO2 98% on room air, CRT
No pallor, icterus, cyanosis, clubbing, lymphadenopathy, Scrotal edema +.
Head to Foot: Microcephaly, Strabismus, Umbilical hernia +
Auxology:
Weight:4.1kg(less than -3SD ), Length: 51cm(less than -3SD ), HC:35cm(less than -3SD)
Development assessment:
prone – lifts head temporarily, hips low
ventral suspension – head in the plane of the body
pull to sit – head lag
Systemic Examination
RS: Air entry bilaterally equal, normal vesicular breath sounds,
CVS: S1 S2 heard,No murmurs
P/A : Distended, Splenomegaly+ , umbilical hernia+, Bowel sounds heard
CNS: Conscious, alert, PEARL. Normal tone and power with reflex 2+.No meningeal or cerebellar signs.
LABS :
Total Counts:22Ku/L
Neutrophils:10%
Lymphocytes:82%
Platelets:5 lakh
Haemoglobin:10.2 g/dl
LFT: Normal
RFT: Normal
Na:133Meq/L
K:4.2Meq/L
Differential Diagnosis other than toxoplasmosis considered were :
• Rubella
• Cytomegalovirus
• Syphilis
• Congenital Zika virus infection
• Congenital herpes simplex infection
• Congenital varicella infection
Management
Toxoplasma IgM was negative , probably because child is on Septran for the past 2 months. Toxoplasma IgG was positive (40IU/ml).Retinal exam left eye showed mild vitreous haze with macular scars and right eye showed vitreous haziness with no macular involvement, confirming congenital ocular toxoplasmosis . Neuro sonogram revealed small echogenic foci in bilateral white matter suspicious for calcification. USG abdomen done revealed splenomegaly and umbilical hernia.
BERA showed mild bilateral hearing loss. . In view of congenital toxoplasmosis, child is planned to be started on Pyrimethamine(1mg/kg/day) and Sulfadiazine(100mg/kg/day BD) .
Parents were advised to follow up every 2 weeks in order to check for cytopenia
Congenital Toxoplasmosis
Congenital infection may present as a mild or severe neonatal disease. It may also present with sequelae or relapse of a previously undiagnosed and untreated infection later in infancy or even later in life.
common clinical findings include
●Chorioretinitis (85 to 92 percent)
●Intracranial calcifications (50 to 85 percent)
●Hydrocephalus (30 to 68 percent)
●Abnormal cerebrospinal fluid (CSF; 63 percent)
●Jaundice (40 to 60 percent)
●Thrombocytopenia (40 percent)
●Anemia (20 to 50 percent)
●Fever (40 percent)
●Hepatosplenomegaly (30 to 40 percent)
●Lymphadenopathy (30 percent)
●Pneumonitis (27 percent)
●Rash (25 percent)
●Seizures (20 to 40 percent)
●Microphthalmia (20 percent)
●Microcephaly (15 percent)
When the infection is acquired in utero and the fetusis treated drug therapy of the pregnant woman with pyrimethamine , sulfadiazine , and leucovorin , signs and symptoms in the infant may be prevented. The newborn infant may appear normal with no CSF abnormalities and no brain or eye disease. In utero therapy initiated rapidly results in a reduction of ocular and neurologic sequelae.
Take home message;
It is vital to treat and diagnose antenatal infections promptly so there is less complications in post natal period for the child. This is essential especially for diseases where antenatal treatment has excellent prognosis.