ABSTRACT
PURPOSE: There is significant prevalence of overt and subclinical hypothyroidism in pregnant women in rural areas. Maternal hypothyroidism is known to cause congenital hypothyroidism resulting in sensorineural hearing loss. Anti-Thyroperoxidase antibodies are known to cross placental barrier. There is no literature on hearing assessment in infants born to women whose hypothyroidism was corrected during pregnancy. Do these infants suffer hearing loss? Our study addresses this question. METHODS: 140 infants born to women on treatment for hypothyroidism during pregnancy and 140 infants born to euthyroid women were evaluated for hearing by Brainstem Evoked Response Audiometrry at 1 and 4 months age. Anti-TPO antibodies were estimated at 4 months of age. RESULTS: There was no clinical hearing deficit or delay in neurological development in infants born to women undergoing treatment for hypothyroidism during pregnancy. However wave V latency on BERA was slightly prolonged in them compared to infants born to euthyroid women. There was absence of wave V when maternal subclinical hypothyroidism persisted till parturition. However within 6-8months of age the wave V latencies corrected to normal. Anti-TPO antibodies were within normal range at 4months age. CONCLUSION: Maternal hypothyroidism when corrected before parturition does not affect hearing in the infants clinically. The mild delay in wave V on BERA corrects within first year of life. However larger studies to assess hearing in infants born to women having overt hypothyroidism during first trimester of pregnancy may be desirable to assess whether hearing is adversely affected in them.
Subject(s)
Congenital Hypothyroidism , Hearing Loss, Sensorineural , Pregnancy Complications , Female , Hearing , Hearing Loss, Sensorineural/diagnosis , Hearing Loss, Sensorineural/epidemiology , Hearing Loss, Sensorineural/etiology , Humans , Infant , Placenta , Pregnancy , Pregnancy Complications/epidemiologyABSTRACT
UNLABELLED: Parotid abscess is a rare complication of acute parotitis in children. Acute parotitis occurs due to infection of intra-parotid or para-parotid lymph nodes or glandular parenchyma of the parotid gland which may progress to parotid abscess. OBJECTIVES: To document the causative organism, clinical behaviour and response to treatment in paediatric parotid abscess. MATERIALS AND METHODS: A retrospective study was done in our tertiary rural hospital from May 2007 to May 2015 to identify and analyse paediatric parotid abscess in 80 unilateral parotitis cases. RESULTS: 7 cases of parotid abscess were identified. 4 cases were diagnosed clinically and in 3 cases ultrasound was done showing heterogenous, hyperechoic, solid and cystic areas. In 2 patients, abscess was extending to the submandibular space. Incision and drainage was done in all patients. The most common bacteria was Methicillin Sensitive Staphylococcus aureus. Escherichia coli was reported in one patient, and was rare in parotid region. 2 patients had House Brackmann grade 2 marginal mandibular nerve palsy, and they recovered within 4½ months. CONCLUSION: Parotid abscess is an uncommon but life-threatening condition in paediatric age group. Poor orodental hygiene was most important predisposing factor. Abscess can be diagnosed clinically and ultrasound scan is also an important diagnostic tool. It is commonly caused by Gram positive cocci and responds well to incision and drainage followed by appropriate antibiotics. No fistula may result if treated early.
