Vol 39 # 2 June 2007 - Kma.org.kw

June 2007KUWAIT MEDICAL JOURNAL 179Fig. 5: MRI neck T2W axial image showing globular lesion with air-fluidlevels and isointense rim in retro and left parapharyngeal spacesFig. 6: Post Gad T1W axial image showing enhancing thick abscess wallwith compression of the oropharynxFig. 7: Post Gad.T1W sagittal image showing vertical extent of the abscesswith compression and anterior displacement of pharyngolarynxsymptoms in infants include fever (100%), neckswelling (84%) and anorexia (58%). The physicalsigns include cervical adenopathy (69%),re t ropharyngeal bulge (43%; do not palpate inchildren), fever, stridor (23%), torticollis (18%) andrarely, cyanosis [5,6] . Early-onset of sepsis in neonatesis associated with acquisition of m i c ro o rg a n i s m sf rom the mother. The micro o rg a n i s m s m o s tcommonly associated with early-onset infectioninclude group B Streptococcus (GBS), Escherichia coli,Haemophilus influenzae, and Listeria monocytogenes.Late-onset sepsis occurs at 7-90 days of life and isa c q u i red from the care-giving enviro n m e n t .Organisms that have been implicated in causinglate-onset sepsis include Staphylococcus aureus, Ecoli, Klebsiella, Pseudomonas, Enterobacter, Candida,Fig. 8: Follow up CT scan after 10 days showing completely resolvedabscess with opened up airwayGBS, Serratia, Acinetobacter, and anaerobes. Studieshave shown that premature infants and low birthweight babies have an increased incidence ofsepsis [6] . RPA of bacterial origin were reported inlate neonatal period with Staphylococcus as maincausative organism.C a n d i d a, like bacteria may infect fetus byhematogenous dissemination from umbilical