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Aberrant right subclavian artery (ARSA) is the most common embryological abnormalities of the aortic arch. It is seen 0,5-1,8 per hundreds overall the population. Aberrant right subclavian artery can be seen asymptomatic in infants; whereas it can also occur severe symptoms such as respiratory distress, stridor, wheezing, dyspnea, dysphagia, recurrent lung infections due to compression on trachea, main bronchi and esophagus. We report a three month- old girl who received a long-term treatment due to recurrent pneumonia with atelectasis. Without any etiological abnormalities about recurrent pneumonia, aberrant right subclavian artery that was compressing right main bronchia, right upper bronchi, and right pulmonary artery was detected via cardiac catheterization. We aimed to emphasize the possibility of aberrant right subclavian artery in who have recurrent or non-healing pneumonia without any etiology despite receiving long-term treatment., Aberan sağ subklavian arter(ARSA), aort arkının en sık görülen embriyolojik anormalisidir. Toplumda %0,5 -1.8 sıklıkla görülür. Aberan sağ subklavian arter infantlarda asemptomatik görülebileceği gibi; trakea, ana bronş ve ya özafagusa bası yaparak solunum sıkıntısı, stridor, wheezing (hışıltı) , dispne, disfaji, tekrarlayan akciğer enfeksiyonlarına kadar değişen ağır semptomlarla da ortaya çıkabilir. Bu makalede rekürren pnömoni ve atelektazi nedeniyle uzun süre tedavi edilen 3 aylık kız hasta sunulmaktadır. Etyolojisine yönelik yapılan testlerinde hiçbir anormalliği saptanmayan hastanın; kardiak kateterizasyonu sonrası sağ ana bronşa, sağ üst lob bronşa ve sağ pulmoner artere bası yapan aberan sağ subklavian arter tespit edilmiştir. Amacımız, uzun süreli tedaviye rağmen düzelmeyen dirençli pnömonilerde ve neden ortaya konulamayan vakalarda, nadir görülen aberan sağ subklavian arter olasılığını gözler önüne serebilmektir.

Guillain-Barré syndrome is an acute inflammatory demyelinating neuropathy characterized by progressive symmetric polyradiculoneuritis, predominantly manifested by weakness and areflexia. In this article, we report our findings in 25 children treated with intravenous immunoglobulin and compare them with the remaining 30 children who received supportive care only. Only supportive care was given to 30 children who were not able to receive intravenous gammaglobulin because of shortcomings in intravenous gammaglobulin availability owing to a poor import during those years. Twenty-five patients were treated with intravenous gammaglobulin; they received intravenous gammaglobulin 0.4 g/kg/day for 5 consecutive days. Seventeen of the intravenous gammaglobulin group had received intravenous gammaglobulin within 10 days after the first symptoms, and eight of them had received intravenous gammaglobulin after the first 10 days. The average time elapsed for the symptoms to reach the maximum level was 6.9 (range 4—12) days in patients receiving intravenous gammaglobulin in the first 10 days, and it was significantly shorter than the time elapsed for the supportive care group (6.9 versus 8.8 days, respectively) (P < .05). Admission to the hospital after the first symptom, disability grade, time to improve in disability grade, the period of hospitalization, and mortality were not different in the intravenous gammaglobulin and supportive care groups (P > .05). Our suggestion for intravenous gammaglobulin treatment in Guillain-Barré syndrome is that if the patient has risk factors for respiratory insufficiency, then the treatment should be started. We more confidently carry out the follow-up of these patients after the results of this study. In conclusion, although it has been reported that intravenous gammaglobulin facilitates improvement in the disease and the decrease in mortality in children with Guillain-Barré syndrome, it has been mentioned in some studies that the intravenous gammaglobulin treatment was not better than supportive care, as in our study. However, further studies are essential to determine when intravenous gammaglobulin should be given to patients having which clinical and laboratory findings. (J Child Neurol 2006;21:972—974; DOI 10.2310/ 7010.2006.00214).