Superior mesenteric artery (SMA) syndrome is a gastrovascular disorder in which the third and final portion of the duodenum is compressed between the abdominal aorta (AA) and the overlying SMA. Our case presents an 11-year-old female with chronic intermittent vomiting that started since she was 6 months old. Contrast enhanced computed tomography scan for abdomen and pelvis guided to the correct diagnosis and the patient received the adequate treatment. Awareness of a broad range of differential diagnosis of vomiting and a high degree of suspicion of SMA syndrome is fundamental in order to direct the proper diagnostic investigation. Duodenojejunostomy provides the best results in severe cases.

Introduction and importance: Intussusception is one of the most common causes of acute abdomen and surgical morbidities in the childhood. In a paediatric presentation of intussusception due to Meckel's diverticulum there may be acute onset of abdominal pain, vomiting or painless red currant stools. However, Lethargy has been described as a rare presenting symptom Case presentation We present a case of 2,5 – year old female complained of acute alternation in consciousness followed by continuous vomiting two days later. Clinical discussion Her neurological examination showed a lethargic child, not reactive and hypotonic. Her past medical history was unremarkable. Abdominal ultrasonography was compatible with ileocolic intussusception. The necrotic bowel and diverticulum were resected, followed by anastomosis of the viable bowel segments. postoperatively the infant recovered dramatically. Conclusion Although lethargy is a rare presenting symptom of Intussusception, it should be kept as a differential diagnosis when a child presents with acute onset of drowsiness with or without abdominal symptoms.

Introduction and importance Congenital cystic adenomatoid malformation (CCAM) is a rare malformation, with unknown causes, that affects distal bronchi. It accounts for 25% of congenital pulmonary malformation s and most cases are found in neonates and babies. The mortality rate of prenatally diagnosed cases ranges from 9 to 49%. The risk factors for poor outcome include hydropsfoetalis, microcystic CCAM and the overall size of the lesions. The mainstay of CCAM treatment is surgical excision that prevents complications such as recurrent infections, pneumothorax and malignancy. Case presentation Our case is a 4-month-old boy born presented with shortness of breath and poor suckling. He was admitted to intensive care for respiratory distress. Clinical discussion A working diagnosis of pneumonia was entertained and the patient given humidified oxygen through nasal prongs, intravenous fluids and antibiotics. Thoracic CT showed a cystic malformation in the left lower lung lobe. Due to continuing recurrent infections and the risk of rupturing of the cyst with subsequent pneumothorax, it was decided to proceed with a left lower lobectomy. The post-operative course was uneventful and the patient was discharged home on the fifth post-operative day. Conclusion Congenital cystic adenomatoid malformation should be a differential diagnosis of pneumonia. A real awareness of this rare entity among pediatricians and radiologists should allow early diagnosis and proper treatment.

Rasmussen encephalitis (RE) is a rare disease of unknown etiology that causes severe chronic unihemispheric inflammatory disease of the central nervous system mainly in children. It leads to intractable seizures, cognitive decline and progressive neurological deficits in the affected hemisphere. We report two cases of RE, as defined by fulfillment of the 2005 Bien criteria. The diagnostic challenge of characterizing this rare disease will be highlighted by the extensive serum, CSF, MR imaging and EEG data in the two patients. In addition, we will review the various forms of therapy attempted in these two patients, namely anti-epileptic drug therapy and immunomodulatory therapy. Hemispherectomy was done for the second patient with favorable outcomes of controlling seizures, but unfortunately, he died because of meningitis. Until the causes of Rasmussen's encephalitis are known, it is difficult to anticipate how treatments will improve. Such a situation creates a therapeutic dilemma; hemispherectomy is not favored because of the inevitable postoperative functional deficits, but a real risk exists that treatments used to delay progression of the disease will defer definitive surgical treatment beyond the time when an optimum post-hemispherectomy outcome could be expected.

Introduction and importance Chickenpox (Varicella) is a benign illness caused by varicella-zoster virus, predominant in childhood. Chicken pox related neurological complications are seen in less than 1% cases of chickenpox. Cerebral Venous thrombosis due to primary (VZV) infection is very rare, and it may occurs secondary to primary or re-activation the virus. Case presentation We report a case of 5-year-old female complained of ataxia, vomiting, headache, and drowsiness 7 days after the onset varicella zoster infection. She had vesicular lesions with scab over the trunk and limbs. Clinical discussion Neurological examination revealed left hemiparesis. Her blood counts and metabolic parameters were normal. Computed tomography brain showed hemorrhagic infarct in the left temporo-parietal region. Coagulation profile was normal. Magnetic resonance imaging (MRI) brain revealed hemorrhagic infarct in the same region. Magnetic resonance Venogram showed thrombosis of left transverse sinus and sigmoid sinus and internal jugular vein. VZV- IgG antibody was positive but CSF VZV PCR (Polymerase chain reaction) was found to be negative. Intravenous acyclovir for 15 days, and low-molecular-weight heparin for 3 days overlapped with oral Warfarin for 3months,. After 3 months follow up, the patient experienced a complete recovery. MRI repeated after 3 months showed recanalization of the sinuses. Conclusion The pathogenic link of occurrence of CSVT after VZV infection is unclear, but some articles showed that it is related to direct endothelial damage by the virus. Early recognition of this complication of VZV infection and prompt treatment is essential to prevent catastrophic complications.