Normally, there is no obvious communication between the intracranial and extra cranial venous drainages in the head. In Sinus Pericranii, there is an abnormal communication, either from the extra cranial system to the intracranial venous sinuses or from the intracranial venous system to the extra cranial draining veins. Venous anomaly is a collection of non muscular venous blood vessels, adhering tightly to the outer surface of the skull and directly communicating with an intracranial venous sinus through diploic veins. The varicosities are intimately associated with the periostium, are distensible, and vary in size with changes in intracranial pressure Sinus pericranii is not a single clinico pathologic entity, rather a symptom complex with diverse clinical manifestations.In this article,the authors present a case of 8 mo old boy having Sinus Pericranii.

The Epstein-Barr virus (EBV) infection commonly manifests as fever, malaise, cervical lymphadenitis, pharyngitis and splenomegaly. Leucocytoclastic vasculitis is a rare complication of acute EBV infection. Clinical manifestation is often limited to the skin, but the renal, gastrointestinal or pulmonary system may be involved. 1 We report a case of leucocytoclastic vasculitis with crescentic glomerulonephritis in association with acute EBV infection.n ep_1440 617.. 618 A 14 year old male presented to us with history of sudden onset of fever and skin rashes initially over the trunk and gradually involving the entire body including the face for 10 days. He was febrile and breathless with a blood pressure of 110/60 mmHg. He had conjunctival suffusion with a diffuse erythematous maculopapular rash. Systemic examination revealed hepatosplenomegaly with pulmonary congestion. His laboratory investigations revealed thrombocytopenia (87000/cmm) with acute renal failure (creatinine 1.7 mg/dL). Urinalysis showed 2+ proteinuria, haematuria and red blood cell casts with spot urine protein to creatinine ratio of 1.74. His blood and urine culture was negative and 2-D echocardiography was normal. Serum complement 3 and 4 levels were low and vasculitis work-up was negative. Serum for EBV capsid antigen (VCA) was highly positive with increasing titres. He had normal bone marrow studies and skin biopsy suggestive of leucocytoclastic vasculitis. He was treated with i.v. ceftriaxone and other supportive measures but he continued to have high grade fever with worsening azotemia (creatinine 5.2 mg/dL). Percutaneous kidney biopsy revealed severe proliferative glomerulonephritis with cellular crescents in more than 50% of the glomeruli (Fig. 1). He was treated with i.v. methyl prednisolone 500 mg once daily on 3 consecutive days followed by 1 mg/kg day p.o. Following this, his respiratory symptoms subsided, rashes started fading and his urine output improved. His serum creatinine dropped to 0.8 mg/dL with disappearance of proteinuria and haematuria.The finding of leucocytoclastic vasculitis on skin biopsy is suggestive of small-vessel vasculitis. The possible pathophysiological mechanism is either direct invasion of endothelial cells by EBV or by immune complex-mediated inflammation. Renal involvement in EBV infection is predominantly interstitial, 2 overt renal failure is uncommon 3 and crescentic glomerulonephritis has never been reported.Crescentic glomerulonephritis and small-vessel vasculitis in the presence of Ig M VCA antibodies in our patient may have resulted from an intense immune response to the EBV infection. Simultaneous decrease in C3 and C4 indicating classical complement activation along with prompt response to immunosuppressive therapy supports this possibility. Thus, we hypothesize that EBV infection should be included in the differential diagnosis while treating a patient with crescentic glomerulonephritis.We report a 35-year-old man with suicidal carbofuran ingestion who developed shock, renal failure and excreted gr...