 Hello everyone, today I will be presenting a case report on Clipple Trenonus syndrome based on the radiological aspects. The case history was that of a 56 year old male patient came with left lower limb pain and non-healing ulcers in the lower one-third region of the leg and lateral aspect of the ankle joint since one and half years. The past history was that of a trivial trauma on left leg two years back. On examination, patient has stable vital signs and was not in any cardiorespiratory distress. Pertinent physical examination findings revealed multiple compressible varicose in left lower extremity. There was limb lung discrepancy and generalized atrophy of the right lower extremity. Evdematous and prominent superficial veins were seen in the anterior middle aspect of the left leg. There was tenderness also elicited in this area. The images of the lower limb of the patient where we can see bluish discrepancy in the left leg in the distal part with multiple ulcer formation. The patient was then subjected to radiological investigations. The first investigation was of ultrasound Doppler in that there were multiple varicose seen along the middle aspect of the leg which were seen draining into the great saphenous vein. There were incompetent perforators seen 10 centimeter below knee along the great saphenous vein on the left side. There were enlarged lymph nodes in the left femoral region. The patient was then subjected to CT scan. The findings were on the scout film and the 3D CT reconstruction of the lower extremities that showed left femur and the left tibias longer than the right femur and the tibia. Overall the patient had a longer left lower extremity by 1.8 centimeter as compared to the right. There were multiple dilated torsus venous channels seen along the subcutaneous fat plane in the lower abdominal pelvic cavity and inguinal region and seen communicating with the great saphenous vein on either side. The dilated venous collateral channels were seen along the left lateral pelvic wall obturator region with venous channels extending along the pre-sacral space posterior to the rectum and crossing the midline and joining the left internal iliac vein. The common iliac vein was absent on the left side. We can see in this image the right common iliac vein is present however there is urgenesis of the common iliac vein on the left side. There were multiple arteriovenous collateral channels seen involving the left lower limb below knee region and extending up to the ankle region mildly increase muscle mass on the left side as compared to the right side possible muscular hypertrophy. The persistent lateral marginal vein was seen on the left side. On coronal images we can see the multiple arteriovenous collateral channels below the knee region extensively along the distal leg and the ankle region. On in the anterior medial compartment muscles along with the subcutaneous fat on the left side is showing hypertrophy as compared to the right side. The diagnosis of 56 year old male patient with non-elum ulcers, pain and swelling in the left lower extremity. Radiological evaluation revealed features of unilateral soft tissue and bone hypertrophy, persistent lateral marginal vein, multiple dilated torsus varicose veins, dilated grade and short saphenous vein, left common iliac vein urgenesis and multiple arteriovenous collateral channels seen involving the left lower limb. On the basis of above findings the diagnosis of cliplet renowne syndrome was made. Case discussion, cliplet renowne syndrome is a rare congenital disorder with the incidence of 1 in 1 lakh people worldwide. It was first described by two physicians in 1900, cliplet renowne and after which it was named that. It is characterized by vascular malformations that is capillary, venous and olfatic and bone soft tissue hypertrophy. Any of the two features are enough to diagnose KTS. It occurs sporadically and has no sex predilection. Usually it is seen in birth or childhood. Ideology is unknown but hypothesized that it causes by mesodermal abnormality. The most common side is unilateral lower extremity. Cutaneous capillary malformations in the form of port wine stains with limb soft tissue hypertrophy are most common clinical findings. There may be involvement of both superficial and deep venous system. Superficial venous malformations include varicositis and persistent embryonic vein. Deep venous malformations include hypoplasia, aneurysmal degeneration and segmental erplasia. Lymphatic deformities include cystic hygroma, primary lymphedema or lymphenjectesia. Visceral malformations can also develop. Vain GI tract, cardiovascular system and genitourinary tract involvement can manifest. Common complications are thrombosis in the extremities, the current pulmonary emboli, lymphedema and hemorrhage secondary to vascular malformations. Persistent embryonic veins are characteristic of clipper trinone syndrome in which the lateral marginal vein and persistent sciatic vein are more common. When they regress after birth, the lateral marginal vein is a superficial vein and the persistent sciatic vein is a part of a deep venous system. During embryonic life, the large primitive axial vein drains the lower extremity. Persistency of this vein instead of its regression is defined as a persistent sciatic vein. The serous canogram CT or other standard radiographic studies can be done for assessment of limb length discrepancies to assess the anatomy of the deep veins and embryologic veins. Ascending and descending venography is useful. Doppler ultrasound is usually the first imaging modality to differentiate between vascular tumors and vascular malformations. To visualize the extent of legions and hypertrophy of bone and muscles, malformations in pelvic and abdominal region, CT and MRI are of benefit. Cintygraphy may be utilized for assessment of bone vascularity and regional blood flow. The closest differential diagnosis of clipper trinone syndrome is Pax Weber syndrome which also presents with limb hypertrophy, vascular and capillary malformations much in the same way as clipper trinone does clinically. However, Parker Weber syndrome also presents with high flow artery venous malformations while clipper trinone does not. Clipper trinone syndrome has a more benign course while Pax Weber syndrome patients usually have a significantly decreased lifespan due to complications brought about by the artery venous malformations. The non-operative medical management is the main modality of treatment in case of symptomatic clipper trinone syndrome. A multi-drug regimen may be needed and a short-term course of steroids may be deemed necessary. Compensatory shoes or heel inserts are advised in limb-lend discrepancies. If discrepancy is more than 2 cm, then surgery should be considered. Surgical management is usually reserved for symptomatic cases. The success of surgery depends on the preoperative evaluation of the deep venous system using techniques such as CT, arteriography, duplex scanning contrast geography which can help ascertain the extent of vascular involvement and the presence of artery venous fistulae. The laser treatment and radiotherapy. The treatment of port wine stain often involves the use of laser treatment. Laser therapy can also be employed in cases of ulceration, raised lesions or lesions under the skin that usually do not respond well to the laser treatment. Endovenous laser therapy on the greatest saphenous veins can also be used in patients with clipper trinone syndrome for the management of varicocities. Radiotherapy has been reported to be of help in some cases of clipper trinone syndrome. The radiation may help to induce regression of the hemangiomas. However, the results are usually slow to develop.