 Good evening everybody. I'm Dr. Venithra doing second year DNB radiology residency at Bilrod Hospital's Chennai. My topic for today is tit for tat, a K series of vascular and hollow viscous compressions. And why is it called tit for tat? We'll see that in upcoming slides. Introduction. Abdominal pelvic vascular compression syndromes comprise of either compression of hollow viscera by adjacent blood vessels, examples includes Wilkie's syndrome, uretro pelvic junction obstruction, portal biliopathy, or the other way round. That is the compression of vessels by adjacent structures. As examples for this includes Dunbar syndrome, nutcracker syndrome and methanol syndrome. These syndromes can be diagnosed incidentally in asymptomatic patients or those who come with atypical symptoms. These patients are never going to come to us with a direct clinical picture. In this K series is an extended list of three other unexplored compressions who came to us with varied presentations. Names and objectives of this paper is to share our department's experience in witnessing few interesting imaging findings and their radiological diagnosis and how we arrived at that diagnosis in such unusual clinical settings. This is my case one 22 year old male presented with complaints of post-prandial epigastric discomfort, indigestion, reflex and regurgitation for past one year. The medical gas routine they proceeded with upper GI scopi which did not reveal any significant findings. Patient symptoms were not relieved by proton pump inhibitors or the routine anti-reflex medications. The patient came referred to us for CCT abdomen which showed us compression of mid portion of D3 segment of the orenum between SMB, its venous rebutaries and iota. And we also saw that stomach D1 and D2 segments of the orenum appeared distended. This is figure one venous phase CCT abdomen axial sections taken at the level of D3 segment which is showing us. This D3 segment is shown by the yellow arrow which is getting sandwiched between SMB which is shown by the star and iota which is shown by the arrow pin. The other two images are also showing the same thing that is the D3 segment of the orenum getting compressed between SMB, its rebutaries and iota on the other side. This is the CCT abdomen venous phase oblique coronal section which is showing us the similar findings. Moving on to in order to confirm the functional status of this kind of obstruction we proceeded with barium male study which showed us a distinction of second and proximal third parts of the orenum with a persistent filling defect at mid portion of D3 likely due to an extrinsic operation. And this is the figure three which is the RAO projection showing us a contrast filled stomach C loop of the orenum with an extrinsic compression at mid portion of D3. And this is figure four supine AP projection which is showing us partial holdup of contrast in D2 and proximal D3 segments with a persistent filling defect at mid D3 segment. And so our diagnosis very well becomes SMA like syndrome or SMB syndrome. Discussion, risk factors for this condition includes mega diodenum which may be caused by multiple connective tissue disorders or other autoimmune conditions like systemic sclerosis, dermatomyocytes, SLE, diabetes mellitus, amyloidosis, chronic idiopathic intestinal pseudo obstruction or OGLB syndrome. Small rotation of midget congenitally shortened suspensory ligament of the orenum, rapid and severe weight loss, hydrogenic alteration of anatomy due to surgeries, surgical correction of scoliosis or chronic external compression by the hip spica cause other other risk factors for this condition. And this is a small review of literature which is made which includes all the SMA like syndrome so far published. These are this includes this is a compilation of all the SMA like syndromes caused by SMB and totally we have eight cases out of which the major chunk is the diodenal compression between SMB and IVC. And all other minor cases includes anomalous venous anatomy, co-surgical and diodenal compression between SMB and IOTA. All these comprises of one case each and so our case becomes second case which is causing diodenal compression between SMB and IOTA. So the treatment options available for this for these patients are conservative that is gravitational manoeuvres, postprandial, prone niches and left lateral decubitus positioning, nutritional augmentation that is multiple small feedings, parenterial hyperalimentation and surgical bypass. Moving on to case two, this is a 47 year old male who presented with complaints of left loin pain for one month. The pain was intermittent in nature and it was not relieved by the usual NSAIDs. No history of renal or urethric calcule was given by the patient. No recent fever episodes took. We proceeded with ultrasound KUV which showed us moderate left hydronephrosis and proximal hydro urethra. In the study we were not able to demonstrate any proximal urethric or left BUG calculus. So no obvious cause for HUN was detected in the study. Figure five is the longitudinal BU ultrasound image which is showing us hydronephrosis of left kidney and this is the figure six which is showing us proximal left hydro urethra. In order to confirm the, in order to know more about the cause for the HUN we proceeded with CECD KUV which showed us left moderate hydronephrosis up to the level of testicular vein crossover at the level of L4 vertebra with smooth narrowing or clean. The portion of urethra distilled to the crossover was also unremarkable. The testicular vein at the crossover was most importantly of normal caliber that is 3.2 NM. Usually in other similar cases what we saw was the testicular vein was pathologically altered but in our case it was normal in caliber. And this is the figure seven which is showing us CECD KUV cortical midlary phase axial section image at the level of renal pelvis showing us left head to end. And this is figure eight which is CECD KUV excretory phase axial section which is beautifully showing us the urethra at the, which is showing us urethra at the level of testicular vein crossover. Laterally what we are seeing is the proximal urethra which is enlarged in caliber and distilled to the, sorry, and medium to that we are seeing the urethra of normal caliber that is distilled distilled to the testicular vein crossover. And this is figure eight that is CECD KUV venous and excretory phases coronal section at the level of left testicular vein crossover and this is also showing the similar findings. So our diagnosis is testicular vein syndrome discussion moving on to discussion the risk factors for this condition includes congenitally enlarged testicular vein from the phlebitesticular vein or varicoseal of testicular vein. And this is a small review of literature which is made using the details of the cases published so far and our case becomes the ninth case. And in this review I have included the authors details then age of presentation of the patient then side of involvement and vertebral level at which the testicular vein crossover happens. And our conclusions are the age of presentation ranges from 20 to 55 years, and on which the mean age was 37.5 years and we also found it is also like seen that the left sided involvement is more common than right sided involvement. And also the other thing was the testicular vein crossover which is happening at the L3 vertebral level was found to be more associated with the testicular vein or testicular vein syndrome and treatment options available for these patients include resection or transaction of the vein at the crossing point plus or minus excision or uretro uretros to me if the uretral segment at the crossover is at the tick. Let's follow for clinical improvement and with IVU if needed between three to five months post surgery. Moving on to the third case, 15 year old normal female child with no developmental abnormalities came with complaints of left low limb pain predominantly on the proximal aspect for past four days. The patient had history of chronic constipation, which was gradually progressive in nature and also gave us history of on and off episodes of abdominal pain. Since the patient had low limb pain and also swelling we proceeded with left low limb venous Doppler and what we saw was echogenic thrombus within the lumen of visualized portions of common femoral vein extending into the superficial femoral vein. Neither color flow nor spectral wave pattern was demonstrated. These vessels were incompressible and no flow augmentation was seen on distal compression and we were completely shocked with the findings of dvT and we were wondering what would have caused dvT in a normal otherwise normal school going child and also since the patient had complaints of abdominal pain we proceeded with CCT abdomen which showed us a literally huge finding and this is a CCT abdomen which shows us gross dilatation of sigmoid colon and rectum with significant fecal impaction measuring and so extending up to the level of left hemi diaphragm compressing and causing thrombosis of left common iliac external iliac veins and visualized portions of left common femoral vein. This is a figure 10 which is showing a CCT abdomen arterial phase coronal section with gross fecal impaction in the rectum and sigmoid colon which is extending up to the level of left hemi diaphragm and this is figure 11 which is the CCT abdomen venous phase sagittal section which is showing a significant pressure effect on the urinary bladder and uterus of the patient and this is figure 12 CCT abdomen venous phase axial section which is showing us the thrombosed left common iliac vein whereas the right common iliac vein is showing normal contrast filling and this is figure 13 CCT abdomen venous phase VR image which is showing us non visualization of the left common iliac external iliac and common femoral veins whereas on the contralateral side we are seeing the normal opaspication of the veins and so our diagnosis becomes giant fecal impaction causing DVT and risk factors for this condition includes Terspring disease, Chava disease, diabetic neuropathy, neuropsychiatric diseases, inflammatory or neoplastic diseases, clereoderma, inner rectal malformations, chronic bedridden patients and long term drugs like antidepressants and opioids and this is a review of literature which is made based on the acute presentations of fecal impaction or fecaloma and among this among the totally like overall published cases, 15 cases of fecal impaction presented with intestinal obstruction and 5 cases presented as toxic mega colon and 7 cases presented as acute urinary retention and 2 cases presented with DVT and 3 cases presented as an up terminal mass and again there was an overlap that is one case presented with both intestinal obstruction and acute urinary retention and one case presented with both toxic mega colon and acute urinary retention and treatment options available for this patient's work, conservative that is laxatives, enema, manual evacuation, colonoscopic guided fragmentation of fecal matter and surgical intervention will be required if complicated by bubble obstruction, toxic mega colon or it had any underlying cause of Hirschman's disease and this is an interesting fact that the colonoscopic installation of coca cola is another interesting therapy that is tried and proved to be successful in dissolving calcified fecaloma in 2 of the literature published cases and so here are the results, why is it called tit for tat, we will see that now, tit for tit we have unusual hollow viscous compressions by vascular structures, the examples are SMA like syndrome or SMB syndrome and testicular vein syndrome and for tat we have unusual vascular compressions by hollow viscous structures and for that we have giant fecal impaction causing DVT so the conclusion is thus abdomen being a compartment with various vital structures in closed vicinity and eagle eye for compressions and drones like these can aid in establishing appropriate differential diagnosis, this will in turn lead to early detection of these rare syndromes and cause reduction in associated morbidity and mortality, thank you everyone