 Good morning everyone. My name is Dr. Prathamesh Nank. I'm from Guam Medical College and I'm going to present the case of mycotic aneurysm. Introduction, the infected aneurysm or mycotic aneurysm is defined as an infectious break in the wall of an artery with formation of a blind secular outpouching that is contiguous with the arterial human. The non-treatment or delay treatment of the infected aneurysm often leads to fulminant sepsis, spontaneous arterial rupture and an earlier detection of infected aneurysm is critical for time to time the treatment to optimize the patient outcome. Coming to the case report, a 45 year old man with no significant prime medical history presented to Guam Medical College and hospital with complaints of non-radiating, non-specific low backache with an insidious onset over past one week. The patient also complained of bilateral pain in my last five days. Patient did not complain of fever, chills or I guess no other clinical significant clinical history could be elicited. Physical examination revealed a temperature of 98.4 degree pulse rate of 90 beats per minute, respiratory rate of 18 per minute and blood pressure of 110 by 60 mm. The heart rate was regular without a murmur, lungs were clear, abdominals soft, non-tender without any organically. The logical examination was normal. The lower limbs, however, had bilateral pyridine. Lab parameters are as follows, the hemoglobin was 8.5 gram, the hematocrit was 36% rate lead was 1.2 lakh, total liver foresight count was 32,000 and serum creat was raised which was 5.8 milligram, serum urea was 19 milligram. Microscopic analysis of the urine showed 18 erythrocytes to 46 lymphocytes and 99.8 bacteria per high power fit. The bilirubin levels were 3.2 with a direct fraction of 2.4 milligram. SGOT was 39, SGVT was 59 and ALP was 325. The serum albumin was 2.4 grams and HVA1C was 14 whereas the serum crocal was 2.9. Ecocardiography revealed my left ventricular systolic dysfunction with an ejection fraction of 45%. CT was performed, plane CT was performed after giving paroral positive contrast. It revealed an iso to mildly hyperdense lobiluted structure in the retroparitoneum in relation to the infrared in the lauta. The soft tissue collection with air globules and retroparitoneal fast stranding was also noted adjacent to the structure. This retroparitoneal collection was seen in close proximity with the bowel loop synchrony and air focacivus in tracking along the lefsoas muscle as well as in the inferior vena carot. The contrast enhanced CT scan was performed after taking the high risk consent. It revealed a large bilobiliated sodium aneurysm on the infarinal abdominal outer with a defect along the posterior wall. However, there was no extrapolation of the contrast and there was no thrombosis within the aneurysmal cell. Coming to the image, this is the plane CT with paroral positive contrast. Here reveals an iso to mildly hyperdense structure in the retroparitoneum that is surrounding retroparitoneal soft tissue collection. On contrast enhanced CT we see aneurysm of an outer with surrounding soft tissue collection and air globules. The societal reconstruction shows a defect along the posterior wall of outer with mycotic aneurysm. Coming to the discussion, mycotic aneurysm are localized irreversible vascular dilatation. They caused by weakening and destruction of the vessel wall. They caused by invasive organism. So it becomes like an infective arthritis. Due to effective and prompt antibiotic therapy, their incidence is rare but potentially life threatening. The term mycotic derives from the mushroom like appearance of the aneurysm and not the underlying microbiological etiology. They may arise through the hematogenist root, lymphatic roots, contiguous extension and direct inoculation. The patients usually often present with non-specific complaints. The most common being fibril illness within serious onset. General malaise, weight loss. Diagnosis of mycotic aneurysm relies on contrast enhanced autography. CT scan reveals a secular or multilobulated aneurysmal sac. There may be vertebral erosions. In case of autic wall rupture, contrast exacerbation will be noted with thrombus formation within the pulse lumen. Mycotic aneurysm carries a high mortality prompt treatment should be initiated using a combination of intensive broad spectrum antibiotic therapy alongside surgical repair. Based on microbiological results, further modification in antibiotics may be performed. The results of surgical repair are to confirm the diagnosis, achieve microbiological source control and prevent or contain the rupture and haemorrhage and reconstruct the arterial treat. The medical therapy alone is associated with poor outcome. Although antibiotics may control the sepsis, they do not reduce the risk of rupture of the weakened vessel wall. The surgical management of infraternial outer can be accomplished by proximal or distal arterial ligation. Endovascular repair is well established for non-infective aneurysm, but persistent infection is a strong predictor for long term mortality. Coming to the conclusion, mycotic aneurysms are rare but universally fatal without appropriate management, diagnosis and surveillance remains clinical challenges and CT angiography is currently considered the modality of choice. The surgical or endovascular intervention alongside intensive antibiotic therapy remains definitive treatment although patient must be assessed case-to-case basis. These are my references and I want to thank CTBus for giving me this platform to present this case and I want to thank everyone for patient listening. Thank you.