 Hello, everyone. My name is Dr. Vivek Rameshwaragar. I'm a junior resident at Justice K is a medical academy at Mangalore. I'm going to present a paper on CT hypoperfusion complex recognizing shock before it's too late. Shock, as you all know, is a medical emergency that represents one of the most common underlying causes of mortality. The choice of imaging mortality depends on several factors associated with the clinical condition and on the presence or absence of localizing signs and symptoms. CT hypoperfusion complex refers to predominantly abdominal imaging features that occur in the context of profound hypotension. Originally, this was described in post-traumatic pediatric patients by Taylor et al. in 1987. Multiple abdominal organs can display atypical appearances which are not related to the initial trauma, but it reflects alterations in perfusion secondary to hypovolemia. A small bowel is more commonly affected than the large bowel and probably any other organ in the body. The term CT hypoperfusion complex is now preferred over the older and the lesser accurate term which was called as the shock bowel. The aims and objectives for this study, the aim was to signify the importance of a radiological imaging in evaluating the patients with hypovolemic shock and the objective being to illustrate vascular and visceral features of CT hypoperfusion complex. The MDCT features of six patients which included five male and one female who presented to our emergency department in year 2022 with documented hypotension and blood loss following trauma were introspectively studied. The CCT examinations were conducted with GE120 sliced CT scanner at our department. The images which are obtained during arterial venous and the delayed phases were analyzed for the presence of findings comprising the CT hypoperfusion complex. The age distribution ranged between 10 and 60 years with male predominance. So out of these six, five male who presented with hypovolemic shock for an acute history of trauma whereas one female patient presented to us with septic shock and this female patient had no history of trauma. The GCS scores of all the patients who presented with chromatic history was more than 11 by 15. While that of the patient who presented with septic shock was eight by 15 at initial presentation. So this is a result five male, one female. Again, etiology five had history of blunt abdominal trauma and one patient had septic failure. The most common CCT finding that we found in this was the presence of what was described earlier as the shock bubble that is abnormal enhancement of this small bubble loops. We found that in about seven patients that is seven out of seven patients that is monitored to cross societies was found in six out of seven patients followed by slit-like accuracy or compressed inferior vena cava followed by pneumoperitorium and mild bilateral pulveria fusion. Violatory pulveria fusion could likely have been just an associated finding, but this is what we found. Whereas the least common finding was hyper enhancement of any other viscera, which will be discussed in the upcoming slides. So this is what has been described as a shock bubble. So here we can see that is mucosa hyper enhancement here along with submucosa edema. So you can see mucosa is hyper enhancing and the second middle layer, what we can see is slightly hypo enhance submucosal edema. And this is classically how a shock bubble appears, especially in cases of hypovolumium. Along with that, some intramural pockets within the small bubble loops or small bubble walls were also noted. The pathophysiology of this particular enhancement of small bubble is because of hypotensive shock, there is sympathetic stimulation which causes splanthic vasoconstriction and reduced bubble perfusion, which will result in altered permeability of the bubble, which will cause interstitial leakage of fluid and the contrast. As a result of, because of this interstitial leak, we can see there is prominent mucosa enhancement and some submucosa edematous oil technique. This was another patient here, you can see intensely enhancing small bubble loops because of the permeability is broken. And hence the contrast material will accumulate which will result in hyper enhancement of these bubble walls. The second finding was hyper enhancement of bilateral kidneys. So this is axial and coronal images of the patient where we can see the kidneys are so hyper enhancing that the corticometallurid differentiation is hardly made out here. Again, this is another example where we can see that the kidneys are very hyper enhancing. So the reason why these particular findings is found is because of the reduced blood flow to the kidney, secondary to hypotension. This will activate the renal angiotensin system, which in turn will increase the production of angiotensin to and cause its increased concentration. So what this particular, the next step would be is this angiotensin to, it causes constriction of the effrin renal arterial. As a result of this, the contrast that is going through the effrin arterial will not be allowed to be going out through the effrin arterial. And as a result, there will be prolonged cortical enhancement, which we just saw. What we also noticed was there was hyper enhancing bilateral adrenal glands. So here we can see that the right and the left adrenal glands are hyper enhancing. So is also the hyper enhancing left kidney here. So this hyper enhancement of adrenal has been attributed to because of there is, of the redistribution of the blood flow to adrenal, why? Because to maintain production of adrenaline and thereby to maintain arterial pressure. Hyper enhancing spleen was also noted in one of the case. So here we can see that there is significant reduction in the enhancement of spleen compared to the liver. So the reason for this is that spleen is most vulnerable abdominal organ to hypotensive shock. And it often shows extremely decreased enhancement in early phases of the CT. So spleen hypoperfusion is a very useful predictor of poor prognosis among patients who have cystary hypotension. Another finding that we quite formally saw was in the presence of something called as a slit like all flattened IVC. So here you can see that the abdominal aorta is very well made out here. And on the right lateral side, you can see a slit like enhancing structure. So this is basically a flattened inferior vena cava which is appearing like a small slit. So this flattening of the inferior vena cava is the result of decreased circulating blood volume. And it indicates that there is reduced return of the venous blood in patients with systemic hypotension. So we will classically call it as a slit like IVC when intra-hypatic vena cava or particularly any vena cava is measuring about less than three mm anterior posterior diameter in more than or equal to three segments. So this was another case. Again, here where you can nicely make out the aorta is the caliber of the aorta looks okay. And this is a flattened inferior vena cava. So this diameter was less than nine mm here. And this was a concomitant finding in that patient what we saw was shock bubble. So you can see that there is thickening, but it's the small bubble mucosa is very intensely enhancing. Along with IVC, IVC represents reduced blood flow. So also that blood flow. So basically the whole venous and the arterial blood volume reduced. So in some patients we can also see a small caliber aorta. So small caliber aorta is called when the AP diameter is less than 13 mm above the renal arteries or when it is less than even below the renal arteries. So this occurs in about 30 patients of 30% of patients with hypovolemia, but however, it's not very specific. So this was a case where the aorta measured 8.3 mm in anterior posterior diameter. So this was the presence of a small caliber aorta in the patient with hypotensive shock. There is also presence of periportal aphids. So we can see here, these are just the left branch of the portal with the right branch of portal. And we can see a cup of fluid surrounding this main portal, right and left main portal branches. So this periportal edema is often seen in conjunction with CT hypo coefficient complex. It is thought to occur if hypovolemic patients are vigorously rehydrated and then there is subsequent deep distention of the periportal lymphatic vessel. So just like how we saw here, periportal edema. In few cases, we can also see this edema surrounding the IVC. So that is called as a halosine. But we could not demonstrate this halosine in the six subjects that we studied. But literature shows the presence of this halosine in cases presenting with CT hypoperfusion complex. Along with that, we wanted to cross societies was seen in all the cases. So here we can see that free fluid lying in the epatorineal space and the left spinorineal and the paracollic atom. So this was more than the cross societies in this patient. So the presence of a site is here correlates with multi-organ dysfunction and is a non-specific sign, but it's usually found in these cases. So we want to discussion. So as we saw that shock is a state of oxygen delivered to the tissues is insufficient. Although there are multiple causes of shock, the most commonly discussed cause is hypovolemic shock, which occurs secondary to a blunt trauma. So hypovolemia will always lead to hyperperfusion, but we must always remember that this hyperperfusion need not be always secondary to hypovolemia. So what is the difference between these two is that suppose the volume of blood in a patient is fine, but the organs are not getting perfused. It could be either secondary to say cardiac failure, for example. So this signs to have, they have been described predominantly in cases with hypovolemic shock, but the literature showed that these signs can also be found in patients with other types of shock, like septic shock, for example. So the signs that we found in our study, it can be grouped into two, basically vascular signs and visceral signs. So what are vascular signs that is related to the vessels? So what we described was a slit like or a flattened inferior vena cava, IVC helosine, however, IVC helosine, what we saw was in the periportal edema and a small caliber aorta. Whereas the visceral signs is something that is typically described as shock bovell or hyperenhancement with submucosal edema of predominantly the small bobbles, more than the large bobbles, hyperenhancement of visceral, like gallbladder wall, kidney and adrenal glands. The reasons also we've discussed. There could be heterogeneous liver enhancement along with hyperenhancement of the spleen and pancreas. In certain cases, there is something called as shock thyroid. So along with that, the heterogeneous enhancement of thyroid with some free flow, with some fluid serum that can also be found. So the TECOM message from this discussion is that the CT hyperperfusion complex has very important prognostic and therapeutic implications. CT imaging represents a useful tool for a complete rapid and detailed diagnosis of clinically suspected shock, which can be used to improve patient outcomes. Though we have described these findings in post-traumatic cases, literature exists about the presence of these findings in patients even with septic shock. These were my references for today's paper presentation. My name is Dr. Vivek Targa. Thank you very much for your time. Thank you.