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Cochin Clinical Society Meeting - May 2022

May 19 | 2:00 PM

Cochin Clinical Society brings to you case discussions from 5 different specialties presented by the doctors of VPS Lakeshore Hospital: Dr. Vinitha: Not just skin deep,Dr. Gladwin: Silk Road woes, Dr. Shwetha: The secrets that eyes tell,Dr. Rajesh: Feet that don't feel the floor,Dr. Jazeel: Breaking the Taboo

[Music] good evening everyone my name is dr tandy and i welcome you all on behalf of netflix team today we are gathered here uh for a very interesting session by coaching clinical society they have a monthly meeting and uh this month we are having it on 19th uh we have very interesting case presentations from different specialties which would be introduced by dr matthew so handing it over to dr matthew please take it forward very good evening uh first of all i would like to thank the clinical society as well as the vps lake shop for give me this opportunity to be with you and uh society is you know the oldest uh clinically oriented discussion um platform which we have been having for many years and uh this was found to be one of the most useful sessions for all specialty doctors and uh as an old timer i really enjoyed attending presenting and watching uh coaching society but unfortunately because the coffee we had a break for some time but now we are back and that too in the virtual platform allowing more people to participate and um at the convenience of your home and uh i think that we have a very interesting cases five different specialities presenting very interesting problems common problems but sometimes difficult to diagnose and i appreciate and thank the doctors who are presenting uh these cases and i have noticed when i looked at the cases i have noticed that it shows a high quality clinical material and that is an indirect evidence of the high quality work you people are doing at vps lecture i appreciate and congratulate you for that so we will start with the first case actually dr sridhar shania has another meeting so she wants to present their face as the first case so we will have doctor srydas and i from the department of end at a vps election to present her case on secret that is 10 and as you for your information we have five cases 10 minutes each for presentation and five means for discussion so try to finish your case in 10 minutes so that we can encourage more people to ask questions so dr singha can you share yours yes sir at the outset i'd like to thank coaching clinical society and the netflix app for bringing us all together for this discussion on very interesting cases so i will be starting mine it is about the secrets that eyes tell here we we have a 65 year old lady who was no who was diagnosed with cirrhosis since 2011 she presented with fatigue slurs speech but we saw her for dizziness since one month so this dizziness was episodic it wasn't triggered but it was rotatory vertigo that is she felt herself and her surroundings spin in rotations and it lasted for a few seconds this worsened while she while he walked because of which she was wheelchair bound there was occasional vomiting as well this patient had stopped consuming alcohol since 10 years there was previous history of decompensation in the form of hepatic encephalopathy during the period of alcohol consumption presently he did not have jaundice ascites or any there was no decomposition decompensation in the form of jaundice or bleeding in other comorbidities he was a diabetic on medication with sleep apnea using overnight cpap hypertensive and recently since the last six months he is diagnosed with chronic kidney disease as well he was diagnosed with pneumonia sometime back in august and also icu psychosis admitted in a tertiary center in tissue he required medications especially haloperidol and lorazepam over a period of time to control his symptoms these medicines the dosage of these medicines were increased so it was increased and also respiratory tone as a pump were all added and these tablets were escalated up to 100 milligrams and one milligram of clonus epm respectively so here we are seeing a patient who in the background of cirrhosis but has stopped drinking from the last 10 years also has other comorbidities notably recent history of starting of psychotropic medicines coming to us with episodic non-triggered vertigo on examination the important finding here is that there's a hepatomegaly of two centimeter being two centimeters below the costal margin coming to ent examination tympanic membrane and ear nose throat examination was normal speech was slow comprehension articulation normal neuro-autological examination we tested him for succuds the card is when two objects are placed at a given distance from each other and the eye has to move from the right object right point and the left point we have a method to test this this is called as medio nystagmogram we have a graph that comes out the green line shows the target the red shows the right eye blue shows the left eye so it shows that sakai is the near normal in the horizontal plane this is his vertical eyes vertical isocard is okay vertical isocard is not very robust in most people so we did not take this as significant but his smooth pursuit smooth pursuit as you can see the picture image here this is smooth pursuit with the eye focuses on the target and moves right and left in a continuous manner unlike in a faced manner in the in regular succulents what we see here is that this patient has a psychiatric pursuit that is his eye is breaking into a step like fashion when it is moving from right and left this is a significant finding it is actually a central nervous system problem indicator now coming to nystagmus he had spontaneous nystagmus but uh it was not very there are few nystagmus beats we can see but this is not from right and left it is a downbeat variant of the nystagmus i'll show a video of the same so here we are concentrating only on his eye movement and we see that how his eye beats in a vertical fashion vertical nystagmus is always indicative of a central pathology so we can see how his eyes are beating in a downward fashion so with down gaze the downbeats increased then when his gaze was to right and to left there was persistence of the downbeat so when there is a lot of downbeat we have a follow these are the following diagnosis that we thought of degenerative diseases ethanol abuse in background of cirrhosis anti-convulsants when given above a certain dose can cause similar downbeat nystagmus and our patient was started on clonazepam at a very high dose and demyelination itself can cause paraneoplastic lesions can cause inflammatory pathology like encephalitis all can cause downbeat syndrome of relevance in his investigation was um that we thought that this could be a vernicas pathology many case disease because uh downbeat syndrome in a serotic patient is very very typical of many case syndrome so we gave him high dose of thymine thousand milligram diluted over five days and it was tapered slowly over three days the improvement was drastic he could walk within with minimal support a wheelchair bound patient could walk with minimal support by day five there was no giddiness no swaying while walking he did not have what i go uh after we gave him thymine a feeling of well-being we repeated the vng traces and we could see that there were no more downbeats seen in any of the uh nystagmus especially guess when we tested at central case there there's almost absent down beats in his readings so in this story till now the hero is thymine now why is thymine important it is an important core factor for trans ketolist transketolase enzyme in the glucose pathway is important for the generation of coenzymes steroids fatty acid and neurotransmitters also nucleic acid and complex sugars of importance is that um when there is absence of thymine it is a cofactor for pyruvate dehydrogenase as well there is absence of myelin and this leads to demyelination of the central uh demyelination at mostly the fourth ventricle level leading to neuro-autological findings such as downward nystagmus it is a life-threatening disorder and uh occasionally there's mental confusion oculomotor disturbances and ataxia it may present with only one or two of the criterias as we have uh as we have described a lot of neuropathological studies have after death have diagnosed and have indicated undiagnosed thymine deficiency related encephalopathy as classical symptoms and signs were often not present the other finding is that of korroskov syndrome where 80 to 90 percent may lead to psychos uh psychosis like behavior becoming a chorus cuff like syndrome so here right now in our patient we thought it is vernicase encephalopathy with features of karuska and it was confirmed was reversal of symptoms objective evidence with high after thymine loading but the twist here is that he has stopped drinking alcohol 10 years ago so what has triggered this this time is was up for um evaluation so we still had lots more coming up in this session a ct abdomen showed features of hepatocellular carcinoma so hepatocellular carcinoma is again related to thymine deficiency malignancies have increased basal metabolic rate which may induce the thymine depletion this could be another reason why our patient came up with these features in the event of a non-alcoholic background and also in cirrhosis the drug handling becomes very different and there is increased toxicity of of medicines mostly psychotropic drugs which act on the central nervous system so what we have what we see here is that it worsens cirrhosis leading to decompensation leading to thymine depletion also a concurrent hepatocellular carcinoma resulting in a high metabolic state of the liver both resulting in thymine deficiency which is why our patient must have come up with these features even in the absence of active alcohol intake so imaging is more it's low sensitivity of mri to diagnose wernicke's that's why it sometimes remains untreated the only ending is the mamillary bodies may show enhancement in the thalamic region now from an ent surgeon point of view what we see that um vertical nystagmus is most commonly seen in vernier case that too when the the situation of timing depletion is acute it is an upbeat nest atmosphere converts to a downbeat when the deficiency remains chronic sometimes patients they compensate over a period of time but provocative manure such as convergence of the eye head shaking and eye movements bring out the hidden nystagmus of a downbeat so why because there's astros astrocyte cell death leading to and mitochondrial damage and this uh this happens across the blood-brain barrier therefore the commonest pathways to uh get affected is those at the floor especially the fourth ventricle now what happens when there is a fourth ventricle problem that is the medial vestibular nucleus gets affected this is why the medial vestibular nucleus and the midline structures get affected so this is called interstitial nucleus of kajal this is a vertical neural integrator that means the upbeat and downbeat nystagmus is controlled by these regions in the fourth ventricle whereas so there are different tracks um the paramedian tract affects the upbeat nystagmus over a period of time the perihypoglossal complex recovers but the the parametric tract neurons remain affected which is why we have downgrade nystagmus when it becomes a chronic issue so the take home message is that multiple comorbidities come together in one case our patient and ex-alcoholic had hepatocellular carcinoma and psychotropic medications which worsened the delicate balance that he was on thymine supplementation is important diagnosis was made after we found downbeat nystagmus with video nystigmography requires high index of suspicion and i findings keep changing over the course of disease which is why we need to catch them early thank you thank you dr seda for his interesting case and i think it's time for uh discussion but uh anyway i'm not able to get into medford it was gone and still it is rotating so i don't know whether there is any question doctor remission i can help me by asking those questions so that we can put across to dr sveda and um i did uh see the comment section there isn't any question just yet so if there would be i'll let you know okay it was a very interesting case and we had you have presented in such a way that the different mechanisms involved in uh vermicase and probably perceptive psychosis were discussed and how this works and in this patient there could be many reasons why it is this has happened we are not sure what is the main reason but i just want to say that alcohol is not the only reason we always think only this alcoholism is important because i have seen patients with the pancreatitis not having adequate food or only on um [Music] or we have started giving them on iv feeds and dot those patients also i have seen developing uh many cases in philippi but i think you know unless you don't uh think about this you will never diagnose it that's very important so any patient having an altered behavior and you have to think across fine now so okay and uh i i think it is important and the dosage of timing is also very important you have to actually give very high dose nearly to the tune of around 500 video or even 2 000 and then only they actually recover and doing an mri in the right time is also important but don't delay mri because of uh you have to treat this patient because if you don't treat at the stage of any case and kepler they can go in for course of psychosis almost 80 percentage if unlimited will go into portion of psychosis then because it is more their recovery is delayed and we are not sure about what's uh what is the residual level in that i think the mri picture you showed is very classical and it is the very ventricular and the mammary body changes are very classical on that and how you manage this patient now will you give supplement of timing continuously for this patient yes sir because till his uh his carcinoma is addressed he will be on supplementation because that could be another reason for depletion because you know we repair almost one to two milligrams of time in per day and the body has a store of uh nearly only 30 to 50 milligram in the whole body and if somebody is not taking food for almost 16 15 16 days two weeks or more then there's a likelihood that they can go in for time induction so what would be the reason the patient is not on diet the patients are in iv feed or if you are even if an ngf adequately not supplement with the thymine because our body cannot prepare diamond plants can do that but if he require and once we as we know first everybody's research we study about krebs cycle tca cycle node and it requires tpp is a very important enzyme in that and the diamond becomes very important that of course alcoholism really is an important cause and very important cause in production of thymine deficiency and another thing what we have noticed that when patient comes with this and if you give them glucose iv fluid no that can actually precipitate this because of diamond deficiency i think the most important triad we should also know about that and the voltage sensorium and the eye movement abnormalities and the gate abnormalities these are all three important areas which we need to look at any other questions on the box uh yeah we have a question from dr uh it has been asked that can we use timing profile x is an alcoholic patient and if yes what is the dosage so whether when they are admitted to the hospital we know there is a alcohol depression we are going to stop alcohol and the patient goes for alkaline alcohol dependence and symptoms of that in those regions usually we give 200 milligram per day but actually in patients with a heavy alcoholism if they have got any abnormality in behavior then we give 500 milligrams and psychiatrists usually start with 500 milligram and we then continue with 200 milligram and then 100 milligram while they are in the hospital so 100 million twice daily is a reasonably good dose to give those who are not having any serious problems if the patient has got significant issues like waters and sodium try to give higher doses like 500 don't wait for the only thing is that we cannot do a serological estimation of this one because time in estimation is quite difficult you need chromatography to do that but there is actually the tpp and same can be some days you can actually do i mean sorry you can't do that go in same in this one sometimes but generally people do not resort to a diagnosis of time and estimation as a diagnostic molarity so imaging and i think most important thing is clinical suspicion so say that it is a wonderful case and you have discussed it very well you have presented very well i think you will go on to the next case in fact you have uh picked up a case of which that neurologist would have done and the gasoline should have done no i really appreciate that so we'll move to this next case it is done by dr vinida gabalekistan from the department of dermatology and uh dr vinida if the title is not just indeed so something else is coming up doctor thank you sir thank you for that introduction so let me start my case of a 64 year old female who presented with pain and redness of the left ankle of five days duration and she gave a history of strenuous household work 10 days prior and the symptoms were associated with occasional chills and tiredness and on clinical examination there was the lesion was tender to touch there was edema there was erythema there was a local rise of temperature and there was no nodularity one week prior to the onset of the skin lesions the patient gave a history of pain and swelling around the left ankle one week back and the patient does not have any other commodities so she had consulted department of orthopedics and they noticed fullness and tenderness around the distal attachment of the left atlas for which an mri was taken which showed retrocalcaneal bursitis distal third tendinopathy so the patient was advised some stretching and strengthening exercises and analgesics if needed so a routine blood investigation was carried out which essentially turned out to be normal except for an elevated esr or 56 millimeters the crp was high so having a provisional diagnosis of cellulitis the patient was started on oral antibiotics and analgesics so the patient was started on oral antibiotics initially but was later changed to systemic or iv antibiotics as the patient was not showing enough response so after 10 days of systemic antibiotics the pain persisted the edema persisted and even the erythema was remaining the same and the patient continued to get high grade fever associated with stills and myogen so further investigations were carried out as to look into the etiology of the fever and the skin symptoms so blood cultures were negative asu was negative all the viral serology was negative the total count remained the same except for a marginal elevation from the previous blood report like esr was 56 initially later it became 65. the patient was given clindamycin and cloxacillin for additional star fouriers coverage an ultrasound was taken of the left lower limb which showed subcutaneous edema there was no evidence of any venous thrombosis there was no stasis a punch biopsy from the skin lesion was taken and it showed edema of the dermis there was some lymphatic dilatation and inflammatory cells in addition there was no vessel infiltration no granuloma and the cultures turned out to be negative so the patient continued to get hydrate fever chills and the skin lesions persisted and there was no significant resolution clinically and in addition the patient started developing pain along the small joints of the hands wrist and ankle which warranted a rheumatology worker so the blood investigations were done the total count essentially remained the same but esr there was a marginal elevation in the esr from the previous one from 65 it went higher up to 110 but the rheumatological workup the rheumatoid factor the ccp antibody a nap and kasianka to rule out any systemic vasculitis turned out to be negative a mantle was undertaken and it was non-reactive so chest x-ray was also done which was essentially normal so to summarize we had a 64 year old female with no comorbidities presented with high grade fever chills arthralgia cellulitis of the left lower limb and an elevated esr so the differential diagnosis could be an infective etiology would be an inflammatory pathology like a zero negative arthropathy or a sarcoidosis malignancy or a paraneoplastic even as till now the blood investigations were not conclusive of any diagnosis so as a part of further workup and evaluation we decided to con to go for a pet ct scan which showed multiple intensely hyper metabolic and large lymph nodes and few of them were necrotic and it was seen in the prevascular right upper and lower paratrooping periodic symbiotic subcarrinal and even para esophageal and bilateral hierarchies so pet ct had essentially mediastinal lymphadenopathy and suggested a granulomatous etiology or a lymphoma and further ultrasound ultrasound-guided fnac was taken from the mediastinal lymph nodes and it gave necrotizing granuloma granulomatous inflammation which was consistent with tuberculosis so is near shore multiple scattered multinucleated giant cells and granulomas some of them showing necrotizing cascading granuloma fb stain was negative but tppc was positive so the diagnosis was necrotizing granulomatous inflammation consistent with tuberculosis so the patient was started on antituberculosis treatment and the symptoms subsided within two weeks of starting the antituberculosis therapy so we had a patient initially who presented without any trigger or without any allergenic or pathogenic factors and started on anti-tuberculosis treatment and after starting after initiation of the treatment we had complete response clinically there was clinical resolution of the lesions and there was radiological clearance of the lymph node after six months of completion of anti-tuberculosis therapy so the final diagnosis thus becomes mediastinal tuberculosis presenting as cellulite is probably a reactive response to the presence of tuberculosis so coming to the discussion part cutaneous tuberculosis or tuberculosis per se the difference the clinical manifestations of tuberculosis is very varied and it varies and it depends upon the host immune response the mode of infection and the immunity of the host so the presence of tuberculosis bacilli in the body can initiate varied pathomechanisms causing different variety of the symptoms so the presence of tb bacilli can mediate hypersensitivity or a reactive response to the presence of the tb bacilli or it can even induce antigen antibody complex reaction leading on to joint pains and arthropathies as far as cutaneous tuberculosis is considered it accounts for around point five to two percentage of all the extra pulmonary tuberculosis and the most common classification that we follow for cutaneous tuberculosis is a tapinger and wolf classification which is essentially based on the mode of infection and the immune response of the host so you can see there are extensive or various varieties in which cutaneous tuberculosis can present so what is essentially common in all these varieties of cutaneous tuberculosis is the presence of a tuberculoid granuloma but when you look into our case the cellulitis that we had we took a biopsy from the lesion but it didn't it did not reveal any tuberculot granuloma there was no vessel wall infiltration also which makes it different which means that the case that we had was not a direct infection which is caused by the tubercle bacilli but a reactive inflammatory response to the presence of tb antigen when we looked into the literature there was very rare and very few numbered case reports of atypical presentations of pulmonary and extra pulmonary tuberculosis some were presenting as skin oxygen popura some presented as cutaneous leukocytoclastic vasculitis and even tuberculosis silhouette is directly tuberculosis causing cellulitis where you get a tubular granuloma was reported but our case is unique for its rarity and the atypical way of presentation so to conclude tuberculosis itself pose diagnostic challenge and as far as skin and tuberculosis is concerned it is varied presentations and atypical presentations as well so high index of suspicion is needed to get into a diagnosis and thank you thank you thank you veneta for this excellent case and it was actually questions and i think you know one important thing is that when you are stuck with a puo you don't have anything i think you always think about the possibility of doing a pet scan which can actually cleanse the diagnosis yes because he could have gone through a ct screen and then gone through pet scan but you know when you will effect ct that you like to look at the whole body and give you an answer so i think you know uh other than magnesium indications so in this case as according to this patient has got an abnormal immune reaction or probably a hypersensitivity to a process yes you know somebody says that we always think about concept syndrome they actually manifest with arthritis in manifestation certainly especially because if you show me the picture of telling that this is a tuberculosis patient then i would attempt to think that only one yeah that is where the skin biopsy differentiated it so even in arithmetic when you do a skin biopsy you will get a panic lettuce like a reaction but in our case there was no particular there was no separate paniculatus and it just showed some inflammatory cells and and the other thing is this patient is an elderly female and yes type of manifestations you know this uh high percentage reactions occasion and the manifestations are different there what i think yes so whatever it is i think the ending is good and we have got a diagnosis of tuberculosis and which is actually good for the patient so if i ask you again what is the stimulation what do you do your answer is just a cellulitis it could be a reactive value like this i would like to coin that because cellulitis just means inflammation of the subcutaneous tissue which it is the only thing is what is the etiology so is it possible that it is unrelated or you think it is related because you think it is related because the patient responds yeah because nothing the patient was not responding to the normal course of treatment it was not responding to the antibiotic force and the lesions the fever the symptoms were all substituted only after starting the anti-tuberculosis treatment any questions on the chat box i am not able to open yeah so uh so there are no questions no questions thank you dr vinita will move to the next place thank you that is from the department of nephrology dr gladwin jimon and that is the tightly silk wrought voice that means that and thank you sir good evening uh today i am presenting a case in wrestling yes we have the case of 27 year old gentleman who was from chiang mai who had a renal transplant on august 2019 this native kidney disease was chronic glomerulonephritis and induction agent used was anti-thyroid globally and he was on maintenance human suppression of acrolomus microfinance optile and stave steroids he had a stable growth function post transplant the one year post transplant he had presented to us with a persistent diary of three weeks of duration and this diary was multiple episodes blue batteries tools no pain or hematopoisias associated with diarrhea no fever vomiting jaundice or no other any systemic involvement the general examination at this time only revealed he was pale and tachycardia was there otherwise no significant finding systemic examination within normal limit so this is the when a chart of the patient there that have a post post-transplant infection the highly positive cme infections more than six months and lymphoma is also there there so at this moment this possibility with history we consider the diagnosis of definition like cme colitis or it can be directed to drug induced maybe like microfinance marketing which is known to be caused for a typical impressions isosceles cryptosporidium or tuberculosis following again post-transplant lymphocytic disorders the relevant investigation shows a hemoglobin is seven point five gram legislator otherwise total count platelet was normal serum reaction was two point four milligram per deciliter liver function rest was normal and other stool routine was saying no obvious vital test was negative that during stool currencies were sterile and usd abdominals taken was normal and we went to the further investigation it's showing colonoscopy which was showing large electrical ulcer biopsy of this colonoscopy was taken which was showing inclusion bodies and then we sent a quantity cme pcr which came as negative and afb also was negative so we considered that the possibility that this point was cma colitis here even though quantity pcr it can be negative cma quantity cme in if it is localized infection other possibility considers drug induced that is mrmf and treated with ocme or gancyclovir for 14 days and mmf stopped and converted to everlasting part of cma treatment and as a part of suspicion of mm of india's diarrhea this diary was reduced and over three weeks later while on the hospital he developed ulcer on the uvula there was no genital ulcer this time the culture was showing plenty hdr which was treated with iv antibiotics and this also healed after 14 days all then for the next five months he was asymptomatic and on february 2021 he had presented to us with episode of lava gi blade the ultrasound taken was normal and ct abdomen showed bald thickening in the cecum and terminal helium ascending poland and it met helioc conjunction with few miscentric lymph nodes again we have done a colonoscopy which was showing persistent helium large heliosical ulcer with necrotic base and few clots source also there at this point of time argon plasma coagulation was done and again this colonoscopy biopsy was done there was no evidence of tuberculosis malignancy for bronze disease the mantle was done which was negative the even though no evidence of tuberculosis i know he's highly immunocompressed patients and illusive answer and see it is going ct scans running power world degree we thought to start an empty trial of empirical att for him and again one month later he developed another ulcer over the umla which is our culture was again culture grown as pseudomonas aerogenesis this time also treated with antibiotics the solstice is filled and responded and one year later he had again presented with the lower g8 second episode now other systemic features we had on a colonoscopy which was showing persistent helio sequel also biopsy was again non-contributory this is a timeline of our uh course of the events 2019 he had underwent regional transplant september 2019 with acute diarrheal disease suspicion of quality cme qualities and also oh you will have treated for cme and mmm stores 2018 again lower ga blade helios equal answer with necrotic beast biopsy is now non-contributory and try treated with empirical atg it's like uh ionization parasymmetric thumb terminology and again january 2008 lower the a bit persisting ilioc cluster biopsy non-contributory at this point of the moment we considered again differential diagnosis like inflammatory bowel disease or any undictated malignancy or you know it can be again interesting to work losses but repeated biopsy if you have to show any evidence of any of this above this odd point in this diagnosis recurrent oral answer without any obvious cause there and we thought that could this be a versus this is we thought so recurrent oral ulcer helios equal ulcers are the fairest point pointing towards the budgets but pythagorean was negative and no genital answer over so this is the criteria for diagnosis for biases in our patient this is criterion is not many not [Music] fit into this criteria so biases with recurrent or analysis and plus any of the two of the following weekend diagnosis are the biases then our problems is recurrent or analysis persistent heliocentral answer then of course i defined for this heliocentric trial of an atg given which was not responded he wasn't so this thing of we are thinking of the multiple course various costs of helios equal answers this all of the most common was like tuberculosis and other malignancies and other these are reasonably limited this whole process we are excluded then other three major diagnosis in this helioc classes measure three depressions are like biases this is industrial tb crohn's disease and versus this is after celsius can be seen but in distance levels is rare and elastical analysis is the most common site for in the past disease for the ulcers then final diagnosis he keeps us embarrassed this is a typical manifestation and stopped att and started on enough alpha inhibitor uh diamond map is uh 80 mg first dose and then followed by 4 tmg taught two weeks apart total seven doses was given on follow-up now for falloff after three months now for the gab or oral ulcers hemoglobin improved to 12 and four long colonoscopies showing there is significant reduction in size of this large heliocentral ulcer then discussion about interstitial viruses diseases can occur in three to six percentage of vicious disease patient with higher frequency of gastrointestinal involvement in east asian countries versus diseases involving gastrointestinal 10 to 15 percentage of cases with block lysation that occur in heliocentral region versus disease is a is mainly seen in multi-system middle east and east mediterranean region along the silk road this is why i chose this name silk road silk road moss and knowledge laboratory test is pathogenic and is usually clinical diagnosis only one other case of new onset of biases this is pos kidney transplant has been reported in literature this case was published in kidney international in 2019 2009 and this is case of recurrent oral analysis and diary in renal transplantation as our case then this is when a person presented the patient in the ulcer in idiocycle area we okay we have suspect we can suspect biases we must suspect vascular disease this impression is a typical industrial ulcer as ours and plus oral answer we have to suspend an industrial biases disease this as in our case when take-home messages persist this disease that can evolve over a prolonged period all described menstruation may not present at the same time heliocellulars are the rare cause of biases disease but put in criteria for diagnosis common differential to be ruled out are tuberculosis and prosthesis these are my references and thank you for coaching clinical society for giving me this wonderful opportunity to present in this case thank you clapton jimon for this challenging problem and i just want to um of course i agree it's really a challenge after the transplantation especially on mmf developing diarrhea you need to know but it can be because of the drug or because of some opportunity infection all these are quite important there so i just want to ask you certain things one is that before coming to the final diagnosis i just want to ask about this particular patient is that you have told that you have taken biopsy from the vesicle region and asked for suspected nutrition bodies in the uh so suppose if you are getting an immersion body i think you can always ask for hc did you get an isc on that yes sir it's your scene here to make your diagnosis of cmv our actual evidence are quite low but i agree that in post renal transplant even a low threshold for cm we need to treat them here actually tissue psr is negative i'm not aware about the i am not aware about uh about the serological test for cme on that and histologically also there is no strong moments so i don't know how you are just different giving treatment but i agree that probably because the posterior transplant transplant that may be the reason another another thing is that you know you have start you are told that you have given treatment for tuberculosis and the medical treatment should have a time so at what time did you reassess the patient after giving it well i am [Music] and tuberculosis this happens to us also sometimes we find it difficult rare situation but in those situations where we are forced to start empirical therapy with the att in an idiosyncrasy we always get some other evidence like igr atoms a demand vertices positive because immunosuppression matter may be negative and we also always take it just city to find out whether there is a tuberculosis in there in spite of that if the pathologist says probably this i cannot defeat between tba versus processes we give usually eight weeks of treatment and maximum three months twelve weeks then you repeat a colonoscopy and look at the elastical region if there's no change there is no healing then you have to stop it so that is the time period eight to twelve weeks is the maximum period i don't know i don't know but anyway there was no creative response in this though i agree that the diagnosis of uh bachelor disease is is generally clinical with the laboratory support is minimum tissue astrology some dsl but it's a conglomeration of clinical features but you should have a criteria for that and it does not fit into criteria and before starting a dialogue how you arrived at a diagnosis and how you are you are justified in giving treatment for this patient is it because that you felt that probably this patient can have crohn's also no not possible no evidence in him without grand llamas or is nothing but no possible in some cases but biopsy also can be normal in some cases and there are some serological tests which can be done for uh no no no pathogenic laboratories is there only some xla can be associated and other uh these three months we stopped now we are stopping your response and repeat colonoscopy also know uh ulcers so we are not continuing so he has to respond to a dilemma so you are given a trial of only three months and then he stopped did you use the full injection regime or you started with only 18 millimeter started faster industrial region by 80 milligrams 80 milligrams and 40 milligrams [Music] all right okay anyway so i think you know this is actually a clinical challenge that is very difficult to make a diagnosis but it was quite interesting we learned a lot from this case that saying that anybody who has got oral arse is an illegal uh of course they agree that in patients with the precious syndrome electrical region is the common site for ulceration and uh we also have sometimes had this problem and we have diagnosed even some days we uh could not get a diagnosis and we operate and finally we go to dinosaur problems with special syndrome by just looking at the specimen not any pathogenic features because you don't have any granulomas you don't have any uh changes of crohn's or tb but sometimes you pick up masculinities that can help you to make a diagnosis thank you so much i think we need to move on to the next case and that case is from the department of authority and ever since we learned neurology diabetes syphilis and um [Music] angel joins the abnormalities we start hearing about charcot joint and something uh rajasthan is telling about uh today is that feel that you don't feel the floor and the surgical skills that have made the difference in the patient so dr daisy simon from the department of orthopedics especially on the foot and angle center coochie thank you sir thank you clinical society for giving me the opportunity the talk is the feet that does not feel the flow as the name suggests it's kind of a neuropathic foot so this is so this is a case history of a 55 year old male who came to us with a complaining of an oozing corn from since last 8 months of course it was a diabetes diabetic for 12 years hba1c was about 9.7 he also had hypertension and ckd the history started about 10 months back when he had a twisting injury and uh followed by a kind of diffuse swelling and he was being treated as cellulitis and an antibiotic was given but the the the swelling persisted and he started seeing that there was a gradual change in the shape of the foot he was given footwear modification but he continued to walk with little discomfort and two months later he developed a small blister and ooze from the foot so he was diagnosed as a non-healing corn with an infected non-healing corn with the diabetic mellitus and he was advised antibiotic and dressings this continued for about almost next six to eight months but the wound never healed when he came to us he had this diffuse swelling the feet was broadened the foot you can see we called this as a rocker bottom foot the rock of bottom deformity with an infected serotonin ooze and there was good pulsation but there was absolutely no sensation what we call as the loss of protective sensation and this was the x-ray and now you can realize that how the midfoot had completely uh has dislocated and what was once upon a time the cuneiform bones is down here and that is the actual cause of the non-healing ulcer because he was actually stamping on his cutie from bones and that had got infected secondarily because of the continuous pressure and since he did not have any pain he continued to walk but with a little discomfort so our treatment was treat the ulcer and give a stable planting rate ulcer free walkable feet which was a challenge which is always a challenge when it comes to a neuropathic foot one because he had infection he was actually having staph and klebsiella so we had to do a bony debridement and we did a bony debrip and we did something called an exostomy and started on an appropriate antibiotic once we did that we continued him on non-weight bearing strict non-weight bearing and was a very compliant patient and he had got a good diabetic control and this is what we got at the end of it at the end of almost one month his wound started to heal and that is the time we thought now it's time because if you again ask him to walk normally he would again probably have the same story for which he had presented to us so this was the limp when after one month of treatment of the initial treatment of exhaustory so time for the second step so that is what we did we went ahead and did what we call as the mid-foot reconstruction we did the medial column exhaustomy and osteotomy and then plated both medial and lateral side i'm not going into the details of what all joints we reduce but this is how we went and this is how the x-rays would look like a lot of implants but that is what the because the bones are completely soft uh very fragile and so we have to reconstruct with what we call as a super construct so this is how the immediate post top looked the wound looked good and the now if you look at the x-rays this is what the pre-op is what we call as a mary's angle the complete correction of the mary's ankle leading to the arch recreation the calcaneal pitch the fire the feet which was completely a rocker bottom now has regained his arch and is completely normal and after one year we could see a good fusion of all the bonds which we had uh fused and so this was the clinical picture after one year the post-op picture you can see compared to what was pre-op in the air in the broadening of the feet the feet has become narrow and both dorsally and plantarly you can see the difference so uh this what is this charcoal foot initially it presents like a cellulitis severe swelling erythema but patient does not have so much of pain and he because of the neuropathic scene this is a differential diagnosis here is the cellulitis osteomyelitis and that is where everybody misses the bus because we almost always treat this as cellulitis so this is like you know comparing between these two tummies which are completely opposite cause but that's how it looks similar clinical assessment is very important you have to look at clinical part the cardinal features are there might be a skin breaks and the when you elevate the limb the redness fades which is something of an importance in a very fair skin but not very important when it looks when we look at the browner or the darker skins which we have the blood parameters usually helps in assessing the inflammatory markers x-rays are essentials but the more important ones are the mri scans which we use here in india the ideal thing would be bone scan the indium bone scan but unfortunately we don't have that so we rely more on x-rays and mris x-rays shows different types of changes from hypertrophic to atrophic changes and there these are the classifications i would uh go slower like what is called as the each and holds classification the stage 0 is the sign the stage of cellulitis which is often missed stage one this is the most important part and this is where the x-rays are seen and this is where the limb can be saved without major surgery even if you pick at this stage but unfortunately patients still continues to walk on these feet when the bone is fragmenting it's like you know you have put your limb under in a bomb when it is fragmented in different shapes but patient still continues to walk with swelling it is a having and though it does have an acute inflammatory response but then there is no pain in stage two the the collapse has happened the deformity has happened and the x-ray is very much evident in stage three the whole thing consolidates and this is the time when we most of the time we operate and this is the time when we have to do something if there is a problem in anatomical basis it is a midfoot that is the most common type though hind foot is very dangerous and often leads to major structural instability and this hind foot charcoat is the one which leads to amputation if not treated well so you can see how the bones would completely change its shape the limb would change in management level what we we do in the acute phase is what we call as the total contact cost this is the plaster the specific specialized way of putting a plaster and you put a total contact cast and and later on orthosis to save the limb and to save the feet from having further problems medical management yes medical management is given different drugs but doesn't help surgery is what it helps so at the end take home messages to carefully examine the feet high index of suspicion in diabetic patients investigate the slightest of doubt and remember amputation is not a solution that would lead because 50 percent of the patients would lead to uh the second application so this is our patient who's walking uh and so then again don't ignore the feet that does not feel the flow because if you ignore it this is the catastrophe that happens thank you very much for your patience thank you rajesh for this excellent reconstructive surgery which is actually a big wound for the patient and preventing amputation is our goal and that improves the quality of life of the patient and anybody who has a similar problem i think you know it's very important that the right diagnosis at the right point of time and the right type of management is quite essential and as a media students we always know that charcoal joint is actually due to syphilis and now we know that very rarely you come across siblings and mostly it's because of any neuro neuron neurological manifestation which can actually lead out to loss of sensation in the feet which can ultimately don't develop on the charcoal zone and diabetes is our most common disease which we come across now and i i feel that uh it's uh what do you think the this type of manifest is only because of neurological uh involvement or is it because of vascular involvement also because we know that there are two theories uh the vascular theory as well as the neurological theory but it is mostly the vascular that is because of the autonomic sensory in your neuropathy uh and uh so so this leads to hypervascularity so most of our sharp foot has got bounding pulse unlike the diabetic feet where there is a lot of atherosclerosis so this sharper feet most of the time are hypervascular and that leads to resorption of the bone and destruction of the bone any questions from the audience no sir can i ask you a question it's actually a different question that's actually to help people general uh practitioners dehydration etc who manages diabetes at what point of time the diabetic patient should be referred to a diabetic food specialist for evaluation at what point of time most of the time when we see an ulcer which is not healing over a period of time the diabetic there are two things which hap needs a foot specialist is a diabetic foot ulcer and the second is the charcoal foot charcoal foot need not have ulcer it could be the change of the shape of the feet but diabetic foot ulcers is where which does not heal it is not by foot specialist it is a multidisciplinary approach we need a vascular person we need an endocrinologist and a food it's a combined effort that saves the food and that is what is the need of our a combined approach to uh to to save the feed as most of the time we see when we amputate it within three to four years the other limb comes into a picture and they'll lead to a double amputee which is disastrous thank you rajesh for this wonderful presentation wonderful skilled procedure for a reconstruction of a very difficult issue and it was really wonderful to listen to you and yourself your techniques on this particular procedure uh i think we'll know the last case that is by jazeera from the department of surgical breast technology at the center of excellence of hungary surgery of the country or even upside and the title is on breaking the taboo and jazeen you are going so thank you for the this opportunity wonderful opportunity so whenever every surgeon whenever he enters into the field of surgery all the three rules which actually apply to him are eat when you can sleep when you can and don't mess with the pancreas so this was an old school thought of don't messing with the pancreas is that actually true so let's break that taboo that don't mess with the pancreas i'm dr jasil from uh department of surgical gastroenterology so i am briefly presenting about two cases which we have done we have re-explored we have done three surgeries on the pancreas my first case is in her story started from 2013. she's a 54 year old female patient non-diabetic evaluated for abstractly jaundice and found out to be we can see in the ct there is a mass in the head of pancreas with the dilatation of the pancreatic duct and the bile deck so which is called a double deck sign with a dilated pedi and bile deck that is typical of a carcinoma head of pancreas so usually for all the customer head of pancreas we will proceed with the ripple pancreatic odor anatomy which we did in 2013 and the biopsy came out to be moderately differentiated you know customer and for which she received six cycles of hydrogen chemo with the cardboard black and gemsy topic then after that she is on constant follow-up under us in from 2013 to 2021. uh during that time she had good weight gain but in between some exoplanet functions has been affected so enzyme supplementation was started on glucose and also her diabetic status also worsened a little bit but it was well controlled with a fixed process of a small doses of insulin and their last imaging is from 2019 by an mri uh there is showing there is only a normal pancreatic oxygenostamine but there is a dilated there but there is no recurrence there is no disease recurrence and her ca 99 was always normal uh during this period of fallout but he lost follow up for the one year after 2019 because of the pandemic and in february 2021 she again presented to us with uh hypoalbuminemia back pain glossophate and uncontrolled diabetes so obviously we were thinking about another malignancy another pancreatic malignancy or a recurrent sovereignty ct so in the city you can see this is the old pancreatitic oxygenostomy so there is a proliferative growth at the pancreaticosuginostomy site of course it's a new tumor so we proceeded with an eu fna usfna also you can see there is a hypo enhancing lesion with the some cystic components we written fna there is a suggestion of an adenocarnoma so since it is a second tumor after eight years we have to roll out any sort of uh dischargement so we did the pet city so pete city only confirmed it is a lock lace disease so obviously uh we we can't afford to lose the patient that much so after eight years of surgery the patient came with another tumor so we have proceeded with the re-exploration of that patient already operated people we have re-explored so this is the old pancreaticogenostomy we can see here in the pancreatitic organism and this is a mass inside that we are feeding that mass so we could able to reset that mass with a very good negative margin and here you can see there is a small stump of pancreas some four centimeter of the pancreas is actually normal so we could able to see the pancreas here and this is a splenic vein this is a portal vein so we could able to do a new pancreaticostomy so we resected that tumor affected that pancreas then there is a distilled pancreas there was there and that has been reconstructed with the new pancreatic orgasinostomy was that and this is that the second specimen of the local uh recurrence or the new tumor so this is the ct image showing the new pancreatitic oxygenostomy so the biopsy came out to be again multi-differentiating customer after following which she again received six cycles of chemotherapy with oxalic uprising uh last years on november 2021 and she was on constant follow-up with us now almost one and a half years after the surgery so diabetes status has not worsened no brittle diabetes because there is some sort of pancreas is still remaining through the patient so there is no brittle diabetes and also the enzyme supplementation is also not increased previously she was taking 10 000 units tedious and now also she is taking 10 000 units tedious and there is no recurrences till now and she is having a very good quality of life so the take-home message from this first case is customer pancreas has got a poor long-term survival but the long-term survival can be achieved by a radical surgery so our lady has got a disease free interval for almost eight years then developed a new tumor which was also resected and has got a reasonable quality of life after that even after the resurgence that's my first case and my second case is a 22 year old male patient male patient he is a non-case of chronic calcium pancreatitis and the patient was put only on enzyme supplementation for the past three years by a local physician so of course exocrine deficiency is controlled with the enzymes but there is no endocrine deficiency he is not a diabetic patient and pain is the main criteria for we are offering him surgery just because of the pain because it is so severe that it interferes with the patient's day-to-day activity so he came to us with an mri mrcp which you can see there is a dilated pancreatitis there with atrophic pancreatitis atrophic pancreas was there so uh directly we proceeded as per each institute protocol or routinely we usually do phrase procedure we did on 4th of january 2022 almost same finding a set of mrcp so this is a finding so whenever we are doing phrase procedure or any surgeries related with the pancreas all these sort of complications like infection wound infection pancreatically case everything can happen but the most drunkard complication is always the postoperative bleeding so whenever we think about the post-operative bleeding always this anatomy should come into our mind so we have got the abdominal iota here first branch is the syriac trunk second branch is a sma so from the celiac rung we have got the common hepatic artery splenic artery and the left gastric artery the common hepatic artery has got a branch of gastrodional artery screening has got a branch of dorsal pancreatic artery and there is communication between the sma that is superior my centric artery and the celiac arteries so the most common site of bleed after pancreatic surgery the most common is always gastrointestinal laboratory then it will be having the common hepatic artery then the splenic cataract and finally the left gastric attack so our patient also had even though uh majority of the patients will not have a bleed but this patient had a bleed on post operative day five which is represent which came out to us melina so routinely we go ahead with a ct and geography the ct and geography showed there is a pseudo aneurysm so you shall cause this urethra from the inferior pancreatic category so obviously this is a role of radiologists who come there the international radiologist will come there but in this patient there is a very important finding which we could able to add in defensivity and geography the patient has got a median arcade syndrome that means it is a celiac axis will be compressed with the median arcade so you can see the severe narrowing of the origin of syria country with the extensive collaterals in and around the pancreas that is very important factor so whenever the radiologist will come he has to embolize this vessel he has to cannulate the celiac artery first but because of the celiac artery has got a serious stenosis he could not cannulate the celiac artery but he calculated the sma and finally he could able to achieve a blue embolization of the bleeding vessel so this was the bleeding muscle but with this with this angiography you can see there are extensive collaterals between superior centric artery and the celiac artery so but the issue because of this collaterals again the patient is in a high chance of bleeding the patient can go ahead with the bleed again again again so the question will the patient bleed again yes biod7 again the patient had melina hypotension hemoglobin form we read the ct angiogram again there is a pseudo aneurysm in one of the collaterals so we could able we we again tried a conventional angiogram but you can see this is a pseudo aneurysm and that pseudo aneurysm is getting branches from almost all the collaterals in and around there so that we could not super selectively cannulate any of these collaterals or we could not able to we could not able to embrace any of these vessels so there comes a sergeant's load we explored him so the re-exploration after the phrase the first free exploration is on post-operative day seven so what we did is we opened the regime so this is a pancreatic oxygen atomy we opened this jejunum so there was an arterial bleeder was there which has been bipolar by using a bipolar coagulation so we uh bipolar coagulated that and what we kept is we kept a selastic brain a small small bore needle small bone drain has been kept into the pancreaticozynostomy loop why we did that because that is just to create a controlled external fistula so that that will reduce the pressure inside the pancreatic vaginostomy as well as it will reduce the chances of local consumption prior globally so even if there is some sort of bleed happens there is not that much of pressure is building up in the pancreaticozynostomy so that the bleed can get controlled as its sort so that is the role of uh why we have inserted a selastic drain into the pancreaticozynostomy and we have closed this region atomy but the question is because it is a very small bore uh train that drain got blocked one day and again on period the patient again blood so the re-exploration number 2 on pod 2 so that was very difficult because of the dense additions and we again uh approached there we did the genotyming and all the clothes were evacuated and there is another active leader was there that was also controlled and what we did is this elastic drain has been replaced with another whiteboard uh train of twenty four friends of foley along with an irrigation tube in order to avoid further blocking and uh almost all these pod told days his oral intake was very poor so for nutrition wise also we did the feeding giant ostomy for that patient so after this three exploration he gradually improved during the hospital stay so there was a controlled postoperative pancreas through this strain but there is no further episodes of melina hypotension or hemoglobin drop and orally as well as feeding the anatomy where geogenostomy were tolerated by the patient and he was discharged with this drain in situ and which has been downsized on the during the follow-up or during the past past month we uh during your copy visit we actually downstage that rain also and so the thing is even after his surgery he did the surgery for his pain so is there any post-operative benefit for the patient so what is a post-operative functional status of follow-up after going through all these hurdles so at three months we examined him and there is an exocrine efficiency still the enzyme supplementation is going in ten thousand international tds which he has been using previously but there is no diabetes no endocrine insufficiency and the most important thing is we did surgery for pain and the pain is now the pain score is mild on only on occasional days so the take-home message for my second presentation is even the most structured complication of pancreatic surgeries can be managed without any mortality and for which the multidisciplinary approach is crucial in these sort of scenarios so coming to my first life eat when you can sleep when you can and don't mess with the pancreas we don't agree with that we can't mess with the pancreas and still get out of the uh morbidity or the mortality which is happening thank you thank you uh jasil for this wonderful cases i think you know the brave patients handled by the brave group of surgeons that is what i think you know when you get your postability complications the relatives get upset and pancreatic surgery even with the in the hands of excellent gi surgeons it is a difficult surgery and any possibility complications are really drugged complications yes when you get a leak after people that is mostly is one of the dangerous complications that can have and bleed happens when it is not able to be tackled by an angiographic by a radialist then it becomes another difficult uh thing to handle because you know you cannot go and reima with the anastomosis there and wonderful thing what i have noticed that you have gone through the jejunum you have to do the genetome we didn't dismantle the anastomosis an excellent way of looking at the problem and least damage done there and allowed to heal by itself by tackling the bleedings and the excellent cases and i also think that the first case you know it's actually excellently followed up i just had a question on that case under the first surgery and what was the um type of say did you achieve an arcelor section yes sir it wasn't it was an rco resection uh moderate but the biopsy was also it's a moderately differentiated customer but with the lymphoma invasions were there and one lymph node was also positive and very rare that you get a different management even because we never get a chance to follow patients of ca pancreas this long with uh and why do you say it is uh actually a different mechanism because the timeline because because the thing is uh the follow-up is almost eight years so if it can be any local recurrence it won't happen after eight years because all these eight years is her cna indian was was normal there was no like we were routinely imaging her for every one year every six months we were routinely imaging her there is no evidence of recurrence at that time and cnn engineering was always normal and after 80 years getting a malignancy it can be because pancreas is an organ which can actually have multi focal tumor can happen from there so it can be a primary to a new tumor also but there is a possibility that it can be a local difference also but we will keep that new tumor as a uh first possibility rather than ignorance not have any chronic pancreatitis electronic pancreatitis then you know they can have interactive neoplasia changes uh dysplasia occurring multiple levels of the pancreatic attack if you look at this you get if you take the specimen of the pancreas and chronic pancreatitis when you resect it now you can actually see that the areas of abnormal diff is plastic epithelium and which can be done to tumor the balance of pancreas actually looks normal and historic strategy also they haven't mentioned any of these yeah technical question while doing surgery for this patient that's the first patient you know there is only a limited amount of pancreas now the head is not there only the ocean left over [Music] definitely sir intraoperatively we actually examined that angrier so we were also the first we went ahead with the two options were in our minds one we will do that limited reception that is a radical resection and we will keep some distal pancreas and the second one is total pancreatity but whenever we went there the distal pancreas the 4 centimeter of the pancreas looks absolutely normal and that frozen was also negative for the malignancy so that we can save some at least some 20 30 percentage of the insulin uh beta cells so that can actually avoid the brittle diabetes which that decision was actually right after one and a half years after the surgery she doesn't have any brittle diabetes so the diabetes is always in a controlled state so we could able to achieve that outcome by conserving some sort of pancreas some amount of pancreas yeah i fully agree with that i'm not a surgeon but i think you know doing a frozen station at that time is very important and crucial because you are leaving only very little pancreas there to re-operate the patient again it becomes difficult uh but i know sure it will be okay with your hands uh because your unit is pancreas excellently well and regarding the second case i just want to ask you in that patient uh you have told that the patient endocrine insufficiently has not developed developed after three months that is not okay because they develop uh exogenous little later so just like following them for three months that is not something yeah that you have not because any chronic pancreatitis that you know that the functional reserve is very less and most of the most of the [Music] because you have we have done a fry surgery and all those things and because of vascular comprehension or many of the islands would have gone in the head region now so probably if they may develop but if it doesn't help it's very good for the patient and you're done extremely well in the second case and basically the surgery has happened in january this year so only agreement but constantly we are having the follow-up all the questions excellent and very two interesting cases and extremely well so congratulations thank you for the wonderful presentation thank you because now you come to the end of the presentation and we had five interesting cases and i think all the cases had a message on this and some of the cases especially the silk group case actually it was a very fast case and they attended so well and managed uh reasonably well because in spite of this even today we don't know what is except dinosaur patient but that and each of the patients where exa worked up variable handle very well i really appreciate and thank the doctors of vps lakeshore for this wonderful presentation and excellent workup of cases and beautiful management of the cases that actually reflects the quality of work you do and i really appreciate that and i would like to thank chicken society for giving me this opportunity and i know how lakeshore is doing in all these things because i was a part of lakeshore in the past and i don't see hms here but anyway i'm sure he will be listening to this uh i have a lot of i got so many friends there and rajesh and everybody is my friends there anyway thank you so much back to thank you sir thank you for an excellent evening all cases were very interesting and beautifully presented and carried away take home message and i thank all of you for having me the possible questions that you can still run on experimental interests thank you for an excellent job as a moderator okay thank you thank you bye to everybody night thank you bye thank you everyone for attending the session thank you thank you

BEING ATTENDED BY

Dr. Darius Justus & 327 others

SPEAKERS

dr. Vinitha G

Dr. Vinitha G

Consultant Dermatologist VPS Lakeshore Hospital Ernakulam

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dr. Gladwin Jeemon

Dr. Gladwin Jeemon

DNB Resident, Nephrology , VPS Lakeshore Hospital

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dr. Shwetha Shenoy

Dr. Shwetha Shenoy

Consultant, ENT Surgeon, VPS Lakeshore Hospital

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dr. Rajesh Simonhwetha

Dr. Rajesh Simonhwetha

Senior Consultant, Foot and Ankle Orthopaedic Surgeon, VPS Lakeshore Hospital

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dr. Vinitha G

Dr. Vinitha G

Consultant Dermatologist VPS Lakeshore Hospi...

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dr. Gladwin Jeemon

Dr. Gladwin Jeemon

DNB Resident, Nephrology , VPS Lakeshore Hosp...

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dr. Shwetha Shenoy

Dr. Shwetha Shenoy

Consultant, ENT Surgeon, VPS Lakeshore Hospit...

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dr. Rajesh Simonhwetha

Dr. Rajesh Simonhwetha

Senior Consultant, Foot and Ankle Orthopaedic...

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