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Cochin Clinical Society Meeting - March 2022

Mar 17 | 2:00 PM

Cochin Clinical Society brings to you case discussions from 5 different specialties presented by the doctors of Lourdes Hospital: 1. Dr. Manoj: Air Hunger: What we shouldn't miss 2. Dr. Anjana: A middle-aged gentleman with sudden onset unilateral deafness 3. Dr. Renjith John Mathew: A swelling in the bone of many months 4. Dr. Anju: In pursuit of a cause for recurrent weakness 5. Dr. Tinu: Taking the path less traveled

[Music] my name is dr tandy and i welcome you all on the behalf of netflix today we are gathered here in association with the coaching clinical society for a session uh for the clinical society meeting for the march 2022 where we have five speakers that will be presenting their cases we have dr manoj kumar dr anjana along with them we also have dr ramesh dr george follows dr binu dr vasantha nayar and dr subramanyam on board with us for this particular session now i'll hand it over to dr subramanyam if he's on stage uh to initiate the discussion as we couldn't get dr george follows on board on stage i mean dr subramaniam can you come on stage yeah good evening everybody so welcome again to another interesting bunch of five cases from luth hospital so as usual they have selected five very interesting cases for all of us so the beauty of these meetings are that these cases are completely investigated and followed up and have gone to their logical conclusion so it's a landmine of information for all as clinicians to learn a lot from these so i thank the doctors of load hospital to get all these cases together for the benefit of all of us so let's start the ball rolling uh i invite dr manoj probably he's the first presenter with his interesting case of sudden onset respiratory failure over to you dr manoj good evening everyone we're going to see an interesting case um air hunger 44 year old male came to our hospital on 21st jan 2022 with the productive cuff aggravated on laying down and lived on sitting up which was sort of inconsistency and three episodes of non-village vomiting on a next day early morning followed which he started developing breathlessness which wasn't over hours and he had two episodes of him of crisis uh then there was a reduced uranus local hospital and management steroids bronchodilators and broad spectrum antibiotics in view of human faces and worsening of breathlessness they have referred him to our center in suspicion of sepsis with a rds and bipolar disorder on twitter for last seven years he was a non-smoker non-alcoholic and there was no history of blood transfusion vaccination in restoration past summary a 44 year old male with 3 ssdf systemic hypotension surveillance history of bipolar disorder on treatment came with two days history of productivity cough and three episodes of non-videos vomiting followed by sudden answer rapidly progressive breathless breathlessness and two episodes of mild hemorrhages with the history of follicular for last 24 hours systems likely involved were respiratory cardiovascular and renal my possibilities were sepsis with multi-organ dysfunction involvement of a rds uh acute lv failure secondary to one acute coronary event acute pulmonary secondary to hypertensive failure pulmonary embolism drug overdose and aspiration leading to chemical immunities on further estate taking he had a history of allergy intake of 30 amlodipine 5mg tablets on this day before of symptoms 18th june 2022 at home and he was stagnant with saturation of 88 on rumor and respiratory rate of 28 per month abc shows common set of respiratory closest cystic the initial operator parameters were hemoglobin are 14.4 with a neutrophilic leukocytosis normal platelet count yuria was on the higher side on 11 18.7 crp was elevated 81.4 calculates on the left two are normal union examinations of microscopic hematuria with a few passes trophy was negative ddamer negative and probably np was negative after examination and preliminary investigation possibilities were narrowed down to non-codogenic ulnar due to amlodipine orders there was few case reports and second possibility was uh sepsis with aids then it shows normal uh lv and rv with uh liquidated ejection fraction cthrox was done uh this shows a polynesia without any cardiomegaly ultrasound shows a normal adrenal pancreas and spleen and kidneys blood sputum and during culture was direct leptoids done it was negative low calcitonin was also done it was also negative serial x-rays uh was taken uh for consecutive three days it shows there are rapid clearance of bilateral opacities final diagnosis non-coordinated polynomial likely due to amlodipine toxicity treatment he was started on non-invasive positive pressure ventilation with a fa auto of 50 percent for initial two days and wind up on day three it was stated after 10 days the chest x-ray was clear and laboratory parameters are within normal limits this was the x-ray on discharge review day i'm loading up the second centralization ccb ultra long acting drug cost personal office for 36 hours daily uh it was useful in hypertension with the stable antenna common side effects we used to see were palpitation dizziness hypotension peripheral edema when it comes to overdose they have refractive hypotension and radicadia hyperglycemia metabolic acidosis non-cardiogenic called edema amlodipine-induced non-cardiac mechanism at least in last 10 years there are uh 10 to 12 studies published uh which shows the ccb are more prone for non-cardiogenic pulmonary edema is as evident in multiple case reports clinical presentation of non-cardiogenic pulmonemia due to ammunition orders takes 24 to 48 hours after injection of tablets hyperinsulinemic eugliasmic therapy is supportive in management of refractory shock thank you thank you dr manoj a very interesting case uh just one question here yeah yeah this patient did he have a hypotension as part of the presentation actually uh symptoms uh amlodipine intake was take uh here he was taken i'm looking on 18th jan he came to our hospital on 21st june uh previously he was consulted in nearby clinic where they have documented there was bp was around 160 and there were symptoms such as generalized iron myalgia holly guria he might have a hypotension which was corrected with iv crystallites in other hospital they might have transfused iv crystallized for which uh the breathless may be aggravated then they might have referred to us uh symptoms more suggest uh suggested that uh there might be a hypotension episode but after admitting in our hospital he was he had a baseline bp around 110 60. okay and alegria was improved within 24 hours what was the treatment you gave actually uh the patient doesn't have any refractory hypotension or hyperglycemia or bradycardia so we just tried with iv diuretics broad spectrum antibiotics and steroids how many tablets your family been did you take 30 tablets uh i have a 5mg tablet totally total 150. right thank you very much yeah quite interesting case and without uh any complication or requiring dialysis he you could salvage him out isn't it yes okay around 10 to 12 uh published cases only one case i have underwent dialysis now can i have the second presentation i think is who is a doctor anjana yeah anjali she's actually presenting on an acute hearing loss what we should not miss during an acute hearing loss yeah you can carry on good evening all my name is dr anjana i'm a dmv resident from luth hospital so today i'll be pressing a case of acute hearing loss so my patient is a 53 years old male he is a electrical appliances shop owner he's and past history he's a known casey systemic hypertension on anti-hypertensives for the last four years complaints he presented to us with complaints of fullness and heaviness of head since 10th of february 2022 and this is uh five days before presenting to us and it was non-localizable there was no said photophobia or homophobia or loss of consciousness and along with that he also started having complaints of ringing sound on the left ear which was roaring in time it was constantly present and it was disturbing his sleep the next day morning he noticed that he also had an illustrated hearing loss it was near total hearing loss it was suddenly nonsense and it was not progressing and he had difficulty in identifying the source of sound the next day after that he noticed that he has numbness of left side of the face and what he goes and saying towards the left side while he was walking and he had difficulty in pursuing hot and cold water while he was washing face then he also noticed deviation of angular moves towards right side and a foreign body sensation of the left side uh it was suddenly onset and non-progressive and this relative said that there was decreased link rate of the left eye and uh he kept frequently rubbing his left eye because of body sensation there was deviation of angle of mouth while speaking and associated with the difficulty chewing of foot on the left side and slurring the speech of saliva on the left side now there was no history suggesting of weakness of any other limbs no history of trauma or seizures or loss of consciousness so based upon this history uh since he has a unilateral left side and hearing loss along with the tinnitus uh he probably has an involvement of the left side eighth nerve or the left side left hand there is uh numbness of the face and there is difficulty chewing food so that's a sensory motor involvement of the left fifth knob and he also has an element type of facial nerve calcium on the left side and he also has swaying towards the left side while walking so it would be involvement of the left side and cerebellum or its connections on examination we noted that he was conscious oriented cooperative and obeying commands weight is 82 kilogram height is 180 centimeters bmi 25.3 vitals were stable memory recent remote memory was normal speech splattering speech was noted but he had a normal comprehension fluency repetition reading and writing on examination pregnancy 1 2 3 4 6 9 10 11 and 12 the bilateral normal examination of trigeminal nerve we noted that there was reduced touch pain and temperature sensations in the central portion of the left side of face in all the three division of asparagus muscles of mastication were normal bilaterally but the spatula test revealed a decreased impression of the white mark on the left side which means a subtle weakness of the left side of muscles of mastication carnal impenetrables were absent on the left side and normal on the right side the jaw jack was normal facial nerve examination deviation of anglophone towards the right side on smiling and frontalis orbicularis oculi vaccinator orbicularis and platysma was weak on the left side day sensation of the anterior two-thirds of them was impaired and sure must haves revealed an impaired tear production in the left eye vestibular cochlear nerve there is hearing loss in the left ear venus test revealed an air conduction better than both conditions webbers showed lateralization towards the left right side and abc test was normal under its rights and absolutely examination uh the rest of the sensory motor system examination was normal over the trunk and the limbs the superficial reflexes except for the coronal and conjunctival reflex where normal bilaterally and planetary was also bilateral cerebellar functions were normally bilaterally eight ataxia was present he had a tendency towards uh to fall towards the left side tandem walking and robustness could not be performed there were no signs of men's irritation after examination uh he has sensory and motor involvement of the trigeminal nerve and the corneal conjunctival reflex was also absent so there is an interaction involving the nucleus of the trigeminal nerve he also had water impairment and impairment of day sensations and lacrimation on the left side of things so there is also nuclear lesion of the left facial now and there is hearing loss ah there is evidence so there is an extracurricular involvement of the left leg because function tests were normal and speech was also normal exercising so probably his attack say was due to the involvement of left circle of predominance there is nothing to suggest involvement of the surveillance test so based on all these structures involved the possibility only is considered where since he had an acute onset of hearing loss and acute answer to all these symptoms the first cause was a vascular cause it's a vascular accident and we considered a nico syndrome because anti-inflammatory cerebral artery supplies the cerebellum ponds and the middle circle which can explain all the symptoms then since his fifth seventh and eighth graders were involved we cannot rule out a cp angulation and although cp angle tumors usually have a chronic subjective presentation in around 10 to 20 percentage of cases uh if the tumor itself is compressing the abdomen artery causing ischemia then the patient can have an active presentation so that was the second dd that was considered and also we consider multiple sclerosis the first presentation of the plaque over the lower bonds and seriously and analysis he was admitted with the above mentioned complaints and uh evaluated the routine blood investigations all came out to be normal renal and liver functions were all normal and uh we did appear out on audiometry which revealed a left side of mixed hearing loss with a predominant sensory neural component and uh the two etiologies which we considered were icar syndrome and the angulation so mri brain was done it showed an area of diffusion restriction and clear high signification involving the left inferior circuit and the entries so that can explain all the symptoms with the patient and this is the territory which is supplied by android inferior cerebral artery so this is a normal anti-inflammatory cerebral artery tertiary and this is a mri brain of the patient showing an infect an area of depression restriction in the area which is supplied by anti-infinity surveillance suppose he was managed as a case of stroke with antibiotics and statins at discharge he improved there was no attacks here he was able to walk without support hearing loss was persisting but improving numbness and the facial weakness were also included so aika syndrome uh so anterior inferior cerval artery supplies it also has responsibilities and uh the recently several studies have been published based on hyper syndrome that acute auditory symptoms are usually seen as a prodromal features in patients having high customers they usually present with symptoms of tinnitus or hearing loss around one to ten days before the actual event our patient also developed hearing loss three days before he developed symptoms of seventh and fifth nerve involvement and causes anterior circle and lateral inferior quantity that is in function and this is a branches of uh the aika gives out the internal auditory branch internal auditory artery which then supplies the former cochlea as well as the labyrinthine apparatus there is no collateral circulation in this system so whenever the uh operation occurs the patient will develop hearing loss or interest and the take home message that i want to convey from this presentation is that whenever a patient presents with unilateral hearing loss we tend to search for peripheral causes like labyrinthitis or something like that but we should always keep in mind that a central cause like a stroke is also a possibility in a patient with persistent hearing loss and uh especially in uh in a case like syndrome the patient the hearing loss may be the first presenting symptom before the patient virus so always be on the lookout for such causes and uh do mri or imaging as soon as possible and thrombolyze the patient if necessary before the patient develops a full register thank you thank you dr angela thank you very much for an excellent presentation basically and uh yeah and this is the anti-cerebral this stroke is not very common it's an unusual stroke so i think it's very good that you picked up the soft neurological science because that's where the problem is i think in a pcopd when you have a accuses you know you have the tendency to refer straight to the ent and get an audiogram done so i think you had very soft science and you picked up the soft science and that was i think the main thing because in neurology the basic things that localized solution if you can't localize the anatomical localization is not there then you won't know where we are going so i think you got that early and a very rare uh kind of thrombus uh location as compared to pica and many other things you know so that is very good the way you did it i just wanted a couple of queries you know did the vision have we know of what risk factors in terms of you know uh diabetes hypertension cholesterolemia carotis stenosis uh any valvular lesions uh there was 30 or anything like that no price thank you that's good anybody in the audience have any questions please you can ask has message did he again regain hearing uh the patience hearing loss was improving when he got admitted he was not at all able to hear anything on the left side he was not able to localize the sound but when we discharged him his hearing loss was improving but he hasn't regained the complete hearing he still in the follow-up i think he'll improve he's a non-alcoholic thank i think the internal acoustic artery is a hind artery so i think hearing improvement chances are not very high you know within the first two days itself he was improving he had a near total hearing loss so we are expecting maybe he will regain 60 30 to 60 percentage of this hearing okay all right somebody yeah very nice case actually is a very important artery for us neurosurgeons also for many reasons one of it of course we should not miss an acute impact but other thing is uh off late we have seen cases where patient comes with intractable tinnitus due to the icar impinging on the earth yeah and though this has been tried to be managed medically for when i started my career in neuroscience but of late we have seen cases where you know you can treat it completely by micro vascular decompression so these patients also have troublesome tinnitus and later on they go into this impact also due to the inking of the artery itself so just wanted to put across this information to all that intractable tinnitus always try to begin a conflict there and off late we have found recently that it is recovering with the microvascular decompression yeah thanks good thank you dr supreme yeah thanks for your comments anybody else in any comments so or we can go to the next speaker okay thank you dr angina the next one is dr ranjit from matthew he's a junior consultant orthopedics and he'll be presenting a very common endless in an unusual way swelling of the bone of many months yeah doctor anthony please yeah uh good evening everyone um my name is dr ranjit uh i'm working as a junior consultant in hospital uh the topic for my presentation today is an unusual selling in a nine month old so this testicle was however normal and the subcutaneous tissues were normal there was no evidence of any calcification and the rest of the soft tissues were also normal so certain differential diagnosis were offered by the radiologist in the form of a fibrous cortical defect or a non-ossified fibroma which are basically benign tumors of the bone so then an mri was suggested by the radiologist so we went ahead to do an mri so on the mri uh an exophytic soft tissue mass firstly scene which is approximately measuring 1.8 into 1.4 centimeters there was an evidence of break in the cortex the inner table of the cortical bone is scalloped and there was a there was some soft tissue involvement as well there was no problems in the the capsule and the synovium the surrounding tendons were grossly normal and the rest of the visualized bones were normal so the diagnosis given by the radiologist was an osteochondroma so still we were not satisfied uh the diagnosis which we actually had in our mind versus some sort of a pyogenic osteomyelitis or a subacute osteomyelitis so we we proceeded to get the blood investigations done and uh the blood investigations i'm sorry uh you could if you can't make out it was largely unremarkable the only things which are elevated was there was mild elevation of the total count which is around in the range of 15 000 and crp was elevated 8.6 and the esr was mildly elevated so uh so thinking that it might be a sub acute osteomyelitis we proceeded with an open biopsy and then intraoperatively we saw an organized collection of soft tissue and bony fragments which were seen over the andromedal aspect to the right proximal tibia but there was no growth plate involvement this was confirmed on the cm images and then we rooted out the whole thing and we sent out the specimens for bacteriological studies and for histopathological examination and then two a slab was given just for protection sake and uh to our surprise actually the histopathology came as necrotizing granulomas which is suggestive of tb so the culture was also negative uh there was no acid fast bacilli which is seen on microscopic uh tb pcr was however uh negative uh tb pcr was positive that's how we made the diagnosis uh on the uh if you see you can see the histopathology there were lots of epithelial cells uh stencils and foreign body giant cells with gaseous granulomas so the diagnosis was made as tuberculos osteomyelitis so then we did a pediatric consultation and the patient was started on an att in the form of two months uh contin intensive therapy with inh rifam person uh pyrocidemide and a temple troll and seven months he was given hre and then after consultation was given every two weeks to rule out any presence of retrobulbar neuritis and we did an lft every month okay and uh the family members were here given a screening a screening mantle was done it turned out that the the maid in the child's house had a positive mantra so this was the immediate post-op x-ray you can see that the lesion has been well curated out and a drain has been placed in situ a posterior slab has been just applied for just for protection sake and then this is the x-ray at four months you can see that the lesion has almost completely resolved you can see that the callus has formed in the region of the soft tissue on the soft tissue as well as the bony defect and this is the child that almost one year follow you can see that the child has near normal function and his range of movement is complete is full there is a key lord in the region of this car and the child is happy so this is actually a very very rare case so we have searched the literature and we could find only uh one another case which was uh reported in the turkish journal of orthopedics in which a tuberculosis osteomaltis of the distal tibia was seen in a 20 in a 22 year old sorry a 10 month old uh infant in which uh they did a similar management was done where uh keratin biopsy and debridement was done and the child was given on prolonged att and there was no relapse in a five-year young children thank you thank you dr yeah i think in india typical of this can present in any way basically there is no end to the way tuberculosis can present and uh very good and it's good that he picked it up and his pathology is extremely suggestive and by confirmatory of tuberculosis it has all the classical paintings that you will get into there is no way that you can get past how we separation have we completed the treatment now because uh now actually he has been lost he has completed the treatment uh he this patient actually presented in 2018 uh so we had him on follow-up for almost uh two years he last uh visited our rpd in 2020 but after that he has been lost to follow so the limitation of this study is that we we don't have any long-term follow-up and we have to follow him up for a long time to see that he has any if he is if the tv has any effect on his growth uh yeah okay i think everybody seems to be satisfied thank you very much we'll go to the next speaker she is in pursuit of the cause of recurrent weakness and uh what we shouldn't miss she is a dmv in general medicine hospital yeah so tell us good evening so today i'm going to present a case on recurrent paralysis so uh present in the case of a 39 year old female with no history of any prior commodities who is apparently normal three days prior to the admission where at night she observed a sudden dull aching diffuse pain on her upper limbs followed by her lower limbs following which she developed an overnight weakness of all her forelimbs so for brevity's sake this weakness was acute in onset proximal followed by distal rapidly progressively symmetrical and having no association with any activity level so there was no history of any sensory symptoms similar episodes in the past history of a strenuous exercise a high carbohydrate diet race and vaccination or autonomic symptoms or any other sensory symptoms there is no hysteresis of autoimmune disorders for fairy wilson's disease toxin intake vascular disorder and there is no significant past or a family history and when the patient reported she was hemodynamically stable fully conscious oriented and cooperative there were no significant signs on general examination the vitals were stable respect rate was around 16 but when its saturation was maintained the single breakdown was under 32. then on further neurological examination uh there was a normal bulk equal and comparable on both sides however there was a hypertony of all her four limbs then the power was around two by five proximally on both her upper limbs and lower limb symmetrically with a power of around three by five digitally symmetrically on both her upper limbs and the lower limbs and when it comes to the reflexes the all the superficial reflexes were preserved except for the plantar which was mute and for the deep tendon reflexes jojo was absent the biceps were absent then knee jerk and angle jet were also absent whereas the triceps and supinator were significantly reduced so uh sensory systems where normal cerebellar science and other systems are also found to be normal um so in view of an acute plastic quadriparasis she was immediately admitted in isu routine blood investigations were done ecg was also taken so among the routine blood investigations only abnormality was snorted in the levels of serum potassium which was around 2.8 and after an acg was also taken an ecg showed a normal sinus rhythm with flattening of key waves and presence of uavs with a normal qt interval then um so uh in this current picture the primary possibilities of a gbs versus a hyperkalemic periodic paralysis was considered then the patient was initiated on potassium correction and as the correction was ongoing the patient suddenly developed this uh bradycardia and the patient suddenly decelerated to around 20 uh heart rates per minute and she developed a cinco foreign language she was revived with and the heart rate revived around 90s so repeat ecg was taken showed no dynamic changes and the topic values were also negative so the patient was reassessed in this current clinical scenario and we noted that her single breath count was reduced at around 14 which was prior 32 so in view of a sudden autonomic instability in the background of absent reflexes and no prior episodes of paralysis uh which were noted to be very confounding elements from the ecological perspective and hyperkalemic periodic analysis and gbs was considered to be the most likeliest of possibility so uh we did an interior on a priority basis on the day of admission itself and showed and it showed an accidental motor polyneuropathy involving both her upper and lower limbs with reduced component selection potential a cs of study was also done it showed an albumin of cytological dissociation surprisingly the two cells and the proteins of around 75. so gbs was confirmed the patient was started on ivig she became symptomatically better and we researched the patient after a period of five days so uh no the readmission the patient again got readmitted on 12th of age 2021 with painful quadriplegics very similar to the uh the previous picture there was pain on both her lower limbs associated with vomiting and weakness of all four limbs uh so again uh we did the routine blood investigations but this time the seven potential was even much lower it was around 2.1 so the potassium correction was initiated via the eye central and avg was also taken it showed a metabolic acidosis ph of 7.2 a pco2 of 23 and bicarbonate of 210.9 so the serum and gap was normal the urine ph was seven and we calculate the trans tubular potassium grain which is also found to be very high so uh calculating everything there was a normal anion gave metabolic estosis there was a decreased serum potassium levels the urine ph was seven the euro nano gap was positive in the setting of an increased transportation gradient we diagnosed it with distal renal tubular acidosis so there are several causes for the digital renal tubular stress as i haven't mentioned in the slide so as part of comprehensive workup answer the studies were completed the thyroid profile was sent and it showed serum clears up to 0.005 with elevated free treatment temple levels suggesting hyperthyroidism so the patient was started on new microsoft imgtad with beta blockers a usb abdomen was done it showed a nephrocalcinosis then the geological workup or distilled integrable resources were also done that is usually in case of adults it is the autoimmune disorders the connective tissue disorders which are often the reason for distilled renal tubular responses we did an ana by a fan zero angela everything was negative this around primary intact ph levels are also normal so finally we made the diagnosis of hyperkinemic periodic paralysis is secondary to a distal renal tubular acidosis precipitated by hyperthyroidism so uh she was managed with an iv cell correction acidosis was corrected she was advised to have a low carbohydrate meal low salt intake and to avoid vitamin d supplementation and the hypothyroidism was also corrected so what i mean to say uh the take-home message is that there are reversible electrophysiological abnormalities which can be encountered during hyperkalemic periodic paralysis itself so these abnormalities especially with reduced c maps that usually occur with normalization of serum potassium levels and muscle strain can be confusing often at the initial presentation or the first attack and may lead to misdiagnosis such as the ammo and variant of gbs so we suggest a simple exercise test that this time the exercise rate should be at least 15 minutes long so stifling so this particular exercise should be done in all patients where we suspect an aman variant of gbs so um in patients with hypokalemic periodic paralysis normally there is an increase in the c-maps in the immediate two to four minutes after the exercise but if you continue that exercise period for around 15 minutes we will notice that there is a significant discrimination so this particular thing does not happen in case of amman variant of gbs so secondly i would like to say the serum potassium level may not always be helpful for diagnosis because attacks attacks can occur without significant hypokalemia in this particular patient initially the ceramic potassium was around 2.8 with the uh serum potassium around 2.8 itself the patient developed the brady as well as the respiratory paralysis so serum potassium levels cannot be significantly taken in countless how low it is or how high it is doesn't really matter so the third one is an album a cyclological dissociation is often of course there have been several reports reported uh then in a hyperkalemic periodic paralysis and we get an albino cytological dissociation so that can that particular thing cannot be concluded for a gps so that's what i would like to say thank you hello sir okay thank you thank you anju thank you very much for your presentation basically i think the first uh the first presentation looks almost like a classical gps if you ask me anybody would diagnose it as a gps and it has an acura ascending uh probably radical neuropathy like presentation and went into eventually failure and i think there were supportive evidences also too in terms of alphanumeric psychology dissociation and electrophysiological studies so i think without a history of definite precipitation with exercise like you mentioned exercise should be done or excessive carbohydrate meal uh or without a history of any prior episodes i think anybody would come to a diagnosis of you know guillain-barre syndrome to start with basically and i think what made us think in this case is when the second attack came because when the second attack came the scenario was a little different and that is when we thought yeah it is one thing you should always keep in mind when you present with an accurate flaccid cardiopyrasis sometimes the history is not very conclusive but you should always think that it could be first attack or even a missed attack of periodic paralysis and carbohydrate meals and exercise are good but in some cases of you know gps they may be ascending in that phase i don't know how much exercise can be undertaken you know it may be slightly risky if there is an ongoing rapid as an ascending order radically on your property which will you know affect the respiratory muscles and go into ventilation and all that but it is one thing that you have to keep in mind hyperkalemia also like you mentioned is very tricky sometimes you know because it's a cation intracellular so you may kind of under diagnose it and some of the borderline things may not be actually underlined but you tried it all up in the second presentation you know when everything came together and you came to the right conclusion basically and second is the incidence of thyrotoxicosis with periodic paralysis paradoxes per se can produce a periodic paralysis what about the what is the percentage that you have of paratoxicosis and hyperkalemic hypokalemic periodic paralysis any incidents that you have no sir actually i don't have the number of cases with me but i separated several case reports that i have seen it is particularly mentioned that the mechanism responsible for a thyrotoxic periodic pelvis per se may not be the thyroid toxicosis that is the patient may have other reasons for a periodic paralysis which could be precipitated by the thyrotoxicosis only so it is just a a potassium channel defect but whenever we see a case of a periodic paralysis particularly after the age of 25 years uh in a particularly agenda of female then we should always suspect aerotoxicosis because the primary hypokalemia period paralysis will not usually present after the age of 25 years so after the age of 25s i think the incidence of thyroid toxic purity balance is going to be a bit more higher i don't have to accept reports with me sir and i think a correction of hyperthyroidism itself will take care of the metabolic optimization exactly exactly it's good very good and nephrocalcinosis actually is quite it's quite it's associated with this so i there are lots of cases any diseases that could cause nephrocalcinosis can cause a distilled renal tuberculosis and distillery neutral absolutists itself can cause nafta calcium so that's why you did a primary intact ph which came out to be normal yeah and you rightly said that you know vasculitis is an important cause you know and so because some of these could yeah yes very aggressive forms of escalating neuropathy can present exactly like gbsr yeah any drugs in your drug history that you um actually barium is one element which is responsible for a secondary hyperkalemic priority paralysis besides this uh an acute placid quadruperaceous can be precipitated by many heavy metal poisonings but none of which are present in our patients [Music] yeah the floor is open anybody wants to ask any questions very interesting case thyroid toxic causes periodic paralysis gbs like presentation and normally you get hyperkalemia you know with acidosis and whenever you get hyperkalemia you should suspect an rpa yeah i think we know yes it's very very often they they crop up later on they get a big diagnosis of autoimmune disorders most often these patients turn out to have some kind of an autoimmune disorder either necessarily or or a basic syndrome or a sugar and syndrome as they progress but this presentation is very typical in the sense he she had recurrent episodes of acute onset of weakness flaccid weakness and preceded by a high carbohydrate intake or an exertion so the history was typical but then it was painful to start with that was what confused everything and he had some kind of an autonomic neuropathy aspect so initial the initial presentation we were actually in a dilemma whether it was really a periodic paralysis or a or an acute flaccid paradigm or an acute fascicular is due to gps so the initial presentation was more like a gbs and subsequently the present with the presentation became clear we did an acid load test as well on this patient to find out if the acid secretion is normal by the kidneys and it was found to be defective [Music] thank you dr bin everybody's satisfied so we'll go to your next speaker thank you very much doctor we have dr tino alby who is a consultant the ent surgeon in luth hospital and he is going to tell us about taking part less travel we have an ent surgeon who's taking a traveling path dr tenu please thank you thank you sir hi good evening all right my name is dr tinu alvey i am here to present an interesting case in the department of ent hospital this is about taking the path less traveled i have chosen this title because it is about an unusual surgery which is not commonly done and the path is to the most difficult science to tackle surgical management of frontal sinus is considered to be the most difficult and challenging when it comes to endoscopic sinus surgery chronic frontal sinusitis is the most difficult sinusitis to manage both medically and surgically despite of having many advancements in endoscopic sinus surgery the wide variety of surgical options speaks to the difficult nature of managing disease in this location why it is difficult to manage frontal sinus what is so special about frontal sinus first of all its proximity to the orbit and skull base and at most care should be taken while managing disease in the frontal sinus region surgically if you go at least one to four millimeter posteriorly you will inadvertently end up in the skull base if you go laterally you will end up you know definitely end up in the orbit and second thing is the narrow opening of the frontal sinus and it is bounded all around by bone it is bounded by the anterior the mud cells and thick bond which is known as the frontal beak the frontal sinus has great anatomical volumetric and dimensional variability what does it mean the frontal sinus can reach in enormous proportions it can reach up to the zygomatic bond it can reach up to the supraorbital area and it can even reach up to the parietal bone usually in case of frontal sinusitis simply clearing the disease around the frontal races or simply removing the pro-inflammatory cells the polyps and deceased mucosa and bone should be enough but in case of extensive disease in case of tumors in case of extensive uh diseases such as mucosal extensive more bone resection is required mucosal is formed when there is accumulation of mucus within a confined space when these mucus get infected it is called piocele they tend to form when the frontal resource is obstructed over a period of time if left untreated it can expand and cause bone erosion and it can cause displacement of the surrounding structures including the orbital anterior cranial fossa in 1991 wolfgang draft published a graduated approach to the sinus frontal sinus surgery they are called draft procedures draft one is essentially just an ethmoidectomy without any manipulation of the frontal bases like i said it is a graduated approach so draft2a is more resection of the bond that is without again without removing any frontal sinus mucus or without disturbing the frontal sinus opening that all the ethmoid cells are removed draft ub and roughly procedure they extend the surgical resection beyond the frontal bases in draft 3 procedure we connect both the frontal sinuses and make it into one big cavity coming to the details of our case a 50 year old female with no comorbidities presented with chronic sinusitis type of symptoms such as nose block nasal discharge headache and she also had closing of the right eye which has been progressive since last two to three months nasal and oral cavity examination was essentially normal there was right titosis can you play the video the ct scan of the patient shows there is extensive mucosal thickening in bilateral frontal sinuses can you pause the video there is a mucosal there is a erosion of the right orbital orbital roof which shows solution coming into the orbit from the frontal sinus floor and there is also mucosal thickening in bilateral frontal sinuses bilateral angioethamoids posterior the merge and bilateral maxillary sinus sinuses the lesion is pushing the orbit inferior laterally let's continue and mri scan of the same patient shows t1 hyperindust2 hyperintense lesion in on the right orbital group which is again pushing the orbit inferior laterally and as you can see the solution is situated very laterally so it is impossible to manage this disease with the normal with the usual endoscopic sinus surgery steps let's continue so we had to do a draft three procedure that is opening both the frontal sinuses making it into one cavity and opening that cavity into the nasal cavity so the uh this extend of the resection will be from one eye to the other eye that is the skin of the side of the nose from one side to the other side of other side skin along with the septoplasty and functional endoscopic sinus surgery under gel anesthesia what you're seeing is the right nasal cavity please play the video what you're seeing is the right nasal cavity and we are making a window on the nasal septum adjacent to the frontal sinus please pause the video body and that circled area show the extent of the resection that is from one side eye to the other side of the eye and we are removing that septal area just below the frontal beak because the circled area let's continue this is the drilling of the frontal big now the frontal big is a very thick bond so we require special drills to open this frontal beak that is the floor of the frontal sinus to enter into the frontal sinus that indicates the anterior extent of the dissection that is the uh what you're palpating is the skin of the globular and you can see the allotment over there and after opening after drilling the frontal beak we are entering the frontal sinus on that side and you can see the bus coming out from the frontal sinus and we are widening that opening and we have widened the frontal sinus on right side and we can see that this is mucosa this is teditus mucosa now like i said if you go a millimeter laterally you'll inadvertently end up in the orbit and if you go millimeter posteriorly you will be in the skull base we have widened the opening on the right side of the frontal sinus and you can see the bus coming out from there and we have made right and left frontal sinus into one big cavity and it is opening nicely into the nasal cavity and on the left hand side you can see that is the floor of the frontal sinus on the right side that is the defect which is uh causing the mucosal to push into the right orbit and while palpating the eyeball we can see the movements in the frontal lashes frontal sinus and after removing the mucosal completely we have placed a free graft which was harvested from the nasal septal mucosa and from the middle turbinate and on the graph there was place to search the cell and on the surgical cell we applied the tissue seal and there was a single silastic sheet graph this elastic sheet which was cut into t shape was placed on the graph to fix the graft and a nasal packing or spray first operatively the needle that was removed after 24 hours this silicon stent or this elastic sheet was removed after two weeks we are given the patient antibiotics regular nasal wash containing steroids and systemic steroids and anti-allergic medications and spray was given post-operatively we can see that the nice big cavity has formed please by the video that is the common cavity which is which is connecting the right and left frontal sinus and it is opening nicely into the nasal cavity and it is now disease free and the mucosa has formed nicely the epithelium epithelialization has occurred [Music] and here you can see the difference that on the uh left hand side that is the pre-operative image you can see the tosses of the right eye and on the right hand upper image you can see the process has improved dramatically and the lower image shows the common cavity connecting both the frontal sinuses and which is opening nicely into the nasal cavity we would like to thank dr njit peter for his guidance and support at this point thank you thank you dr tino for an excellent presentation and uh that everybody any ent sergeant or anybody who knows or who wants to know any doubts or comments on the procedure does this have any complications these kind of procedures any long term any complications for the procedure that you anticipate short term long term intraoperative complications can occur such as like i said if you go the skull base is situated around one to four millimeter uh posterior direction so if you go if you drill too much posteriorly just about one to four millimeter you will inadvertently end up in the skull base and you can cause a csf rhino area and uh just just before entering the uh skull base you will be inadvertently injuring the anterior thermometer which can cause profuse bleeding and it can uh the anti-automotive artery once it is injured it will reflect into the orbit and it can cause orbital hematoma orbital hemorrhage and it can cause a loss of vision and yeah these are the main interrupt complications post-operatively the epithelial session has occurred nicely and it has become a one big cavity so even post-operative access by endoscopic uh regular endoscopic cleaning and nasal wash there should not be an issue post operatively in long term [Music] so it improves the access in future problems yes yeah dr ramsengersin has asked sir dns slash all mucosal sinuses is the management no in chronic rhinos chronic rhino sinusitis a regular functional endoscopic sinus surgery is the management but this is uh different because the mucosal or the rather the piocele was situated too laterally on the right hand side if you remember ct scan and mri scan it was situated too laterally to access through a regular steps of the functional endoscopic sinus surgery hence we needed extensive drill out and both the frontal sinuses were involved there was mucosal changes mucosal edema and mucosal enhancement in mri scan in both the frontal sinuses hence we had to clear the disease from both the frontal sinuses hence this common cavity was created and connecting both the frontal sinuses and opens into the nasal cavity nerve injury possible what is the prognosis uh optic nerve injury is very unlikely because we are not going into that direction we are confined confining our resection into the frontal sinus region optic never comes much uh posteriorly actually when you try to open the sphenoid sinus and draw extensive resection in the sphenoid sinus then the optic nerve can get injured here the posterior limit of the resection is the first olfactory nerve when you raise the mucosa and see the first olfactory fibers that is the limit of the posterior extension optic nerve comes much posteriorly okay i think uh if you have no more questions thank you dr pino for an excellent presentation and highlighting an area it's not my area of speciality so i don't know much about it so thank you very much thank you thank you um i would like to thank lord hospital for organizing this and inviting me to share this session and it is always nice to associate with a sister institution he had some excellent speakers and what stood out was you know that you shouldn't wish what we should miss i think that was a message in this entire presentation that what we shouldn't miss because most of these things they come up you know as very ordinary things you know just just some weakness there or recurrent weakness there and little things which turn out to be something that you don't know so that's the lesson that i got from this and i hope all the trainees and other doctors thank you very much for attending this function thank you so much dr george uh doctor apparently to come on stage and moderating the session and thank you for attending the session

BEING ATTENDED BY

Dr. Murtuza Zozwala & 229 others

SPEAKERS

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dr. Anjana Sankar

Dr. Anjana Sankar

DNB Resident

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dr. Ramesh Shenoy

Dr. Ramesh Shenoy

Consultant Radiologist | Kochi

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dr. Renjit  John Mathew

Dr. Renjit John Mathew

Junior Consultant

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dr. Anju P A

Dr. Anju P A

DNB Resident

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dr. Tinu Alby

Dr. Tinu Alby

Junior Consultant

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dr. Anjana Sankar

Dr. Anjana Sankar

DNB Resident

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dr. Ramesh Shenoy

Dr. Ramesh Shenoy

Consultant Radiologist | Kochi

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dr. Renjit  John Mathew

Dr. Renjit John Mathew

Junior Consultant

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dr. Anju P A

Dr. Anju P A

DNB Resident

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dr. Tinu Alby

Dr. Tinu Alby

Junior Consultant

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