This clinical case presentation demonstrates a systematic approach to diagnosing and managing portal hypertension with splenomegaly, emphasizing thorough history-taking to differentiate between extrahepatic portal vein obstruction (EHPVO) and non-cirrhotic portal fibrosis (NCPF), with key diagnostic features including age of presentation (younger for EHPVO, older for NCPF), spleen size (moderate for EHPVO, massive for NCPF), and portal vein obstruction level (first-order for EHPVO, second-order for NCPF). The session highlights the importance of complete blood count with peripheral smear to identify hypersplenism, ultrasound with color Doppler for portal vein assessment, and upper GI endoscopy for variceal evaluation, while management ranges from conservative observation in asymptomatic patients to splenectomy for symptomatic hypersplenism and shunt surgery for refractory cases.
PG CLINICS PORTAL HYPERTENSION CARCINOMA GALL BLADDERAdded:
Ma'am good evening.
>> Good evening Dr. K.
>> Ma'am we'll start in a minute ma'am.
>> Yeah. What is the format like?
>> Uh ma'am it is an hour long case. We have two cases. The first case I have kept is portal hypertension uh with the case of spenomaggali. The second one is the caroma gallbladder.
Usually the candidate runs through the history without stopping. At the end they sum the history. So we revisit slide by slide and ask questions or give comments or whatever. If they missed out on something you can address. Same thing clinical part they run through until the end. They arrive at a summary of the clinical findings. Then they give a working diagnosis. This gets over in half an hour time. Then we have full half hour on evaluation, medical management, surgical management, endotherapy and if there are any newer advances candidate should know. This is a teaching format ma'am. So basically if the candidate finds or not is able to answer to your expectation I request the faculty to kindly give the answers what they expect ma'am. So that is the way we have the case.
>> Two twoour session two hours.
>> Yes ma'am. Yes ma'am. each case one hour.
So, Professor Kit Palmer, warm welcome.
Um friends, uh without much ado, it's 8:00. Uh >> good evening. So, this is our uh weekly Friday clinical session. Today, this is the 336th session and this is the 617th and 18th case we are discussing today.
Today is a exclusive habitable program and uh we have a very eminent faculty who has joined us and uh of the lead will be very senior most art teacher professor Jim Man uh she has served as the head of the department at multiple places brilliant student from Christian medical college Balor and right now she is faculty at the global hospitals at Chennai. We have professor Johnson Maria Anthony head of the department of the surgical gastroenterology from government medical college Salem.
Professor Amit Gupta again head of the HPB section of the general surgery department under the general surgery. He is from Ald institute of medical sciences. Rishih again professor R. Khalasan uh is a eminent surgical gastroenterologist and robotic surgeon from Jipma. right now she is part of the academical unit of the Apollo hospitals uh at Chennai. We have professor Wenger Ramari uh again Hod from Shri Weneshwara Institute of Medical Sciences Thurupati who will be joining us shortly. Professor Barat Nara should be joining us shortly. I also take this opportunity to thank professor Simma Kanam, head of the unit at IMSBHU Varnasi and Professor Amit Gupta for kindly permitting their students to present a case here. We also thank the respective HOD's professor Satyanam Khya from IMS BHU Vasi and professor Somra Bashu from Ames Rishi case for permitting their students to be part of it and we have our own eminent faculty uh joining us professor Kirit Palmer Professor Ti Shinimasan and I expect others to join us shortly. So without much ado we'll have the first presentation uh can we have the Dr. Mascan Dugar he she is a postgraduate resident from IMSBHU Varnasi to introduce herself her unit faculty and HOD and start your presentation. Good luck to you doctor. I request all the others in the group to be in silent mode except for the student and the faculty. Should you wish to ask questions please use the chat box.
Welcome Dr. Barat Nara. Barat is from Apollo Hydrobat. She heads the hepidelerian transplant unit from Apollo uh hydroat. Thank you sir. M stage is yours. Faculty please take over make it full screen. M >> good evening everyone.
>> Good luck to you. You're perfect ma'am.
Good luck.
>> Uh good evening everyone. I am Dr. from there are three general surgery from uh IMSPHU and uh I'm presenting a clinical case under the moderation of professor simma kaman under the department of general surgery IMSU I'm presenting a case of a 32-year-old homemaker resident of John for Uttar Pradesh presented to surgery op lump in left upper abdomen for 20 years and a single episode of hematimis 20 days back lump Lump in the left upper abdomen was for 20 years which was serious and also gradually progressed to the correct size. Lump was initially confined to the left upper quadrant and has progressively increased in size to extend up to the umbilical region. It was associated with abdominal discomfort intermittently.
She also has a complaint of single episode of hematimis 20 days back. It was scanty in amount coffee ground non projectile not mixed with food particles not associated with pain or nausea relieved with oral medication from a local hospital. There was a similar episode 20 years ago which was released after she was admitted in a local hospital and took oral medications for four to 5 years. No documentation of this admission was available.
There is no history of fever, chills or diarrhea, abdominal pain, abdominal distension or abdominal trauma, malina or bleeding by rectum, altered sensorium, yellowish discoloration of eyes and immaturia or disordia and early satiety or weight loss.
history of hospitalization for similar complaint 20 years back was and was started on oral medication which continued for four to five years then stopped abruptly with no documentation.
She also has a past history of one unit of blood transfusion which was done 20 years ago. No documentation of the same is available with us. There is no history of any surgical intervention in the past and there is no history of any known coorbidities.
There is no uh similar history in other family members and her menstrual cycle is of 28 days which is regular and her last menstrual period was on 4th of May.
She is a par to life to par and both of the children were born by normal vaginal delivery and the younger child is of 20 years 12 years of age.
She takes a mixed diet with a normal bubble and bladder habit. uh she has a normal sleep pattern and has no free of alcohol intake or substance abuse. There is no known allergies and no birth histories available with us. Summarizing the case, a 32 year old senior with complaint of gradually progressive painless lump in the left upper abdomen for 20 years associated with single episode of hematimis 20 days back with a history of similar episode 20 years ago and one unit of blood transfusion 20 years back.
So should I um I just ask here. So so apparently the ch patient has been unwell since the age of 12, right?
>> Yes sir. Yes ma'am.
>> Yeah. So that's that's so the history is at the age of 12 she's noticed some lump mass whatever she's had and she's had a bleed then right?
So I just want to know so what is the educational status like?
>> Ma'am I have not formally tested the uh educational status or the economic uh econo economic status of the patient but she was she belonged to a ruler rural area.
>> No she she's been investigated or she's not been investigated at all from 12 years of age.
>> No sir no ma'am she has not been investigated at all. She came to us as a index case. Yeah, she was >> even even during pregnancy she was not investigated. Is it?
>> No. She was >> not possible. So I think somewhere there's a missing link in the history because someone would have picked up this clean which is about almost touching the umbilicus.
Right.
>> So it's not possible that the obstitrician and gynecologist who whoever seen the patient at that time during the first pregnancy would have told her that she has a liver problem and would require an evaluation. So my the thing is otherwise she becomes and it's not a single episode there are two episodes of bleed you have to describe the bleed to a larger extent to know how severe was the bleed was it related to NSA was it a pepicul bleed is it a vicial bleed how would you know that from the history can you differentiate >> I say I say that she's got a spleen which is incidental but the bleed is not u of splenic origin >> peptic bleeds are generally associated with pain and wouldn't take and uh um another point of discrimination is the recent bleeds are if it can lead also lead to massive bleed that is theory what I'm asking is what was it in this patient I just want to know in this patient what was the severity of bleed was it just bleed or was it massive bleed was it was it provocative >> it was a mild bleed and uh >> so so it's not so it's not related to a portal attention okay just a mild bleed Right >> Dr. Muscar.
>> So can you so can you can you you you have to be very clear about this. No, because this is a patient at the now we need to know that bleed whatever is the parents or if there's another person to give you a comment on the patient at the age of 12 it's fine if not then we say that we have no further information as far as that is concerned and you have to tell what was the educational status that is had what's the scholistic history has she has she been doing regular in her classes are we dealing it is it is obviously a spleen so are we dealing with a myo is it more of a a hematological issue we are dealing with or we dealing with a liberated issue. So all these things should come out from the history and it's not possible that at least during the time of pregnancy even if she remained it's not possible no like I mean huge lump right up to umbilicus going through a normal pregnancy two pregnancies normal delivery it's not it's just impossible that the doctor attending her would not have told her that she has a problem that's my okay this is my comment okay others can take over this >> was she suffering from any bleeding disorders in the young No sir, according to the historiation not available but you could have elicited the history isn't it from the relatives parents see from 12 years probably she wouldn't have but that's what madam is asking you could have elicited the history from the parents >> no nothing wrong in it which we forgot to think we telling because you're dealing with something with bleeding an ematological disorder probably we do not know what it is. So from 12 from 20 years she has been bleeding so from 12 years so young age what has she got anyotic disorders the bleeding dithesis you forgot to ask?
>> Yes.
>> Okay. Right.
You can go to Yeah. Can can this patient come to you >> sir? Please sir.
>> Yeah. Muscar, can this patient come to you with history of multiple blood transfusions? Is it feasible?
>> Uh sir, it is feasible. Uh she can come with multiple blood transfusions.
>> So the point has been raised very pertinently by Dr. Janti. She's asking a very valid question right when the spleen is so much enlarged that it is going up to the micers and how come she uh completed two pregnancies that two without much investigations right because no gynecologist or obstitrician will miss this important finding right >> yes >> and she must have been worked up proper thorough worked up perhaps smear etc and complete CBC etc. during the pregnancy itself during the antiatal visits which might have picked up some or the other cause right you asked the history of abdominal pain why you asked the history of abdominal pain >> sir uh in case there is any uh due to uh so if if uh I'm suspecting then it can be due to uh any uh if there is a sudden enlargement in the skin it can go into infection which can again lead to pain abdomen and uh hematimosis if I'm suspecting we can also say it's a peptic release which also presents the pain after >> so you want to say that because of peptic ulcer patient might be having pain with this much huge spleen >> most of but if Sir by the basis of history sir I cannot exact >> you cannot make out right >> this patient has got a massive spleen what suppose this patient had pain what do what do you think could be the causes of pain in a patient with a massive spleen >> related to the spleen >> m patient can have pisplenitis due to infaction or there can be any absess formation in the spleen and uh it can be um because of a >> what are the other possibilities? Can it be portraine thrombosis?
>> Yes.
>> Madam, she has not examined the patient.
Madam, we have not come to the examination.
>> No, no, no. Thank you, sir. I just ask >> pain in a patient with a large spleen.
One of you have asked the question, what are the cause of pain? So, it's not a ner disease pain related to the spleen.
What are the possibilities? Unrelated to spleen, what are the possibilities?
Because the bleed is very mild according to you bleed is very mild.
This this present bleed is almost trivial bleed. No what how do you assess the bleed? How do you assess the sign intensity of the bleed in a given patient? My moderate massive >> massive bleed is said when the patient has lost approx 1.5 lit of what no what we want is just a clinical only clinic.
So what will be the clinical presentation for massive bleed versus mild bleed versus modern.
So is a person bleed is a person who just comes walking to the OP and gets evaluated and just goes back. Okay, this is the simple clinical history taking a massive bleed will present with shock and the moderate person will be the person who will have giddiness, sync copal attacks and blackout. So certain things you can almost pick out by saying this whether this patient could be having a mild moderate. So based on this what do you think this patient has minded?
>> When patient has mind bleed ma'am because she >> okay then you'll take up in a summary and discuss what are the possibilities okay if it's mind bleed.
>> So what are the possible causes? What questions would you ask lead questions to know if it's wide bleed?
What are the common causes of upper GI?
>> Ma'am common causes of upper GI bleed are peptic disease. It is a gastritis.
uh it can be um you know uh basic cell bleeding it can also be malary these stairs >> so from the history so we're asking in this particular from the history that you have what what are the question that you'll ask you say okay it is acideptic or is it erosive is it malary what eight questions will give you a clue >> some we will ask for the history of N6 intake >> so was there any history of NSA was there any history of NSA in this patient Mom, she took oral medications for four to five years which was not documented.
So I cannot uh confirmly say that there was a strip.
>> I'm I'm asking about the present episode this this history you took now or is it >> Yes sir.
>> I just want you not in the recent the recent history there is no history of any >> okay I'm not getting the history right others can take over please until I'm not getting the history right. History will never prove to the diagnosis that's what I wanted to say. Yeah. When she took regular medication for four to five years at what age?
at the age of 12 years of age when she uh when she had first first year history of >> so uh at that age whatever has >> so at that age whatever the chronology of the events probably patient may not be in a condition to tell you exactly the details right yes ma'am >> so then there are certain missing links in the history Right? Because uh continuously for four to five years.
What sort of treatment patient was on?
Was she on some uh iron replacement therapy? Was she on some other drugs that you cannot comment upon?
>> Yes sir.
>> Right.
>> Yes sir.
>> You asked the history of abdominal trauma. Why you ask the history of trauma? Okay, I think >> abdominal trauma can >> so abdominal trauma can lead to any uh either trombosis in the port or the spenic spenic pain. So it can uh to split.
>> So this much huge spleen with trauma what do you feel? How the patients can present?
The patient will uh this is a with trauma. So it will not present with a long history. Uh and patient will have uh the patient will have any symptoms of hemodynamic instability.
>> Yes. So the spleen can be easily ruptured these kind of spleens. So that's why uh it's easily patient can be in hypotension, spleenic rupture, anything can happen right summarize and give your diagnosis and differentials >> ma'am should I move to examination?
>> No no summarize the case and give your differentials. No, you'll have to give your differentials with the history. No, I do not know what your pattern is.
That's the way we we need to know what's a clinical working diagnosis before you go to examination.
>> So what's your working diagnosis?
>> What's your working diagnosis?
>> Mom sens no history taking. No more history. Just what is your differentials in this patient? That's all. We're just asking you what's your diagnosis or differentials. That's all. After history taking no more positive. Sorry >> ma'am. This lump could be arising from stomach.
>> No doctor. See I would just say I'm dealing with a case of splenomegle with two episodes of bleed right if you have any other differentials for the mass then you give a differentials for the mass. So what are your differentials at this stage and then you go to >> why you want to say stomach?
>> No sir I will rule out stomach because there is no because there is a long history so I cannot rule in stomach pathology. What stomach pathology would present for 14 years, 20, 20 years?
>> Ma'am, I have no doubt that at all in your differentials in this patient.
>> No ma'am, I will not consider it as a differential. I will just work move with a working diagnosis of spome >> only.
>> Yes ma'am.
>> What about the bleed? Let's we'll ignore the bleed. You mentioned two bleeds and long-term treatment for 5 years. So, should we ignore the bleed?
No ma'am. Uh spome can lead to bleed hypertension.
>> Okay. You proced your examination because I mean for us it's a different way of approach to the case. You must get a >> it is vice versa. You are sayingomegali leading to portal hypertension. Is it so or is it portal hypertension leading to spinoi leading to spome >> portal hypertension is leading to spome and hematosis.
>> See there are actually no uh coherence in your history presentation. So there is no clearcut diagnosis right after summarizing the history. So move on to the examination please.
On general examination patient is uh examined in a well lit room with proper informed consent. She's conscious and cooperative oriented to time place and person. She's a bile to touch and pulse rate is 80 beats per minute regular was 114 upon 74 mm of mercury in right arm.
16 per minute abdominal thoros and pal was present. There is no clumping sinosis generalized lympadinopathy fedal edema. There is no stigmatis liver disease observed. She weighed 56 kg with height of 48 cm and a BMI was 25.
>> Okay, just stop here. Why do you look for clubbing? Can you just stop here?
Why do you look for clubbing sinosis and generalized lympadnopathy in this patient? How much time did you spend looking for this >> generalized lympadnopathy clubbing sinosis and all? Why did you look for all this in this particular patient?
Ma'am because uh in in case of any u serotic liver disease it can uh patient can have clubbing and uh it uh disease >> which when you get club >> ma'am if the patient sosis what are the cause of sinosis and clubbing in a patient it's >> ma'am if the patient develops hepatal syndrome or put pressure is increased >> so what would have been the clinical presentation >> ma'am in Why why I'm asking this is I am asking generalized lympendopathy basically let it not be like a poetry you know no sinosis no clubbing no lympendopathy this is what we say for all our patients right but when you mention this just think twice when when we are speaking on this why are we why are we discussing at all about this all right that's my thing what else would you look for in general examination in a patient with splenom it's a large mass you presume it's spleen after examination you've said It's bleed then regroup and you will you go back to look for anything in physical examination in a patient what are what are the hematological conditions where you look for some findings in general examination we can look for par we will look for uh ma'am we can look for uh any climotic or perpetic pes um m then we can look for stigmatic trans liver disease I can't hear audio is not good they're not I'm not to hear you properly. What did you say towards the end?
>> Mama, we will look for pal. We will look for and we will look for any kyimotic or pulpitic patches on the skin and stigmata of chronic liver disease.
>> Why do you look forotic patches and all in this patient without a history?
Someone is lying down I think. Please switch off the video. Okay. Because this doesn't look nice. All all consultants sitting here upright and taking the people listening are all sleeping and lying down. Dr. Can you switch off the video for all the others please?
Yeah, please tell.
>> Because you look you look for sternal tenderness.
Would you look for sternal tenderness?
>> I say it's a case of milo fibrosis.
>> Okay.
>> What else will you look for? What are the other conditions that you look for?
>> We'll look for gout.
>> Okay. Please ensure that because in a case like this it's a bedside clinic you know if a short case bedside and they ask you to examine and you say it's a large you should know what are the things you look for in generally physical examination okay that's why we're focusing on that okay continue examination abdominis with central placed and inverted there's a visible fullness of the left hypochondrum and left plumb region moving downwards with inspiration fullness becomes less appreciable on head by raising all corresponding quadrants move forward proportionately with respiration.
There's no engorged veistis or scar seen and external genetic labia are normal. Bilateral renal angles are moving to the palpation. Abdomen is soft non- tender skin is part 12 cm in size below the left costal margin in its long axis occupying left hypochondrium extending towards the umbilical region not crossing the midline. It is smooth in surface per f consistency with regular margins. Not just fetch over the anterior border. Upper margin is not palpable. Fingers could not be insinuated under the sub left subcostic region. Neither botable nor by manually palpable. No other organo mentality or lump noted. All her sides are intact.
Pil are not in spine is within normal limit.
On percussion there is d on percussion over this. Liver span is 12 cm and there is no evidence of intraabdominal free fluid. On oscultation there is normal normal bowel sounds heard and there is no brewing or hum heard over the lump or elsewhere.
On uh digital dexal examination per skin was normal normal anal tone with feal stain was present and there is no blood on glove finger no mass or abdominally felt. On proctoscopic examination there is normal rectal mucosa with no evident hemorrhoids or growth.
On systemic examination central nervous system was higher mental functions were intact and uh in the cardiovascular system she s1 has to be normal with no added sound. Respiratory system bilateral air equally was present with no added sounds.
Summarizing my case, a 32-year-old senior which contain a gradually progressive painless lump and lift up a abdomen for 20 years associated with simple episode of hematimus 20 days back with history of similar episode 20 years ago and one unit of blood transfusion 20 years back. On examination, spleen palpable 12 cm below the left costal margin along its long axis extending towards the umbilicus with no evidence of repatogali asitis and signific disease paral was present.
>> So what is your diagnosis now?
>> So my provisional diagnosis is lenome due to portal hypertension.
uh for the reason of portal hypertention I would like to give my uh uh provisional diagnosis of extropatic portal venus op in your examination finding what is the what are the points which are favoring portal hypertension diagnosis.
So um in the history uh first of all it is a long uh long period of history.
And second is the hematis which uh again favors the diagnosis of total hypertension and spinogalu in case of magaloo. And uh there in the examination uh there was no uh uh >> do you think that such a longl last uh lasting I mean uh portal hypertension patient will have only two episodes of hematis that to mild hematis.
No sir in case in case of portal hypertension genetic patient presence with mass upper GI any other thing in the examination which favors portal hypertention examination sir sir u >> so white cannot be just some uh Uh she may be a case of cickle cell anemia. She may be a case of talismia.
>> Yes.
>> She may be a case of sperocytosis.
>> Right.
>> Yes.
So there was >> so why you want to bring in portal hypertension here?
there was no history of any blood repeated blood transfusion and also there was no this complaint of any jaundice uhation of that's why I have put a provisional diagnosis of the type of portal hypertension rather than herited >> do you see jaundice in all the patients of portal hypertension >> no sir so we but in hemolytic there is generally jaolysis What are the causes of massive splenomegali >> causes of massive splenomegali is uh one is extra extraatic portal venus obstruction.
>> Extraatic never causes mass extraatic never cause a massive massive plan is very specific for one particular type of categor coming up to dumbus in a patient with EHPVU.
Give us the differentials for a master spenomi. Give us just classify and give a differentials for the master that's your diagnosis.
My massive spali can be due to infected pathology like in case of tropical spomeali and it it can be due to kala and in case uh it can be due to due to in case of portal hypertion it can be due to >> classify can you classify? Can you please classify causes of massive?
>> How do you classify them neoplasmic infiltrator causes? Tell what are the infective causes?
>> Ma'am infective we have tropical metal syndrome and kalaza. In mam infiltrative we have a chronic myoid leukemia CML and in case of conveyus metal we have nonerotic.
>> What are the hematological causes?
Mr. causes of massive spleen.
>> Ma'am, it can be due to chronic myoid leukemia. Uh it can be due to uh cycles uh sorry it can be due to herittois and it can be due to primary myio fibrosis and it can be due to which one sorry last one.
>> Massive spleus and thalismia at this age.
Alismia inter >> what are the infiltrative causes?
>> Infiltrative causes is uh primary >> disloidosis lymphoma you must classify it. You must have infection inflammation plastic miscellaneous storage disorders. You must have a complete list in this condition. Let us see whether any of them your bleed history is where it's misleading us. If you had taken a good history of the bleed would have come to the right diagnosis.
Understand in EHP you'll not get such a massive spleen. When you suspect NCP you mentioned second as NCPF what will be the what what will be the features of NCPL?
>> MP can you can you just differentiate EHPVO and NCPF? Just differentiate the two in a given patient. differentiate EHP and NCP uh presentation age of presentation of EHPU is a younger age and the second decade of life and whereas monotic portyrosis is of older third to fourth decade of life and uh what age what's the age of presentation of NCPF >> third age of presentation >> sorry is 20 to 40 years. H then what are the other differences between the two? Mom uh in case of mom extravenous portal hypertension there is um m there is spleen is not massive uh massive there's moderate spali whereas in the NCF there is massive spleen in the gali and uh it can the the problem is in the second order of portal vein in case of npf while in the espatic portal venus obstruction it is in the first order portal and >> first order first order will be EHP is prehypatic. No >> prehypatic >> prehypatic. Huh.
>> What else?
>> Um ma'am uh uh and NCTF can present uh with jaundice in the later stages. I'm not in this.
>> Can they both present as portal biopathy?
No ma'am portathy will be present in EP can present in both Adam can be can present in both both are similar. So you can get potent number in both PCC and then what are other diff what will be the HVPG in both these take a pressure gradient what will be the difference between the two >> ma'am in case of >> ma'am in case of ESPO pressure gradient will be normal and in case of nerotic hypertension EP uh HPatic Venus grading will be next. What be the value? Tell us the value. You know cannot just say high value. Yes ma'am.
Minut just we'll just summarize it here. So in other words just see that you have a good differentials for all the hemlo for all the massesomely because this can come as a bedside clinic.
Okay. And also have a differential between EHP and NCPF. The whole problem with the presentation was that the GI bleed will always usually be massive.
You'll never get a trivial bleed. You have a trivial bleed is just not related to that. You understand? And some if the person who's given her treatment for 8 years would have told her what is the primary problem at least the doctor would have told her something that yes you have to take this for next five to seven years. So your history is very very very important. Without the history it's very difficult to make any clinical diagnosis in this patient. These are my comments. You can take over sir.
>> Uh very uh rightly said by Dr. Janti Muskan actually so many pertinent things you have missed. Anyway uh u do you think that uh patient who is having total hypertension with whatever the reason is for last 20 years will not have asitis etc. and spleen is enlarged to this point.
Can this really happen? Do you see such kind of clinical presentation very commonly?
>> In case of precinosidal we can ask them.
So there will not be any free fluid in the abdomen then.
>> Okay.
>> So uh when you say that patient is having portal hypertensions >> sir on the basis of theatic venus portal gradient. So when it is more than 5 mm of marketing we can say it is a portal hypertension and for clinically significant it it should be more than 10 mm of and uh for bleed uh to lead it to bleeding should be more than 12 mm of >> so how do you measure pressure?
Uh so by canalating the swimmer beam uh we uh place a balloon catheter in the hypatic vein and on inflating the balloon we take the veg pressure hypatic w pressure and uh deflating the balloon we take the three pressure uh threeatic pressure and on sub subtracting both the pressure we get the port hypatic port.
Okay. Now you have this differential diagnosis in your mind. How will you investigate this lady?
>> Sir, I would like to move forward to uh sir um confirming my diagnosis by ultrasography of cold abdomen along with the color color Doppler of the bottom system.
>> So what can be the uh finding in Doppler study?
>> What will be your level one investigation in this patient? What will be the level one investigation this patient?
Level one, what will be your first level one?
What will be a level one investigation?
We'll have to do a complete blood count with the petrol smear. No, >> we don't know what you're dealing with.
So, you need that. Okay. Ultrasound will be the diagnostic and Doppler. But what will be the role of CBC with the peripheral smear in this patient in >> this patient?
What do you expect?
>> We expect either it can be due uh it can lead to a hyperl hyperplum picture or it can be normal.
If I'm considering a diagnosis of hypertension, >> I do not know what cypressism.
I do not know what cypressism.
>> Hyperplanism will show um cyto by more than radius reduction in more than two cell lines either by cytoenia or pancytomia. It will present as a splenomegali and the symptoms will be relieved after the removal of spleen and the bone marrow will be normal cellular or hyperellular.
I'm asking you what will be the counts in this patient. Can it be that the patient has got 4.5 lakhs of uh plate count?
>> Yes ma'am.
>> So what what is it?
>> All the time you're concentrating only on on port hypertension but why can't you have a can it be a hyop fibrosis cytoenia?
Can it be m can it be myopolitated neoplasm with active mutation?
>> Um m neoplasm I will not keep it likely because for 20 years you will not have survived.
>> No no no we have no idea what we dealing with. We have no idea what we are dealing with. Can it be a storage disorder?
>> Yes mom but present early age. So I have not kept >> what the role of liver function test in this patient.
Mom, it will show the condition of the if the it is a sinosidalism if the liver is involved or not.
>> What what do you expect the LFT to be in this patient?
You expect the liver function can be it can um if I'm suspecting a case of hereditary anemas then it can it can show a raised uncon >> doctor are you suspecting that so your your complete blood count will give you all that information before you proceed through all this in portal hypertension what do you expect you had two differentials EHP1 NCP what do you expect the LFT to be >> may expect to be normal.
in both.
>> Yes ma'am and both.
>> How is it normal that your non-cerotic portal fibrosis is very sinosoidally?
So what are the possibilities? 20% of them can progress to cerosis. We have no idea. No liver span is just normal. So you can still have some changes in the liver function test. So we have we used to do what's called as brome sulfilene retention test in our days and that totally told us that in MCPF it is pericyosidal whereas in EHP it's precinosidal because it's pericyosidal 20% of patients can progress to cerosis so in li function testing supposing alphas and gamma gt was elevated on biochemistry liver biochemistry what is your take >> I will like pathology as well like potential.
>> Yeah. So therefore this is what we're asking. So you can expect no suppose you have raised alphas and gamma GT then you have to suspect PCC in this patient right. So you cannot level level one investigation would be diagnostic. Yes.
Ultrasounded Doppler but otherwise when you go stepwise peripheral smear blood test would be the first one and then you move on from there on. Okay. Okay. Then can you continue with that answer to doctor's question on what will be your finding on ultrasound and doler in this patient?
>> Uh sir in this patient uh we can uh uh either uh or on the basis of portal be in color we can uh say if it is a uh hypertension or not. If the portal be is visualized then we we can have portal vein diameter will be increased and the flow uh the rate of flow will be decreased. So on the basis of the partic CD uh CDSPs we can also say if it is a there are any collaterals or not and uh if uh if at all the portal V is visualized or not we can also see the status of the schemic vein and uh if there all the findings that you look for in the portal Venus system in a patient with portal hypertension.
Now we will see further uh visualization of the portal beam diameter of the portal beam uh flow normal diameter doctor when you speak you know you have to say the normal diameter is about 9 mm to 1 million. Now my patient I expect the diameter to be more than 1.2. So then we understand that you've understood the basic concept. Okay. So one is dilation of the central vein.
Yeah. So then that's number one. Then you say we have a DD of EHP versus NCPF versus cerosis. Can it still be CTPA cerosis? Okay.
Okay. So now tell so one is you see look for the dilation of tell all the findings look for EH perals.
>> What collaterals? What collaterals are you looking for? What is the looking for the collaterals of ultrasound bridging? You're looking for bridging collaterals. What are these bridging collaterals? What are they?
What is this? What is this bridging collaterals? What is it Kevin? What is it?
They're all the commitis which are the communications between the before prior to the obstruction versus the post. So they're all bridging collaterals which which circum circumvents the portal fibrosis which is present in these patients. Okay, that is keloma.
Then what else will happen inside the liver? inside the liver you're likely to have a what will be the finding in the portal vein or what will happen to the hpatic artery in these patients >> non-hypatic artery will be uh I um I can uh we will see the decisive velocity in the hpatic artery which can be increased and resistive index which is again either normal or decreased in case of uh HP view and we will also look for uh the appearance of Total in the case uh in um a liver and we will in the liver we will look for echogenicity and nodularity and any secondary pathology.
>> What is the finding in NCP?
M NCP we will have a attenuation of the portal uh vein and liver uh in the distal part it will be a winter tree appearance >> I do not know what's a winter tree madam I do not know anything about a winter tree Chennai has no winter no we do not know what's a winter tree so I just want to know what happens when once a portraine enters the liver what is how do you describe the branches it's It's a dichotoous okay dichotoously it keeps dividing and goes right up to the periphery. So in NCPF we call it as abrupt truncation. That's the word we use. There's an abrupt truncation after the second degree. So there's a peripheral pruning. So you have two degrees and then after that second degree onwards there will be peripheral pruning. Okay. And some of them you can get surface. So when you if the liver is enlarged the surface will show oscillation. it will be there'll be surface irregularity because of the of the retraction of the capsule due to this peripheral pruning. Okay. So that's the finding you'll see in NCPF. So this is how you describe. So can we have some information on this patient what it was?
So then we can move on to the management some at least give us some more information on this.
>> Ma'am uh this is the uh report of it isography the coloratic port system. Now here we can uh we have a liver of 13.1 cm and plan cordal length which showed altered eco texture with a regular surface and so mine is of 31 cm along the long axis pain dilated and shows multiple peripal and perpicanc Ratic collaterals was not visualized and apartic artery the pistol velocity was 35 and resistive was 71 with a minimal free collection noted and impression was chronic liver disease with massive spomegal dilated spices and multiple peripotic and collaterals with non visualization of main portal pain and minimal assess likely due to extraatic port obstruction. What was the finding within the liver? The protein system within the liver.
>> Mom, they have not commented on it.
>> That that is most important. No, it's such a big massive spleen. How can you say it's EHPVO with the features of cerosis? It's a chronic liver disease.
You expect that in EHP?
>> In EHPVO, do you expect findings of surface irregularity?
alter echo texture and that is why in your differential that's what I said it could still be CTP cerosis >> okay only thing the natural history is the patient would by now would have decompensated over these last 14 years patient would have de 14 or 16 or 17 years should have decompensated but this is most likely an NCPF that is progressing towards cerosis that's that's the diagnosis in this patient and therefore we need details of the vessels is a combination we need details of the portal venous system within in the liver to know what we're dealing with. A simple EHPO would not cause surface altered echo texture and uh this thing her BMI is high. So are we is there a component of massive? We do not know.
Metabolic dysfunction associated to steroic liver disease. Her BMI I think was 25 or 26. She was like slightly on the overweight.
>> Sir uh others please take over sir.
>> Yeah. Uh Musk any any other specific investigation you would like to do for her?
>> Sir I would like to do upper G endoscopy sir.
>> Yes. So what all you would like to see in the upper G endoscopy?
>> So we will see for uh uh uh the site any pathology that can lead to bleeding it uh and we will see for varicuses.
So howis looks on a paganoscopy sophistic looks like a torturous vein. So uh in case of uh sir it can be uh divided into uh f1 which is the small straight be which l uh which does not produce uh after incirculation of uh in endoscoping. uh then it can be of f_sub_2 variety which can present as a top shoe and it can be in f3 variety which can be a coil like and large nodular shaped. We can also we will also see for red signs on endoscopy can be cherry red that spots red veil marks and hemosystic uh socystic uh lesions >> sir and apart from endoscopy any other test >> sir uh as the USD abdomen and CDFBS has suggested a chronic liver disease I would like to go forward to fibrosis first Okay. So what all you will uh what is the basic principle of fibrocan?
>> So fibrocan works on the sheer uh pressure and elastic uh which measures the elasticity of liver on applying the shear pressure.
>> Any other investigation?
So uh the basic investigation so they will would like to do the C >> viral markers doctor would you look for viral markers in this patient and what's the role of viral markers in this patient >> uh repetitive B and hepatitis B >> what markers would you do in hepatitis B what markers would you look for in hepatitis B to know whether it's chronic HPV infection >> mpg >> what test would you do for chronicity you'll stop being HBC is negative you'll just stop there what's the role of anti-HBC total all these are very important no because this patient would require vaccination she's a person who's likely to have repeat get repeated transfusions and she's already she's received some transfusion also and if both are negative you have to get get her vaccinated for hepatitis B so you have to look for viral markers and So maybe she's HBS agent positive and the chronic liver disease she's got an incidental HBB or HCV infection. So what was her viral markers in this patient?
>> Ma'am it was uh I have not mentioned in here but it was all negative. No uh no viral marker was not positive.
Uh Muskan how you are going to manage this lady?
Uh sir in the management sir uh I would like to move forward uh with uh sir uh I can uh so if the patient presents with a absute bleeding so we will manage it if not then we can manage it.
Sir uh with >> tell us tell us the grades of viruses no then only we know the management there are viruses or no viruses what was the blood picture what is blood the HB patient is anemic you said that clinically what is the HB >> so endoscopic there is one column grade two and one column grade one esopacial viruses and endoscopic >> what was the hemoglobin you said patient has got pal that's what the professor is asking what was he tell us the blood First >> the Hindam hemoglobin was 8.4 g per deciliter um with a decreased uh totalite count of 3,500 and platelet was also reduced of 65,000 and uh the viral markers were non reactive ptr was 1.2 2 and the albamin of the albamin is 3.9 and um the uh general blood pressure shows the hypogchromic microtic hypogchromic edia and the TLC is also reduced and plate is also reduced and the CTP CTP score I would like to give it as a grade.
>> So is it hyperplanism?
Yes sir. Hyperplanism there is according to the study of cypus.
>> So your blood count CBC is going to make any impact on the overall management of the patient.
>> So um as it is the case of hyperpinism we will uh one of the goal of management will be spinto.
So that is what Guptas asked that what how will you proceed how will you manage this patient and for the management of the patient first and foremost is CBC right that you should always mention.
So now this is the reports would you like to go for how will you manage this patient?
The uh goals my goals of management would be first to uh uh uh removal of uh spleen and control of the vicial bleeding. So I would like uh to go uh as it is uh she's not actively bleeding. So we can go forctomy with sh surgeries in this patient. I'll leave this patient alone. She's finished her family. She's got two children. She's asymptomatic.
There only grade one viruses. Why would you do a shunt in this patient?
in EHP we use >> for what purpose are we doing short >> ma'am um >> I just go back to the endoscopy when you have grade one and two viruses would you really push in for an EVL one column >> you could do just a small no they're all small vises would you ask for an EVL >> bleed is also not massive did you give a give the patient carbidelon did you give any of the non selective to be termed blockers.
Oh mom uh >> the surgical aspect as far as I'm concerned this patient come to me I'll just leave her alone patient is asymptomatic if the bleed was trivial unrelated to the isopedial viruses and put her on cardinal maintain her if she has any dispmia manager for that and leave the patient alone I will not do any surgical or any other intervention with patient because patient has completed a family she's had no problem all this is very important because pregnancy is not that easy in a patient BHPV advanced cytoenia history history history will give you a diagnosis in 80% that whole history was lacking in this patient because some person during the course of pregnancy the obstitrician would have said your platelet count is only 20,000 30,000 you have a liver disease you have a difficult problem we have problems in your obstetric management there's likely to be a miscarriage all this has to be discussed in this patient these are my comments as far as the management discussion Yeah, agreed ma'am. Uh Kuskan was this even done as a prophylactic measure.
>> So it was done as a prophylactic measure sir.
>> Yeah. So even that was not indicated as madam is rightly saying >> right >> you can >> because patient only two episodes of >> yeah and shant as of now is not at all required in this lady right as per your description whatever history you have told and whatever examination findings you have given to us so uh right now there is no hurry to go for a surgical management for this particular patient.
Yes.
>> So just coming what type of shunts you know for portal hypertension you know selective shs you know non- selective shs.
>> Yes sir.
>> So what are selective shs?
>> So selective shunts are sino sh uh that is a walking shunt. uh it is sinus that is the left gastric venus and uh cable shunt um and select is a sage shant that is a small diameter photo shant and in non- selective sh we can have side to side lenovo shunt that is and we can have s proximal lenovo shunt that is the linton shunt and we can have the miso cable shunt grain shunt and uh sir tips is also non- selective portal non- selective shunt s and sir we can have ect official that is a >> you were asking some question what are the various type of >> can you hear me >> yes sir What are the various types of miso cable shunts?
So miso cable shunt s side to side uh that is >> side to side is it is >> you cannot do a direct sh in between but you can do any end to shid I'm asking about the miso.
>> So, so inferior mentric vein and renal renal veent.
>> No, you can sometimes cut the in at the infior and rotate it to the superioric ve.
So if you are not able to do a drain this is another direct sign which is there between the lower end of the inferior vicular to the side of the superior what is a child's grade in your patient.
So it is a child score of a grade. Grade A.
>> How much?
>> Grade A sir.
>> How much is the score?
>> So it is uh six.
>> Okay. And what is the ME's grade?
>> The meds I have not calcated sir. Huh?
Okay.
Now what are the direct search theory for the portal hypertentionization surgery sir?
>> Do you know any name of the devascion procedure?
>> Yes sir. Sir Tanner uh operation it can hab operation uh it is siguira procedure.
So there are some modifications as well.
uh sir Mil Walker Johnston and sir an in Indian modification sir Shahi's modification okay what is sah modification >> sir it is a modification of tanner's operation wherein uh the anterior uh only the anterior uh gastric uh resection is done and the posterior ball is tated and where and there there is devascularization of the external devascular ization of esophagus and cardia of the stomach. So >> no, you underrun the posterior wall.
Okay. After opening the anterior wall, you underrun the posterior wall and then you s the anterior.
Okay. So that is the t modification and then there is further modification is there you know sash modification again Indian but I don't modification also.
>> Yeah, I I'm co-author in that. I'm hearing everything carefully.
>> There are many Indian sas which are involved in that.
>> Sir, I have some basic questions for this lady. She has answered very well.
I'm very happy about it. in spite of being really grounded.
What are the causes of coffee ground vomit without splenomegali?
>> So without splenome it can be a very uh sorry it can be due to pepicula disease it can be due to erosive gastritis.
>> What is coffee ground? What is coffee ground vomit according to you?
So coffee ground vomitus is uh due to when the bleeding is in the upper uh upper uh GI. So the blood changes into hematin due to the AC.
>> So what should be the speed of bleed?
What should be the speed of bleed in a coffee ground?
>> It would be it would be slow and it should minimum of 30 minutes. Uh >> never answer more than what never answer more than what is required. Just say slow bleed bleed and keep quiet because then I will ask you what is medium bleed, what is rapid bleed. So in examination be very very clear as to how you are going to answer these questions.
According to me these clinics are for to train all of yall for that. What are the common causes of slow bleed in the upper GI tract? Forget portraition right now.
>> Slow bleed ulcer ulcer. It can be due to peptic disease or it can be malignancy as well. And uh uh then it >> you're not thinking of erosions at all.
Right.
>> Erosive erosive gastritis.
Which erosive gastritis, gastric ulcer disease or pepiculer disease and malignancy? Which of these will you give priority in your diagnosis without splenog splenomically?
>> So uh I would like to keep uh um the quickest answer is I don't know. My my next question is what are normal spenic dimensions?
Normal spenic dimensions length breadth width >> length is 13 cm is 7 cm bread is 3 cm.
>> What is normal weight of the spleen?
the uh 200 uh two uh 200 sir 250 >> don't blink your eyes because I'm seeing you >> can you tell me classifications of splenomegali on a CT scan >> because we have been talking about massively moderate I just want you to know >> yeah So massive spomegali is when the size is uh >> no I I have asked you classification of spenomegali on a CT scan >> but on the uh CT volume so we can uh say it is a massive spinome if it is more than one >> I'll give you one one more one more question there is splenomegali on weight and splengali on a CT scan Which of these two would you prefer to know as a surgeon that I'm going in on a spanomeali?
>> I don't >> good very nice. So all this once you prepare for a case on portlap attention you got to be ready with all these questions and answers. Okay, that's that's my take. Basics are more important rather than treatment of bap attention which is supposed to be done by liver people. Thank you so much the fine end. Thank you.
>> I was just asking what are the causes or indications in which you will go for sh surgery.
One is visel blade. This patient is not having varacial blade and what are the other indications for shunt surgery?
>> Infractible asitis uh the refractory uh and this patient already have a huge splenomegali right with hypersplanism that is one of the indication.
>> Yes. Then what is if this patient is having jaundice?
>> How will you manage that and what are the indications? What will happen?
>> The um dais it is more uh it is more in favor of cerosis uh cerotic liver disease. So I would like to manage it according to the uh >> earlier madam had discussed Dr. Guptasar had also discussed that is portal bilopathy.
>> Yes sir. So portal bilopathy will be managed. So we will go for an ERCP. Uh so ERCP strening can be done.
>> I think uh she has answered well. Uh madam you can please give your final comments.
Madam you are mute. Madam you are mute.
>> So summarizing I would like to say yeah you you uh you you you did a good job you know getting all the questions and bombard even from all the examiners around you but I think you did a quite a good job. What do you think what I would say say is you know I would spend a little more time once I I actually what I would do is go straight for the examination found a big spleen and then I just say how long you've had it and once she's had it then I just ask who are you during all these years and then describe the bleed to a larger extent and then just give us you know like it's not like um Sherlock Holmes you know where we're trying to find out what it is we want to manage the patient patient comes to us more for management rather than for basic diagnosis okay patient would have come to you with a diagn Diagnosis of a portal hypertension and for us it's a management and important is very this is most important no facial chronic liver disease that infertility rates are very high menstrual cycles are often irregular these are all the features of chronicity and invariably they they just most of them will have abortions and seldom would they go through all this you know and that too with the large spleen almost the uterus moving up and the spleen crossing so I think that's important and as most of us discussed this case if it comes is a bedside clinic questions will be asked only on splenomegali that in other words you must know a little bit more about general medicine okay and then photo hypertention is because you know what the cases you were skewed towards one diagnosis had you not known what the case is you would have had a wide differentials be at least I did not see the powerpoint so I did not know what the case was so therefore I I was able to discuss more than beyond what you thought because you already knew what the case was but the discussion will hover around cosmos plenomegaly Then splenomegly when can you get portal potential and vice versa and then know the difference between once you've made a diagnosis EHP or NCPF you must read all the papers from northeast parts of the country Kolkata papers by Dr. Mazumar he's done a lot of work on NCPF there are huge papers on the role of arsenicosis there are then you must know what are the other cause of NCPF role of liver biopsy that's very important in this patient and they'll ask you the differences which is a liver biopsy at all so what we tell the surgeons is if they are going in take a biopsy core biopsy we don't ask for a veg biopsy or a perccutaneous biopsy because it will be not be informative so we always ask for a core biopsy and a little bit about endoscopy because surgeons are doing endoscopy nowadays. So therefore you need to know more about endoscopy you you're given the case you're the surgeon patient comes to you will you do an endoscopy will you do banding what are the they will ask you because you're the surgeon who are doing no you all are doing endoscopy so they'll ask you what are the bands how how do you deploy the bands how do you arrange further this thing all these questions will be asked and what's the role there's no role for any of the non- selective beta blockers in patients who have got EHPVO because it's a lower resistive system it's only NCPF and cerosis that we give otherwise there's no role even if the viruses are grade three grade four there's no it's a low resistive system there's no role for any of the beta blockers okay these are my comments but you've done a good job all the best and best wishes I'm sure you do well >> thank you >> thank you ma'am uh Dr. Sema ma'am would you like to come in at this point?
Professor Sema ma'am >> good evening sir.
>> Good evening ma'am welcome.
>> Yeah Dr. Muskan faced all the questions valiantly but yes Janti madam brought out a valid point that during pregnancy if there was massive spinogeli how it would have missed. So I think uh that was uh that should have been taken up in the history and uh maybe the patient did not uh give proper history and when uh when when when did she have the children at the she came at age of 36 years. So maybe it was 10 to 12 years back. So yes that was the that was missed by the candidate but I think otherwise she did well and did a good job.
Okay. Any other faculty would like to give in any comments? Uh Muskan, do you have any doubts to be clarified with the senior faculty here?
>> Yes sir, I have >> Yeah, you can ask the question. Faculty can definitely >> as in this case sir uh the patient had a uh features of hypersplenism.
So should we go for splinctomy? And if we are going for spleentomy then uh we can just leave the patient with spleentomy or we should do any additional procedures as well. So I was not sure about how to proceed in this patient as >> the answer is very simple if the patient is symptomatic with a low platelet count you operate asymptomatic leave them alone. So that's it >> because they worried about the spleen and mind you she's gone through the pregnancy so now she her family life is completed. So what the spleen is not going to come in any way except that no one should kick on her abdomen you know and cause rupture of the spleen otherwise she's safe.
>> Okay. Thank you.
>> Any other doubts Dr. Muskan?
>> No sir.
>> Okay. Thank you very much. Uh madam the next case is a Kasama Galbad. You're welcome to be with us unless you are pressed of time ma'am. So ma'am I'll stay connected sir. I'll stay connected.
>> Thank you ma'am. Thank you. And uh thank you Dr. Muskan for uh taking all that time but I seriously believe you spend little more time on the history part of it either with the parents or with the husbands. Many times uh they may be have been informed uh the patient may themselves may not been informed of considering the gravity of the situation. The volume of bleed has to be definitely taken into consideration because in one slide you mentioned one unit of transfusion. Apart from that spend more time on asking about the how many transfusions were given that gives a very broad thing and was there something like an emergency admissions indirect questions many times if you have asked them and perused the records it would have been more appropriate for this presentation that gives a clue the other thing is if the mom of the girl is there I'll be happy to look into amal sepsis how many days it took for the amicus to fall down onwards intra like intraatal or perinatal sepsis on the mom's side. These are all additional things we'll be very very interested in knowing about it whether the child had extended like for instance patients kept on ventilators for a long time posttop postnatally you know premature child or something their patient on ventilator whether the patient had exchange transfusion in the immediate postnatal period so many subsidiary questions may you may not get a real answer but still no if the child is kept in the post delivery period extended in ICU or repeated hospitalizations in the early natal period. These things all give a clue, right? And certainly any obstitrician doing an ultrasound or perinatal antiatal checkups definitely would have picked up these things. So you gently probe them something else told some other safety precautions would have told. Many times these girls get married, get pregnant and then the first n antiatal checked up the obstetration picks up definitely they would have discussed in the team they would have explained to the family such a risk is there unless she is a totally unbooked mom. These things can easily be proed from the mother and asked whether they took a proper booking or not. These things all matter at least at this point of time make it a timeline and give it a notebook. In fact, Jim ma'am at this age writes a full notebook of information so that if she after 20 30 years if she goes somewhere she has a way of writing all the liver function tests 20 30 40 liver function tests on a sequence. So it becomes a breeze to understand how the liver is progressively improving remaining static or getting decompensated. So documentation per se as much as possible probe the family the previous treating doctors would have certainly given some records ask them to get hold of it if not at least from now on you please give a proper note written document generally notes notebooks are not missed that's what works as well in these type of long patients please write in a notebook and give rather than giving a one page or twopage printed summary even though it has all the information some more people don't lose the notebooks that's what is our experience in our long-term patients keep track of it. Give a very good followup advice to these patients because they have to be on followup at least once in six months. They have to have a liver functions or to be assessed by a proper uh clinical team and then evaluation by way of endoscopy scans have to be a lifelong effort. If necessary, I think you have a fibro scan in your department that has to be on a sequential basis based on the values which are rapidly going up. Sometimes you may require frequent fibro scans and madam has told about the biopsy concepts also. So it has to be very carefully monitored because the more you leave the liver to go to more denser cerosis the longevity of the patient comes down. But at this point India has a fabulous transplant facilities also. So keep the options open. Don't exercise all the options at one go. But this is certainly a patient who needs a closer monitoring by the team.
>> Dr. Kan just one please read about the prothrombotic state. Okay, we didn't discuss that. So please read all the tests for proth thrombotic state and whether the patient will require antiquagulence or it's a long-standing case and therefore we ignore it. In your patient, was this patient admitted under you or the patient was referred from the liver department or some other department for a splenctomy? Can you just answer that final question?
>> Uh sir ma'am she was referred from gastroenterology.
Uh ma'am she presented there with uh that hematamus complaint.
>> No why was she referred to the surgeons?
>> So uh because uh u she was not uh actually when she came to us she said I don't have any problem with the lump.
I'm I'm all right with it. I just >> Exactly. That's what I said. That's exactly what I said. I have no problem.
That's what I said. just leave her alone but was she referred for spenctomy?
Uh no ma'am they uh said for the workup and for the management they have referred to us but uh yeah so ma'am they also mentioned that uh splinctomy is necessary because of the features of >> no that's where no if the plate the so if the platelet see platelet count even of 10,000 in a post- transplant scenario patient the function is retained even the lowest no so long as the function is retained even though the count we don't do anything even the count comes to 10,000 The function of the platelet is retained. So better not to meddle and prothrombotic worker very important.
Suppose she was appla positive. She would have had a bad obstetric history.
All these that's what the history history is most important. Okay. Thank you.
>> Thank you. And the ACG has recently published guidelines on management of anticoagulants in these type of serotic patients. I wish your attention. It's a open access guideline. Please go through that. I think it was in year 2024 at late 25. Please go through the management of anticoagulants in serotic patients or in vasculopathy or bilopathy individuals. So with that word I think I've taken little longer time on this case because not a very common occurrences and with the permission of the faculty we move on to the next p next case discussion. Dr. Aayush you are with us.
>> Yes sir.
>> Uh good luck to you Dr. Aayush and faculty here please take over. Uh Aayush please introduce yourself. your unit chief head of the department and start your presentation. Madam and sir, please take over. Thank you very much.
>> Uh good morning sir and faculty. Uh I am Dr. Aayus third year postgraduate uh from department of surgery MCC case. My head of department is Dr. Slas Basil, Professor Department of General Surgery and monitor is Professor Amit Gupta Department surgery in charge of HB unit and in charge of surgical MCC case I sat please go ahead all of them are listening they are with us in quiet mode but they will ask questions or comments at the respective time please go ahead >> lady miss uh as a 59y year resident of the rat utraand she is homemaker illiterate and belong to low socioeconomic u she had she presented with complaint of pain in abdomen around right upper abdomen for past two months uh stop present illness patient was apparently asytomatic two months back when she developed pain in abdomen around right up abdominis in onset progressive illness which was relating to back continuous which increased on severity after food intake can leave doctor or medication which has not assated vomiting, fever and abdominal distension. He also has history of loss of appetite for past one and a half month and unintentional undocumented weight loss in last one month which was by loosening of clothes. Um there is no history of fever, vomiting, yellow discoloration of ice, vitamin C, passes of black tis, bleeding PR, uh no history of alter bid, no mis generaliz, joint pain, no history of cough, headache, seizure, back pain, no abnormal distension. Meal history she attendop 10 years back. She is married had three children all normal vaginal delivery.
She has history of pulmonary tuberculosis three years back for which she took drug for 9 months and she had no history of asthma hypo hypothyroidism semic heart disease diabetes or hypertension. No history of blood transition no previously. No history of any chronic drug intake. No history of any abnormal surgery in past. No of anyergy. Personal history is completely disturbed due to abnormal pain. She consumes mixed diet. There is no history of addiction. She has no bowel and bladder habit. No history of similar disease in family. No history of any malignancy malignancy related death in the family. Smrising that case u a 59 year old female presented with right upper quadant pain uh for past two months with history of loss of appetite and loss of weight.
>> Yeah. Can you can you just go to some of your previous slides where you ask for no histories and all that?
Go.
Go back to your history. History history, doctor.
>> You're going forward. Can we go back to the history?
>> Yes, ma'am.
>> Yeah. Just just just come come. Yeah.
Just move next slide. Just get just keep moving. Yeah.
Yeah. No, this can you can you give us a what what are the just go back to the previous slide.
Yeah. This one increase in severity after food intake and relieved after oral medication not also in vomiting. So what are the conditions when you can have a pain in the right hypochondrium which increases after food intake?
Um man uh CI increased after uh uh it can be acute um it can be because of bilary uh folic uh like after taking food intake or consuming fat meals they can have pain in abdomen after >> what percentage of patients in your day-to-day practice you find that patient gallbladder disease get a pain after taking food you see so many cases no with pain in the right hypochondrium so what common causes of pain in the right hypoondri which increases after food intake.
>> Yes ma'am. Um >> what are the common causes?
>> Pain in right upper portion mostly uh >> gallbladder disease.
>> Gallbladder disease. What what about the where where's the surface marking of the dural cap?
Where do you think will be the surface marking of the jal cap?
Any so what are the common what just list out the causes of pain after food intake just give us common just what are the common causes of food related pain >> um ma'am uh after due dal ulcer man >> dural ulcer will you get aggravated or get relieved with food intake >> um aggravated man >> aggravated then what happens to the gastric ulcer what is the classical you know internal ulcer moment the patient takes food as it comes down so the relief of pain right that's a du and then so one is pepicula disease most likely either a Johnson's classification pre pyloric or a dural ulcer that will get relieved with pain gastric ulcers can get aggravated with pain number one number two >> and can the pain be due to pancreatic or >> yes ma'am >> how many hours when do when will you get paining I suspect It is pancreatic pathology. When would you get paid?
>> You didn't mention after taking food after how much time patient have pain and is there any specific history of taking specific type of food related to pain?
She had uh pain after taking fatty meals. Sir, >> why should they get pain after a fatty meal?
>> Ma'am, it causes >> when you say when you say fatty meal, every time she takes a fatty meal, doctor, they're just tearing about the history, you know, too much about this fatty meal and all. Gallbladder dyslexia is a little more of a myth. No, you seldom do you get a pain due to that.
What really happens is if they take a heavy meal patient's got stone disease that stone gets gets impacted at the neck and then you get an acute callitis like picture but any other patient will never have a pain related to food intake okay it's never a food related pain although it's described in the text called bladder dispsia what will be the pancreatic what will be the description that's what sir is asking you what is the why do you want to know this pain after meal pain 3 hours after meal and pain occurs One to two hours after meal. What is important?
What will be the presentation of eskeemic bowel?
>> It a pain will aggravate on eating.
>> Pain will aggravate on eating doctor.
How will you diagnose in a given clinical condition? Patient comes to the emergency in the ER and comes >> how will you know it's an eskeemic bowel pain >> that's also food related pain.
What will be the pain?
What will be the type of pain in pancreatic origin? When will you get pain in pancreatitic origin? You said pain radiating to the back.
>> Yes, sir.
>> When you say pain radiating the back, it's my in my mind I'm thinking of pancreatic pathology pain of cox.
>> Simple question of abdominal pain.
Describe the pain of pancreatic origin.
Describe the pain of eskeemic bowel.
We've already discussed some extent peptic ulcer disease.
>> Pain in uh pancreatic patient will have pain in abdomen around uh pest region.
Patient will be uh saying that his pain really on bending forward.
>> Relation to food. I'm asking why do they get pain? Why do they get a pain? Why does a pancreatic pathology cause pain after food intake?
Why does it cause pain? Why should a pancreatic pathology cause pain after food intake?
What happens when you take food? What happens with the enzymes? What happens to the pancreatic enzyme when you take food?
All these basics basics you should be very strong. Okay? You should be very clear because see what happens is with most of us the present days we're seeing the records first then we see the patient and therefore that's it but then if you really spend time taking a history and then doing a proper clinical examination you'll clinch the diagnosis just with the history and examination.
Okay. Now what are the causes of pain in the right? Please read all this eskeemic bowel pain, pancreatic origin pain, acipeptic disease pain, gallbladder pain. Now what are the cause of pain in the right hypochondrium?
>> Uh ma'am uh pain in right hyper quadrum is uh polythesis colopolytheasis. Um >> which one? Sorryis polycyitis.
>> Polycyitis will continue will have pain for two months.
>> Uh no ma'am.
>> They're asking for a dull continuous pain in the right hypochondria. What are the causes?
What are the organs? What are the if you take a right upper quadrant by anatomical uh distribution what are the organs that are there in the right hypochondria?
>> Uh viscus hollow viscus and solid >> gallbladder is stomach and hypotic of colon.
>> Good. What about the liver?
>> And liver man liver is the most important organ.
Yes ma'am.
>> All right. So you have the liver, you have the gallbladder, you have a portion of the stomach and you have the hypatic flexure.
>> Of course.
>> So in can can there be a second and third part of the diodum? Second part descending part of the diodnum.
>> Yes ma'am.
>> Descending part of the diodnum.
>> Second part of >> Yeah. Descending. That's what is descending. Descending a second part.
Yeah. Descending a second part. So what are the causes arising from the liver?
Uh if there is any uh >> she's got loss of she's got loss of loss of weight, loss of appetite and she's got a dull pain in the right corner.
What are the causes?
>> Then if there is any >> classify doctor always classify always classify classify without classification you cannot answer.
Why can't inflammatory or infective cause?
>> Yeah, infection, inflammation give some causes. No, for pain in the right hypocchondria arising from the liver, the gallbladder, hpatic flexure and the d ma'am. In liver it can be liver absess. Um in um um uh acupatitis um in stomach it can be a pepicula disease and >> you're talking of the same patient in the same patient in this context what are the possibilities arising from the liver we're not discussing theory in this patient what are the things across this patient ma'am it can be unknown primary liver m Keep talking doctor. So just tell what are the possibilities? Loss of weight, loss of appetite and pain in the right liver.
>> Uh ma'am it can be intatical and carcinoma. Um >> why not viral hepatitis?
>> It can be viral hepatitis.
>> What are the points is asking for viral hepatitis? Can it be viral hepatitis? It can be parabeties if patient will contain a prodal symptoms like fever. Uh uh patient will have mallay and um but >> can they get pain in the right hyper quadrant?
>> They can get pain >> due to what? Why do why do people with viral hepatitis get pain?
>> Uh because of uh uh expansion of glyon capsule.
>> Good. So that you can get pain. So but that history is important. No, you get that history. Can it be an outflow tract obstruction?
>> Yes ma'am.
>> Outflow tract obstruction.
>> Yes ma'am.
>> What will be the presentation?
>> Um >> what will be the presentation of outflow tract hypatic wave?
>> Sorry ma'am I >> all this you should know because once you get the differentials you know from the history taking that. So you say it's hypatic flexure. What will be the presentation hepatic flexure growth?
Ma'am patient will have contains M patient will have contain a malina and patient will have contain of altered bip. What will be the classical presentation of hypatic flexure growth?
In recepting mass lesion of they're present like incepecting mass lesion.
That's the presentation.
Now what are the causes from the you kept on harping on gallbladder. So tell what are the causes from the gallbladder that can cause this presentation?
>> Uh patient >> the same case same case loss of weight, loss of appetite and gallbladder pathology.
Uh patient will have uh uh >> causes causes just list out the causes.
>> Yeah.
>> Uh patient will have complaint in pain and right patient will uh >> doctor I'm not asking a symptom asking you what are what is your differentials from the gallbladder. gallbladder chronic cyitis man. Um >> chronic cyitis in this patient. What will be the presentation of chronic choleiccyitis?
>> Patient will have complaining uh pain in right upon which will be red to back.
>> The chronic choleiccyitis will never have pain. They'll never come to you.
Only the acute cases will come to you.
Chronicyitis is a radological ultraographic diagnosis.
What are the other causes of gallbladder pain?
Mikosilla >> that will be a dull ache. What else?
>> Uh ma'am uh >> cause of appetite. What are the causes?
>> Carcinoma gallbladder ma'am.
>> Carcinoma gallbladder number one. Why do they get pain?
uh ma'am because of uh uh first if there is any obstruction because of G col stone then there will be uh expansion of the gallbladder which can cause pain and um secondary if there is uh um because of taking any meal uh there is uh stimulation of persistent kind receptor which can cause construction of GB which can cause What are the causes of pain?
One is distended gallbladder.
Number two, it can infiltrate at the porta. No gallbladder forces in the porta of the liver. So it can infiltrate the porta hpatus and then you can get pain arising from there. There can be distension. Then the involvement of the bilary tract. The bilary tract dilotation can cause pain.
You can have involvement of the nodes nodes and that can cause dilotation of the bery tract. Again they can get continuous pain.
Understand? So all these you must keep in mind. So that go to the next slide.
There are too many no histories. Just go back next slide.
Now here see she's not why did you ask for hemoptitis, chronic cough, headache, seizures, back pain and all. You spent so much time asking all these questions in this patient and why did you ask?
meant to rule out any distant metastasis. District metastasis you already made a diagnosis is it that it is called a malignancy in a given patient in the outpatient clinic a patient who comes with you just ask for fever you may ask for cough but you headache seizures and all if it was present patient will come out with that history okay and what how do you get hemises and nina in a in a suspected case of gallbladder malignancy >> ma'am if it is involving hepatic fracture of colon then patient may present with uh passage of black stool and assessment.
>> The other cause more common >> um >> common causes of upper GM leaf more important in this patient is vomiting. Can this patient have vomiting and obstructive symptoms?
>> Yes ma'am. She can have vomiting in >> due to what >> ma'am see uh due to berolic ma'am.
>> Oh doctor what else can you have obstructive symptoms? How can you get obstructive? Can you get obstructive symptoms involved at a malignancy?
>> Yes ma'am. Uh if it is causing any gastric out obstruction >> where at what level >> due to labor?
>> All this you should answer. Okay. Okay sir. Please take over sir.
Next slide please.
Next slide.
>> Even in this slide, why did you ask for chronic drug intake, previous hospitalization, blood transfusion? Did you ask for all these questions in this particular patient?
In a given patient, the outpatient clinic, will you ask for did you take repeated blood transfusion in this patient who comes to you with a pain in the right hypo chronic drug intake? Why did you ask for the chronic drug intake?
>> What? What chronic drug did you ask?
See, it is very simple, you know. Never ever think that you're appearing for an exam. Always think you're sitting in an outpatient clinic. You have to do a quick examination. There are 50 patients waiting outside. Quick history taking, quick examination, making a diagnosis.
So those are the important no histories.
Okay? When you ask when you say like this and the exam knows your chronic drug intake, the examiner will stop. And if that person is a good physician also, they'll ask you all questions on this.
They will not move forward. Okay? Let's move on to it. Move on. Move on.
>> Give your differentials.
>> My first differential first differential will be carcinoma GB and my differential diagnosis is uh intact carcinoma and my second is cellular carcinoma and third is uh unknown primaries of liver medicine.
unknown primary I say it is gastric tumor gastric cancer with mets why do you say it's unknown you've not asked for any history of dysfight no nausea vomiting all those questions are all missing those are the important things no there may be nodes at the port are causing pain it's not an unknown primary but you have not asked for questions what are the causal secondaries in the liver common causes three important causes >> any colonic car three Common causes of secondaries in the liver >> colonic carma and another is um >> gastric cancer, pancreatitic cancer, colonic cancer and then you have the NES. So these are all the secondary causes.
>> Most of the times you'll be able to pick up with the primary history.
>> Understand? You cannot say unknown primary. We've not even investigated it.
Understand? So your differentials please in exam even if you know it's a case of gallbladder cancer please don't give it as a first differential you'll say I consider differential diagnosis of a space occupying lesion in the right hyperchondri that's your first differential and then you say the possibilities are arising either from the liver or arising from the gallbladder or there are nodes at the quarter with invol with the dilation of the intraatic millary system my differentials for from the liver source are this gallbladder must right at the end and in the primary could be stomach colon although the history is not forthcoming and the patient could be having secondaries at the port and the third possibility is primary gallbladder malignancy quizzing then they'll ask you questions on the mechanisms okay okay so we can continue sir how will you manage this case examination examination it's not sorry examination yeah yeah yeah please please is the history Okay, next slide please.
Next slide.
Uh general examination sir. Uh person was examined in well lit room and well lit and ventilated room. Uh maintaining privacy in female presence of female sapron. uh conscious and patient was conscious and oriented time pleasant person was a averageely built uh moderately nourished hydration was adequate patient weight was 53 kg height 166 and BMA 19.23 2 three eco was one and karmosis performance scale was 90.
Uh vital for a while to touch pulsate was 86 bits per minute on over radial artery. Uh rhythm was regular and good volume. Uh BP was 109 by 80 mm of mercury in super position over right arm. Respirate was 20 bit breast per minute and saturation she was maintaining 98% on room. Gen physical examination. No pal actus clubbing sinosis palma gen left super was not palpable. Uh neck when not visible. No vis no swelling in the neck. No sign of chronic liver disease. Uh system examination. Uh CNS no focal neurological deficit. Uh respiratory bilateral air entry was present. No no vascular sound and no added sound. Uh CBS S1 S2 AR no muscular skeleton no skeletal deformity. No gate abnormality.
Uh per abnormal examination uh inspection in supine position. Diffused balls was seen over right upper quadrant. Uh omlucus is central and inverted. All quadrant were moving proportionate with respiration. There is no dilated vein sinus or scar marks. No visible peristis pulsation. Um no visible cough impulse were present. No inspection of back and spine. No scar or sinus over back or in deformity.
Externality appear number and no scratch mark.
uh palpation on surface of palpation there is no localizing temperature or tenderness uh over lump of approximately 4.3 cm in the right upper quadrant just below the uh right coastal margin lateral to lateral border of right uh rectus abdominis all margin are defined except for superior margin smooth surface hard in consistency moves on respiration side to side mobility is restricted liver is firm non- tender palpable 3 cm below the right question margin in midcoline. Uh spleen is not palpable. No other lump palpable over the abdomen.
>> Why did you look for the spleen?
>> Um >> why did you spend time looking for a spleen in this patient?
>> Uh ma'am if uh >> it's important but why did you look for it? Why did you spend so much time looking for a spleen and then say spleen is not palp suppose it was palpable and you've not done your right you've not put the patient on middle you've not done a middle turn test you've not done the all the other test for a splenomegaly drop space dullness and all and you missed it why is it important >> ma'am if there is any uh liver uh uh disease um and patient is having any portal ser >> patient in this particular patient why Is it important? Look on the screen.
Portal vein thrombosis. No. What's the relationship of the gallbladder to the portal vein and hpatic artery and the bile duct?
Can you just tell us the marking portal vein, bile duct and hpatic artery >> and what's the relationship of the gallbladder relation to all these three?
Uh portal portal vein is just uh >> you're a surgeon. No, you need to know this anatomy. Basic basic anatomy of then only you understand why gallbladder involvement of the portal vein is important.
>> It can cause compression on uh portal vein. So it can cause uh portal vein.
>> It can cause compression. Can it cause vein thrombosis?
Sir can you please take this this discussion? may be important from surgeon's point of view. One of you can please take note.
>> I wish actually any medicine may predispose for portal vembosis.
Right? So there are certain coh disorders in the coagulation and even carcinoma per se may lead to portal vein thrombosis may lead to secondary portal hypertension. This is what actually madam wants to ask from right or even splenic main thrombosis. So in that case you will see there will might be a spomegary right this is what ma'am we wanted to ask from you >> yeah yeah photo you have to examine the spleen because you can we still not so no now you've known it's a gallbladder but the patient can have photo it almost becomes a stage four disease no then you should you didn't answer that question doctor what is the cal vein and hpatic artery and buckuct anatomy in the fancy form Um >> what is callous triangle?
callus triangle ma'am uh superiorly it is a part uh um uh medially it is CVD and super inferiorly it is apatic artery and superiorly lial ma'am >> and apatic artery then where does apatic what's the importance of car triangle >> ma'amating okay I think we'll take up a discussion let's move on finish off let's go to the next one. Now, can this mass that you felt, can it be a exopetic mass arising from the liver? That's my only question on this case. Just go back to your previous examination.
This part this particular description that you've given, can it be an exopetitic lump arising from the liver?
>> Uh yes ma'am, it can be. But um it is since it is uh >> I say it's an exopic mass. It's a hard mass arising from the liver. It is HCC.
No intrinsic mobility. It will move with respiration. The shape boid is just a misnomer and it is a is a mass that is arising. This question is often asked no it may be just a heptocellular carcinoma.
>> Yes ma'am it can be but uh >> your differentials are you 100% sure you're dealing with a gallbladder or is it possible that you're dealing with a HCC?
uh it is one of my differential ma but it can be uh it is uh since it is a void lump and it is uh void >> and all is what you feel doctor because you know the case but otherwise gallbladder mass may not have that gallbladder shape once it becomes malignant it becomes like a mass it just becomes like a firm mass the well definfined margins that's all and if you have an exopitic growth a hanger from the liver you will not be able to differentiate so your DD cut should maintain as HCC is but the whole thing is yeah but the thing is the gallbladder cancer is more common in north India and all that history based on that you'll consider the possibility of okay just move on >> so what's your diagnosis now quickly tell what's your quick what's your final diagnosis >> invest your final diagnosis is carbon and >> doctor in medicine there's nothing definite about anything okay you have give us your differential never give just one like what are your >> and my differential are carcinoma intraatic colarcinoma and >> intra no intraatic colio carcinoma they present like this sir what will the presentation of intraatic colarum >> uh ma'am it it has um you get a mass how often will you find a mass moving with respiration in intraatic colicarum >> you understand so when you're discussing thing you're talking of a lump. So, HCC is one possibility. It can be a huge fibroadinoma. It can be one of those tumors. Adinomomas, they're all exophatic tumors. Understand? Intraatic colarum is intrahibatic. You'll not get a mass arising. You'll find a mass, but you may not find it as a hanger from the liver as a DD for a gallbladder cancer.
So, one DD will be GB cancer. Number two would be this >> patellar calcium. cellar and other tumors but it's hard and therefore it's likely to be more neuroplasm malignancy rather than a penile pathology. So can we move on?
>> Can we move on to the next >> just one question please sir?
>> Just one question in in in your >> in your palpation the previous slide please.
No no no palpation palpation on this. So you return there is a 4x3 cm mass. So what is the relation with the liver?
So it is continuous with the mass. The mass was uh the percussion on percussion the mass was continuous with the liver dness >> that you have not mentioned. So I mentioned in a percussion sir >> in palpation it is very important whether the mass is in continuation with the liver or is it arising from the liver or it is different from the liver that you have to defin you have to mention.
>> Okay sir.
>> What is umbilication?
I don't know sir it is seen in the liver secondaries right >> necrosis central necrosis >> central necrosis so whether this is primary liver secondary liver or a gallbladder madam has already told you very nicely so I think we can proceed further with the investigations >> please please yeah so what investigations one so examination over some differentials so what let us see that you want to make a definite diagnosis What's one investigation you'll do to make one diagnosis?
>> Ma'am, ultrasound ma'am. Ultrasound whole abdomen.
>> Answer the whole question doctor.
Ultrasound that's all you'll do only ultrasound. What else will you do along with a Doppler? Always ultrasound is combined with a Doppler.
Ultrasound is always combined with a Doppler. So that in one go you make a complete diagnosis about the invasiveness of the pathology. So now tell us what are the findings you look for in this patient. We do not know what's the case. So what are the things that you look for? U ma'am we look for any liver as well and we'll look for if there is any >> pre when you place the probe no do when you place the probe what's the first thing that you look for in this pat in this patient >> u ma'am uh any leion over the liver and >> doctor first will be IHBR no you'll first moment you place the probe your first thing is you're looking for IHBR dilation >> yes ma'am >> and then you'll trace the IHBR that's the first thing liver of course you'll be seeing you'll look for any So look at the echo texture. You look for surface irregularity and the focus will be on you're already suspecting a case of galler malignancy. So you're looking for IHBR you'll follow it up at the porta you'll follow for the CHD and come down and then what are the things you look for then in the gallbladder >> ma'am?
>> What do you expect in this patient?
>> Um gallbladder thickness ma'am if there is any symmetrical wall thickness >> doctor very definite. You know you have to you're going to be a consultant. So just tell 1 2 3 4 these are the things I look for. I look for the gallbladder mass. I expect calcification which will porcelain calcification which will be irregular which will be interrupted. I I 80% of the patients can have gall stones. So I look for the gall I look for gall stones in these patients. I'll look for the size of the gall stone.
She's a female. One size stone or 1.5 cm means something totally different from multiple stones. I'll also see whether there's an effect of this gallbladder mass whether it's a neck or involving the body and see whether it's infiltrating on the under surface of the gallbladder and whether it's involving the CBD compressing like a miri syndrome all this you'll have to mention >> yes >> supposing this patient did not have when when is a gallbladder not palpable when is a gallbladder not palpable in a gallbladder >> uh ma'am uh when there is uh if there is any chronic uh because of chronic uh choleicit is patient the gallbladder gets >> number one number two number two it is under surface of the gallbladder under surface of the liver so the gallbladder is on the under surface of the liver there's a surface marking in the GB fossa you'll not get one one important differential diagnosis you've not discussed can it be XGC zanthropus policy you've not discussed that at all I say it's XGC it can be it can be you tell me now can it be XGC >> yes ma'am >> it's a very important DD what how will differentiate XGC from GB cancer >> ma'am clinically it is very hard to defiate between uh GBC and >> therefore becomes an important differential diagnosis in your clinical examination so on ultrasound how will you know it's XGC or it is uh GB cancer >> um >> what are the characteristic features of XGC versus gallbladder cancer >> gallbladder cancer will have lymphopathy and there will be uh in uh uh right now we not don't have much time see that you have a table distinguishing HGC from ga cancer so you look for all these things so what do you expect in this patient so what was the finding can we have the findings and then you'll trace the CBD you'll trace the spenicquin you'll see the spleen you'll see the pancreas is normal we'll see for nodes and the porta all these things you'll have to mention okay we're not suspecting pancreatic malignancies so therefore did not discuss about the other signs that you look for. So can you just tell now?
>> Uh >> what are the findings?
>> On ultrasound all abdomen liver was 17 cm. Enlarge multiple hypoquic to hyperquake uh leion were seen in bilateral livelop. Largest measuring 10 10 + 9 mm in left lobe and 14 + 10 mm in right lobe. GB was partially distended.
A hyperquic calculus was noted in GB neck. Asymmetrical GB wall thickening in epatic surface with ecoenic mass like infiltration in uh surrounding liver segment 4B and five. CBT was not dilated and no free fluid impression free of GB mask leion with infiltration adjacent liver segment and liver metastasis.
>> What's your take?
>> Uh ma'am it is uh Gas.
>> This is what I said. So this is the same thing what I said the fossa no in the gall for fossa involving the 4 A and 4 B.
>> Yes ma'am >> that's a bed that's the port hypatis bed. So what is your what is your diagnosis now? Complete diagnosis >> stage. What's the stage of the disease?
uh stage uh ma'am uh three ma'am.
>> What three is already gone? Metastasis in the liver. No.
>> Yes ma'am. Stage four ma'am. This is an advanc advanced gallbladder cancer. No, it's advanced gallbladder malignancy and there's a background of a stone. That's what I said. See that 1.5 cm?
>> Yes.
>> Okay. So, can we ask some questions on this? So, what are the risk factors for gallbladder cancer? What can you do you know of any regional differences in gallbladder cancer across the country?
>> Excuse me, I didn't hear ma'am.
>> What what any regional differences in gallbladder cancer across the country?
Um ma'am >> madam is wanting to ask you what are why there is a geographical variation in the incidence of GBC in India.
>> Uh it is because of uh uh compounds like uh secretion of uh like mustard contamination. You know I'm not asking you the causes I'm asking you is there a regional difference do you know of the epidemological studies of gallbladder cancer >> in gangic belt ma'am >> I don't know what's a gangic belt doctor I'm asking you what are the areas where you have huge amounts of gallbladder cancer and where is it not known or hardly seen which portions of the country where parts of the country where you hardly see gallbladder cancer and why have you read us duta's papers Well, have you read my paper? So, by the way, you understand? So, down south, they're all pigment stones. 90% are pigment stones. Cholesterol gallstones are just about 2%. Whereas in north and northeast, they're all cholesterol. Most of them are cholesterol or mixed stones.
So, cholesterol constitute 60% and 20% and pigment stone is just 2%. Bile in northeast and northern parts of the country are all lithogenic. So, gallstone gallbladder cancer is very high. So any patient gallstone disease in north India we are justified in doing a chyctomy because association of gallbladder stone with cancer is there but it's not we don't say that stone causes cancer we're not saying that but if you take gallbladder cancer 80% will have stone disease okay >> so you must please read the regional differences pre read duta's paper you must know the regional differences in the gall so down south if I get a case of obstructive jaundice gallbladder cancer will never come in my differential Whereas in North India if you get a case of obstructive jaundice number one investigation is gallbladder cancer. Okay. These are my important messages of this case. Sir please take over sir.
Just one thing that I wanted to pointed out that you are in inspection you have not mentioned the left supraular region.
>> Yes sir I have mentioned in general physical examination sir. You have mentioned in general physical examination. Okay.
Okay. Fine. So now what other investigation you have gone for? Now how will you plan the management of this patient? You you have got a CT scan.
>> Yes sir.
Uh I have uh done CCT thorax plus abdomen sir. Um on abdomen uh liver enlarge uh size 17.6 and 6 cm. There was multiple illdefined hetrogenously enhancing leion were noted largest measuring 9 cross 8 mm in segment 4A likely metasis. Um gallbladder was distended GB primary legion uh illdefined heterogenously enhancing mass lesion of size 2.5 + 3.6 6 + 3 cm involving gallbladder fundus and body associated with asymmetrical enhancing mural thickening maximum thickness 9.5 mm extending from fundus body neck of gallbladder to involving cystic duct uh common duct and CBD maximum caliber of CSD 4.7 mm and so what is what is the staging after your CT scan is done the final staging sir it is metastatic advanced GB sir How should you treat this patient?
>> Uh ma'am >> this is the patient. How will you treat?
What treatment options you have?
>> Since it is a metastatic case ma'am, we will go for uh biopsy ma'am. Uh we'll go for um biopsy from the legion and chemotherapy palative chemotherapy.
>> Tell details of the treatment. Doctor tell details of the treatment.
What was the binarin level? What is the liver function test? Give us some information. What are the tumor markers?
>> Um liver function ALP was elevated 195 and CN 999 was 10,000 and CA was 59.2 2 nanog per ml or the parameter was normal.
>> So you do a tissue biopsy and what will be the drug of choice for chemotherapy and what will be the survival benefit?
>> What will be the patient asks you what's the survival >> and patient has got loss of appetite and weight. So how should we manage that loss of >> Yes ma'am. uh we first uh we'll go for biopsy and after biopsy we we can plan for uh gem setabin based therapy ma'am patient is already having loss of appetite so how will you treat her how will you feed her >> u all this you have to know patient is there in front of her patient says I'm not I'm not worried about the pain you give me some pain reliever but I want to eat so how will you manage The patient will this patient will go straight to the oncology department. No, the patient would they will not come to the surgical side because the surgical option is not there.
>> Yes, ma'am.
>> Anyway, this case is not operable. So, the questions will not this case may not come to you except up to the examination. you know they'll ask you up for examination and then they'll just say most probably you'll just say that I'll be referring the case to the oncologist who will take charge of it the patient is inoperable and it's not a candidate for surgery so some of you can ask some questions on surgical aspect of gallbladder cancer sir then we can conclude >> so are you suppose it was a localized disease to the gallbladder and there were no liver metastasis right >> yes sir >> so then how will you have managed this uh if it was not localized uh and it was found to be reectable we can go for a radical choleiccystectomy in this patient.
>> So what do you mean by radical choleicyctomy? Uh radical colctomy is uh envelop uh removal of or invoke resection of gall bladder with uh segmental restriction of 4B and five of liver segment with uh hepatitudinal ligament uh uh and and have to cable lymph sampling.
>> So with lymph along ligament right?
>> Yes sir.
>> Okay. So what are indications of bile duct excision during radicalis technique? uh if it is uh uh involving CBD sir if there direct invasion of CBD and if there is if the cystic dock margin comes out to be positive during frozen section and um if there is any uh uh cystic if the legion is in uh cystic duct which is infiltrating into uh CBD sir >> what are the other indications Uh if there is uh any highlighter infiltration sir >> suppose there is a large nal burden along the >> chain there is any yes sir >> right >> yes sir >> and suppose it is associated with primary celling Colitis or abnormal pancreatic bilary duct junction or collidocalysis. Would you like to excise duct or not?
>> Yes sir.
>> And in many cases of papillary variant of carcinoma gallbladder also there is an indication of duct taxision as there might be a tumor thrombi if not microscopic microscopic tumor thrombi may be there in the bite. Right?
>> Yes sir.
>> Okay. Suppose you are doing a sampling from prioritic group of employee level 16 V1 right they come out to be positive on per of frozen section study. So what you will do?
>> So we'll abandon the processor because it will be considered metastatic at that time sir.
>> Okay.
So what is the role of uh non anatomical or vection of liver versus anatomical resection?
So um it has been found that anatomical and non-anatomical um anatomical uh non anatomical has there is no extensive cervical benefit if we do anatomical resection of a liver.
Are there any condition you know where you should go for a preferably you should go for an automal uh liver resection during radical choleiccystectomy rather than just taking a 2 to 3 cm of wedge of liver >> um >> what literature has has to say on it sir if there is any Um, >> you can tell him the answer sir.
>> So when the tumor burden is very large, right? And when there is direct infiltration on CT or ultrasound, you can see they are encroaching onto segment 4B and five, right? So then it becomes an indication to do a formal right uh sorry formal segmental or anatomical resection rather than just doing the non anatomical resection.
>> Yes sir.
>> Okay. So what other surgeries you have seen in CAD apart from radical chic?
>> Yes sir. Um if there is uh any invasion along the uh extended radical uh colisctomy.
>> So you can do a right hipctomy or you can do extended right hypertic resection right. Yes sir.
>> What else? But more radical surgery you can actually do in >> particular dutctomy sir.
>> Yeah HP. So have you ever seen that? Uh >> I have not seen it but yeah it had been done here sir.
Okay. So what you doing in hypopenttomy?
It's a very morbid procedure.
>> Yes sir. We'll do extended epidectomy with pancreatic duttomy. Sir tell anastmosis also you have to tell you can't just you cannot just be hanging there. No tell the complete procedure you do panttomy and what are the anesmosis that you do? uh we'll do uh gastro see when you in the in the exam just want to like you're little blunt in your answer just to tell you just to improvise on that so you know just just tell yes I will do this and along with this anastmosis so that the continuum is maintained so what are the anesmosis that you will do >> we'll do gastroenostomy and hypatic desenostomy and desenostomy >> liver you're removing hypatctomy you said know which portion of the liver so let I I do not know anything so you must tell me in such a way that I understand which the anesmosis you're doing.
>> Uh we'll do uh anastmosis with the left apartic duct with the u jun and um gastrogenostomy >> and what happens with pancreatic duct >> and will anastmosis with pancreatic women.
So you believe in a row and y or what is it or you just put one where would you take the loop from the jun >> what's at what level would you pick up the jal loop >> 45 cm 45 to 60 cm ma'am >> from where flex >> you have to tell it no answer in a proper way 45 cm from where >> from DJ flexer we'll take 45 to 60 cm >> 45 to 60 is a huge variation. Okay, we talking of 15 cm more >> 45 cm.
So can so suppos supposeding you're doing a cholicisctomy for a gallstone disease and suddenly you encounter that actually there's a small growth there what would you do on at laparoscopy >> uh ma'am uh if there is uh we uh if it is on posttop and we found out to be >> posttop I'm not I'm not telling you intro >> we'll send for present section if there is any uh if we have any uh apart uh we'll We'll go for we'll try to re we'll abandon the process. We'll go for uh restagasing of the disease. Ma'am >> sir can you just take up that question sir that is incidental you pick up and then what would you do?
>> Yeah uh what do you mean by incidental gallb?
Um um previously we have not thought of uh any GB mal latency but interoperatively we found out to be there is uh GB uh growth and when sending out for present section it came out to be car.
>> So what should you do then?
One is you cannot just take over this.
You have to tell the relatives standing outside. No outside the relation will be waiting and sus you suspected XGC and then it turns out to be got a malignancy. So what would you do on the table?
>> Uh ma'am we look for uh reectability if the legion is reectable or not. Ma'am >> how would you know that? How will you do you done it's a gallstone surgery you've gone in for a planned polycyctomy and suddenly you land up with this finding.
So what would you do?
Do do every patient with gallstone disease require a CT scan for staging?
>> Um they can go for PET CT ma'am.
>> CT no doctor this is on the table I'm telling you I'm telling you on the table you picked up a frozen section is positive sir can you please sir Dr. BMAR and Dr. Amid >> hi what is the luck technique or SGPJ technique proposed by Dr. VK capur for such eventities >> we can go for anticipator chic extended chystectomies >> so what do we do during that u we will remove gallbladder with 2 cm with resection of liver >> what about lymph nodes >> uh if the uh GB come out to be negative then uh we'll consider for ext if it is come out to a procedure then we'll further take out the lymph nodes Sir, >> so how many minimum number of lymph nodes you should harvest to call it as a surgically safe radical coristically?
>> Six minimum six lymph nodes sir.
>> Okay. So what are the salient differences between the ACC 7th edition and ACC 8th edition for gallbladder cancer staging? Uh sir uh in seventh edition in seventh edition there was uh uh based on location and on the uh 8th edition uh it is based on number of lymph nodes sir.
On seventh uh N1 uh it involved perodical celiac uh lymph nodes and on uh addition there was uh N1 less than one to three lymph nodes.
>> Okay Dr. Kit you want to ask him some question.
No, I think we have discussed much and at PG level he has answered I think very nicely and uh uh I think with the permission of ma'am we can ma'am you can please conclude.
>> Concluded Dr. Kak you can take over and conclude the session.
>> Yes. Yes ma'am. Yes ma'am. Thank you very much. Uh Dr. Aayush at this point of time uh what do you think is the longevity of the patient?
uh sir less nearly 6 months or less than 6 months.
>> So considering the newer norms where people believe in patient comfort levels and the patient reported outcomes know like be sensitive to the pain and other things. So what are the typical progression do we expect in this patient that is what is the end point? No what is the disease progression and what takes over or heads to the patient towards death.
Um so mostly uh patient will go under uh if the disease uh extends they can go under obstruction and >> okay >> for which we can do paliative uh maneuver also and if the uh this can involve uh okay I will make life easier for you as an examiner what I expect from you is see paliation have to be to alleviate the symptoms what the patient progresses towards death. Here number one, first thing is the disease compressing the bery tract that is a local effect and the disease once it reaches the cerosa it becomes very rapidly transparial spread where it spreads into both paronium as well as to the bowel cerosa and to the other organs. So technically the first thing is subsection to the ber tree. The second thing is subsection to the remaining part of the GI tract.
>> Yes sir.
>> Third thing is as the patient disease spreads out of the it becomes T4 the keexia grows up because the tumor volume grows multiffold higher than the primary volume the metastatic load becomes very high. So once the metastatic load becomes very high the anorctic components the cactic components secreted by the tumor load becomes a major thing. So generally speaking these patients go for sort of a bedriddenness very rapidly become gumolic state because nothing gets absorbed first of all no appetite number two no ber no entropatic circulation possible and the bowel gets rapidly accumulated by the tumor cells if and if very few publications are coming in what is the most recent I won't tell decent like quite some time it is there. Other consideration will you invasive laparoscopic procedure for a time being delay or extension of the lifespan of this patient? In simple words, can you tell what is the role of pipac in this patient? Is there a role at all?
>> Yes sir. What sir? I could not hear you.
>> Sorry ma.
>> What is the role of sir? Pipac P I P A C >> Sorry sir I don't know >> no problem. Uh for the students sake Pipac is a terminally ill patients where you have extensive peronial carcinomtosis in simple words peronial carcinomatus indices plus of eight people should go and read about what is paronial carcinomosis index. So in patients who has colorectal cancer, liver cancer per se or any malignancy, abdominal intraparital malignancy including if it is a lady consider even genital malignancies also in incurable advanced disease where the patient is having reasonable performance status. We don't talk about PS5, we are talking about PS2 and three. If they have patient has performance status good performance status it is a single port laparoscopic procedure where you do a intraaronally aerosolized chemotherapy that is called as the pipack right so it gives an aerosol depending on sing what is the origin of the cell here the role of uh monoconals and other imunotherapy have to be considered that is the only reason you may require a biopsy where you will understand what are the subm molecules you can extend the lifespan.
Please understand extend the lifespan.
Here the most important things which are considered are the PDL1 and the EGFR and VHF. Now SD4 or SD10 are the newer molecules which are being considered. See please note these things show survival increase by 15 days, 30 days like that. But the cost of therapy if you are considering it runs to $10,000 to $20,000 per injection.
So for all reason for scientific discussion you should be aware of these therapies. But for practical reasons in the country like us where the resources are limited you should be aware of such therapy existing but the multi-disiplinary board does not accept these therapies for practical regular use for these patients.
Number two, if and if you are going to alleviate with Pipac, Pipac works well for metastatic gastric cancer, metastatic coloral cancer where you have they they have shown even gastric cancer with liver metastasis patient with PCI up of 18. The recent publications have shown a lifespan of up till 1 year. They are showing more than one year survival status for gastric cancer.
Unfortunately, gallbladder is still not accepted as a regular patient use.
Limited center studies have shown very very meager increase in the lifespan.
So, pipac is not recommended but pipac is an option for increased paritonal costsis especially in patients who has good performance status. Unfortunately, gallbladder cancer patients do not maintain that good performance status even for few months. They become rapidly sick. All right. So most importantly what happens is they develop rapid tumor thrombosis or portal vein thrombosis immediately causing sort of a like emergency portal hypertension. So patient becomes pymic portal pymia sets in very rapidly and hence the gap junctions widen. So patient gets into a systemic sepsis very rapidly whereas in colctal metastasis and other metastasis patient don't deteriorate this fast but many times it is a block of the portal hypertension and systemic spread of the gap junction induced septic anorobic sepsis into the uh system.
These patients become unconscious or become like what to say hypoc consciousness that's what we say in malignancy where the patient rapidly goes into a phase of sepsis and dies of all right these are the things you should have in mind but then I would recommend you to go back to devita and read natural course of progression of death will be a common question whenever you are talking about a malignancy say in gastric cancer how a patient dies in liver cancer how a patient dies If you see that timelines you will be able to understand and you will know what are the potential interventional endoscopic radiological intervention endotherapy or surgical therapy and then guide the way guide the or godge the situation and many times CAGB is a very mortal as of now one of the very highly mortal disease is CAGB. So your question will be p valuation in CAGP. If there is a question you should have a clear path to answer the question. You valid 10 points. I will elevate the jaundice. I will try to increase the longevity of this patient. Only these two things and you also mention what all things the role of supportive therapy. There'll be one big question asked how do you maintain nutrition in these patients.
Many times you end up placing a nasogenal tube and that is all you can do because to an extent at least elemental nutrition can go in.
All right. The next question is what is the quality of life very poor quality of life. So end of life support therapies have to be arranged for these patients.
P spices have to be arranged for these patients and a frank discussion with the family members have to be informed in like you take them along with when you're doing your multi-disiplinary discussion that's the best place to do they can vent their feelings they can ask more difficult questions in the presence of cross specialy experts and please document everything in clearly and then as madam said it is prudent we hand over to the palative group of oncologists where what possible they cannot all Right. So this will be a overall cover but in general metastatic gallbladder cancer what are the treatment options? It'll be a short note question for you number one. And then progression of the events and newer therapies have to be considered as a short note. So SD 10, SD4, EGFR VGF PDL1 therapies have to be considered as the armamentium as a rescue. It is not a primary therapy. as a rescue some form of treatment response you hold certainly you don't aim for any cure in this patient if you can I would say reduce the rapidity of the tumor load or reduce the speed of tumor doubling time to 10% or 20% you are winning in this type of metastatic cancers all right yes sir so these are the word of uh things but again go back to read devita devita gives a very clear timeline how this tumor progresses. The other thing is Bloomgarts is the next textbook to go back. I'm sure your department has a copy of it. So go for the treatment endstage care for CAB bladder. There is a full chapter on it.
Please go and update yourself about the recent updates of the therapy. The last thing I would recommend is whenever you're coming for a presentation, please read the most updated NCCN version. NCCN version gives it does not read only about the surgery. It gives about endotherapy, interventional therapies, imageguided intervention as well as the pure form of paliation. So gallbladder was updated as late as this early January 2026 NCCN guideline. I wish you go through that whenever you're coming for the presentation. Please upgrade yourself knowledge on NCCN and then come and speak with NCCN basis. You have a focus that is a one-stop access for all the information.
>> So Dr. Kaku, there's an ICM or consensus. Okay. There's an ICMR Indian consensus.
>> Yeah. Indian consensus. You should know ICMR ICMR consensus on management of galler cancer.
>> There is IHPVBA consensus mam actually IHPB and Asia Pacific HPV consensus guidelines.
>> Yeah, there's one other I've read ICMR consensus by uh from Jesus hospital I think one of the surgeons has written it.
Thank you. Can we >> Thank you. Any other questions ma'am?
Can we call a close?
>> Yeah, please.
>> Are you?
>> Yes.
>> Amit sir and K sir?
>> Yes we can close.
>> Thank you very much. Thank you very much for all of you and thank you very much for staying sir. Thank you very much.
Good night sir. Good night everyone.
Thank you madam. Good night. Good night.
Thank you. Thank you. Thank you. Thank you.
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