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Microscopic colitis is one of the most commonly missed causes of chronic watery diarrhoea, largely because the colon looks completely normal during colonoscopy. The diagnosis only shows up when biopsies are examined under the microscope, which is exactly why patients spend months labelled with IBS before anyone takes the tissue samples that reveal what’s actually going on. According to Dr. Vipulroy Rathod, Gastroenterologist in Mumbai, “The trap with microscopic colitis is that the scope looks clean, so it’s easy to reassure the patient and send them away with an IBS label. But if you don’t take biopsies from a normal-looking colon in someone with chronic watery diarrhoea, you miss it entirely. The biopsy is the whole diagnosis here, not the colonoscopy view.” What Are the Symptoms of Microscopic Colitis? The presentation overlaps heavily with IBS, which is a large part of why it goes undiagnosed for so long. Chronic watery, non-bloody diarrhoea is the defining symptom, often persisting for weeks or months, and unlike IBS it frequently wakes patients at night rather than settling when they rest. Abdominal pain and urgency come alongside it. The urgency in particular can be severe enough to disrupt work and daily routine well beyond what the diarrhoea alone would suggest. Fatigue and weight loss appear in a meaningful proportion of patients as the ongoing diarrhoea affects nutrition and hydration, and these features push the picture away from simple IBS toward something that genuinely needs biopsy confirmation. It’s more common than most expect in older women, with the risk rising notably after 50 and a clear female predominance, particularly for the collagenous subtype, which helps flag who should be biopsied even when the scope looks unremarkable. Distinguishing this from other colitis types on tissue is exactly what a specialist in IBD management does when the clinical picture points toward inflammatory rather than functional bowel disease. How Is Microscopic Colitis Diagnosed and Treated? The gap between a normal-looking scope and a positive biopsy is where this diagnosis is won or lost. Colonoscopy with biopsies is non-negotiable. The mucosa looks normal to the eye, so multiple biopsies taken from different segments of the colon are the only way to confirm lymphocytic or collagenous colitis, and skipping them in a patient with chronic watery diarrhoea is the single commonest reason the diagnosis gets missed. Stopping the drugs that trigger it often improves symptoms on its own, because NSAIDs, PPIs, and certain antidepressants are strongly linked to microscopic colitis, and reviewing the medication list is one of the first and most useful steps. Budesonide is the mainstay of treatment, a steroid that acts largely within the gut with limited systemic absorption, and it produces symptom remission in the majority of patients who take a proper course, though relapse after stopping is common enough that some need repeated or maintenance therapy. Refractory cases have further options. Bile acid binders help when bile acid malabsorption coexists, and immunosuppressants are reserved for the small group who don’t respond to budesonide, which is where specialist management genuinely changes the outcome. Telling microscopic colitis apart from the more familiar inflammatory bowel diseases matters because the treatment and prognosis differ. Read more on Crohn’s vs colitis to understand how the different colitis types are distinguished on colonoscopy and biopsy. Why Choose Dr. Vipulroy Rathod for Microscopic Colitis? Dr. Vipulroy Rathod has been diagnosing and treating colitis in all its forms at Fortis Hospital Mulund for over 30 years, and the instinct to biopsy a normal-looking colon in the right clinical context is exactly the kind of judgment that comes from scoping tens of thousands of patients. Those referred after months of an IBS label often finally get a microscopic colitis diagnosis and effective treatment here. Physicians from 35 countries have trained under his approach at Fortis. Book your consultation today with one of India’s most experienced specialists for microscopic colitis diagnosis and treatment. Book Appointment Call now Frequently Asked Questions What is microscopic colitis? It is a chronic inflammatory condition causing watery, non-bloody diarrhoea. The colon looks normal on colonoscopy, so diagnosis relies on biopsy showing inflammation. What are the symptoms of microscopic colitis? The main symptom is chronic watery, non-bloody diarrhoea, often with abdominal pain, urgency, fatigue, and sometimes weight loss. How is microscopic colitis diagnosed? It requires colonoscopy with multiple biopsies, because the colon appears normal and only microscopic examination confirms lymphocytic or collagenous colitis. How is microscopic colitis treated? Treatment usually starts with budesonide and stopping triggers like NSAIDs and PPIs, with bile acid binders or immunosuppressants used in refractory cases. Reference Microscopic Colitis: Pathogenesis and Diagnosis — NCBI/PMC, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10342440/ Chronic Diarrhoea Owing to Microscopic Colitis: Diagnostic Challenges — NCBI/PMC, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11507306/

Barrett’s oesophagus is what years of unchecked acid reflux does to the lower oesophageal lining. The normal cell type is replaced by intestinal-type cells that carry a higher cancer risk, and the patients who end up with oesophageal adenocarcinoma are almost always the ones who either didn’t know they had it or didn’t follow through on surveillance. According to Dr. Vipulroy Rathod, Gastroenterologist in Mumbai, “Barrett’s is a condition where the risk is real but manageable, and the patients who end up with oesophageal cancer are usually the ones who either didn’t know they had it or knew and didn’t follow through on surveillance. The endoscopic tools we have now let us treat dysplasia before it becomes invasive, but only if we find it in time.” How Is Barrett’s Esophagus Diagnosed and Managed? Everything runs through the endoscope, and the biopsy result is what sets the entire surveillance and treatment plan. A scope and biopsy is the only way to confirm it. No blood test, no scan, and no symptom pattern can tell you whether the lining has changed, which is exactly why high-risk patients with years of reflux need at least one scope regardless of how manageable their symptoms feel. When no dysplasia is found, surveillance every three to five years is evidence-based and not as infrequent as it sounds, because progression in the absence of dysplastic change is genuinely slow and the annual cancer risk is very low. Low-grade dysplasia sits in more uncomfortable territory because the risk of progression is real enough that some gastroenterologists recommend ablative treatment at this stage rather than tighter surveillance, and that conversation needs a clinician who sees enough Barrett’s to read the individual picture rather than applying a generic protocol. High-grade dysplasia gets treated. Radiofrequency ablation combined with EMR removes the abnormal segment through the scope, without surgery and with outcomes that compare well to resection for appropriately staged early disease. A specialist in oesophageal cancer manages the step from surveillance into active treatment when dysplasia reaches the point where watching is no longer the right call. Why Does Barrett’s Oesophagus Develop? Acid doesn’t have to produce severe symptoms to damage the oesophageal lining, and the change from normal to Barrett’s often happens quietly over years. Long-standing GERD is behind most cases. Duration matters more than severity, and patients with a decade of reflux on and off PPIs often have no idea their lining has changed because the symptoms haven’t told them anything useful. The risk is much higher in men over 50. That demographic profile, combined with longstanding heartburn, is the combination that most clearly calls for a screening scope before waiting for something worse to develop. Central obesity worsens acid exposure at the gastro-oesophageal junction and raises Barrett’s risk independently of reflux symptoms, which is why metabolic disease and GERD so frequently appear together in the same patient. Smoking raises the risk, but here’s the twist — it doesn’t always produce more heartburn, so smokers with GERD often underestimate how much their combination of habits is doing to the oesophageal lining versus non-smokers with the same reflux pattern. Knowing when longstanding GERD has passed the point where medication alone is enough is where high-risk patients should be looking. Read more on GERD and endoscopy to understand when acid reflux crosses the threshold that requires direct oesophageal assessment. Why Choose Dr. Vipulroy Rathod for Barrett’s Oesophagus? Dr. Vipulroy Rathod has been diagnosing and managing Barrett’s oesophagus at Fortis Hospital Mulund for over 30 years, with NBI endoscopy and EUS allowing him to detect dysplastic change and assess early invasion with a level of precision that standard white-light endoscopy alone does not provide. Patients referred with longstanding GERD who have never been scoped frequently turn out to have Barrett’s on their first scope, which is the entire argument for not waiting. Physicians from 35 countries have trained under his approach at Fortis. Book your consultation today with one of India’s most experienced specialists for Barrett’s oesophagus surveillance and endoscopic treatment. Book Appointment Call now Frequently Asked Questions What is Barrett’s oesophagus? It is a condition where the normal oesophageal lining is replaced by intestinal-type cells due to chronic acid exposure, raising the risk of oesophageal adenocarcinoma. Does Barrett’s oesophagus always lead to cancer? No. Most patients with Barrett’s never develop cancer, but the condition requires regular surveillance endoscopy to detect dysplasia before it progresses. How is Barrett’s oesophagus treated? Low-grade dysplasia is monitored with surveillance endoscopy, while high-grade dysplasia or early cancer is treated with radiofrequency ablation or endoscopic mucosal resection. Who is at risk of developing Barrett’s oesophagus? Men over 50 with long-term acid reflux, obesity, smoking, and a family history of Barrett’s or oesophageal cancer carry the highest risk. Reference Barrett’s Oesophagus: Epidemiology, Risk Factors and Pathogenesis — NCBI/PMC, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3178260/ Endoscopic Management of Barrett’s Oesophagus and Early Oesophageal Cancer — NCBI/PMC, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6197218/

Stomach ulcers and stomach cancer produce almost identical symptoms, and neither a patient nor a clinician can reliably separate them on history alone. Endoscopy with biopsy is the only investigation that gives a definitive answer, and skipping it because an ulcer looks benign on the scope is exactly how early gastric cancer gets missed. According to Dr. Vipulroy Rathod, Gastroenterologist in Mumbai, “I’ve biopsied ulcers that looked completely benign on the scope and come back as cancer, and I’ve seen lesions that looked worrying turn out to be purely inflammatory. The appearance tells you something but never enough. A biopsy is the only way to know, and skipping it because an ulcer looks benign is exactly how early gastric cancer gets missed.” How Do They Differ? Shared symptoms and a common bacterial cause make these two conditions harder to separate clinically than most patients realise. Factor Stomach Ulcer Stomach Cancer Primary cause H. pylori, NSAIDs, acid H. pylori, dietary factors, genetics Typical patient Any age, often younger More common over 50 Endoscopic appearance Clean edges, heals with treatment Irregular edges, raised borders Response to treatment Improves on PPIs Does not resolve with acid suppression Biopsy result Inflammatory or H. pylori Malignant cells An ulcer that heals cleanly on PPIs and H. pylori treatment is almost certainly benign, but a follow-up scope to confirm healing is not optional; a cancer masquerading as an ulcer can appear to partially improve while continuing to grow underneath. Irregular or raised edges, no response to treatment, or a recurring ulcer at the same site all push the picture toward malignancy, and each warrants repeat biopsy rather than another course of acid suppression. Unintended weight loss alongside an ulcer changes the clinical urgency entirely. Benign ulcers cause pain and nausea but rarely drive weight loss, and that combination needs a cancer workup, not more time on omeprazole. H. pylori sits behind both conditions, directly causing most benign ulcers and also functioning as the strongest modifiable risk factor for gastric cancer, which is why treating the infection matters regardless of which way the biopsy goes. Accurate tissue diagnosis is the starting point, and a stomach cancer specialist builds the workup around that from the first appointment. When Should You See a Specialist? Certain presentations demand a scope rather than a longer trial of medication. Persisting pain beyond two weeks on a PPI is not an indication for a stronger PPI, it’s an indication for endoscopy and biopsy before continuing to treat something whose cause hasn’t been confirmed. If the patient is over 50 with new upper GI symptoms, going straight to endoscopy rather than empirical treatment is the safer default, because the prior probability of malignancy at that age makes skipping the scope a meaningful clinical risk. Vomiting, unexplained anaemia, or a palpable abdominal mass alongside upper abdominal pain are red flags that point well away from a simple peptic ulcer and need urgent investigation in days not weeks. Known H. pylori infection with new stomach symptoms lowers the threshold for scoping regardless of how mild the presentation seems, given the dual role the infection plays in both ulcer and cancer development. Understanding why endoscopy answers questions that CT can’t is useful here. Read more on endoscopy vs CT to understand why a biopsy from a scope changes the diagnosis in a way no CT scan can replicate. Why Choose Dr. Vipulroy Rathod for Stomach Conditions? Dr. Vipulroy Rathod has been diagnosing and treating both benign and malignant stomach conditions at Fortis Hospital Mulund for over 30 years, with NBI endoscopy and EUS forming a core part of his upper GI practice for picking up early gastric cancers that standard white-light endoscopy misses. Patients referred after months of PPI treatment for a presumed ulcer often arrive with an early gastric cancer that a timely biopsy would have found sooner. Physicians from 35 countries have trained under his approach at Fortis. Book your consultation today with one of India’s most experienced specialists for stomach ulcer evaluation and gastric cancer diagnosis. Book Appointment Call now Frequently Asked Questions How do doctors tell apart a stomach ulcer and stomach cancer? Endoscopy with biopsy is the only reliable method. Appearance alone can be misleading, and all gastric ulcers should be biopsied to rule out malignancy. Can a stomach ulcer turn into cancer? An ulcer itself does not directly become cancer, but H. pylori infection causes both, and chronic untreated mucosal inflammation raises gastric cancer risk over time. What are the warning signs that point to stomach cancer over an ulcer? Progressive weight loss, persistent vomiting, anaemia without obvious bleeding, and pain that does not improve with ulcer treatment all raise concern for cancer. Does H. pylori cause both stomach ulcers and cancer? Yes. H. pylori is the leading cause of peptic ulcers and the most significant risk factor for gastric cancer, so eradication is recommended in all infected patients. Reference Helicobacter Pylori and Gastric Cancer: Epidemiological Evidence and Proposed Mechanisms — NCBI/PMC, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5561585/ Distinguishing Gastric Ulcer from Early Gastric Cancer by Endoscopy — NCBI/PMC, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3950611/

When a foreign object gets swallowed or stuck in the GI tract, the endoscope is almost always the first and only intervention needed. A flexible camera goes in through the mouth or, in colonic cases, from below, locates the object under direct vision, and retrieves it using tools passed through the instrument channel without a single cut. Around 80 to 90% of swallowed foreign bodies pass spontaneously, but the ones that don’t, particularly sharp objects and batteries in the oesophagus, need prompt endoscopic attention. According to Dr. Vipulroy Rathod, Gastroenterologist in Mumbai, “Button batteries are the ones that keep me up at night. They can cause severe oesophageal burns within two hours of impaction, and families often wait and watch before coming in. Everything else can usually wait until morning. A battery stuck in the oesophagus cannot.” How Is the Procedure Performed? The technique adapts to the object, and the endoscopist’s toolkit covers most situations the scope can reach. Rat-tooth forceps, snares, and retrieval nets are the standard tools, chosen based on the object’s shape and surface something smooth and round needs a net, something flat or fragmented needs forceps, something lodged in a narrow segment needs a snare. For sharp objects like fish bones or razor blades, an overtube is placed over the scope before insertion, so the sharp edge can be drawn into the tube during withdrawal and pulled out without tearing the oesophageal wall. Coins and food boluses sitting in the oesophagus are among the most common presentations and usually come out cleanly in a single pass, with the procedure over before the patient has fully woken from sedation. Button batteries need a different urgency entirely. Once confirmed on X-ray as sitting in the oesophagus, they go straight to emergency endoscopy, and the retrieval technique prioritises speed over everything else. Once the object is out and the mucosa inspected for damage, a specialist in foreign body removal assesses whether any secondary treatment is needed for burns, lacerations, or perforation risk before discharge. What Affects the Outcome? Most removals go smoothly, but a few variables shape how straightforward or complex the procedure turns out to be. Time matters for batteries and sharp objects. The longer a battery sits in the oesophagus, the more tissue damage accumulates, and a delayed presentation that might have been a clean removal becomes a mucosal repair case. Location changes the technical difficulty. Objects in the oesophagus are usually more accessible than those in the stomach or small bowel, and deeper objects that have passed the pylorus are monitored conservatively unless they’re sharp or causing symptoms. Object characteristics determine tool selection. A smooth marble and a jagged piece of bone require different retrieval approaches, and misjudging the grip means the object slips and has to be repositioned, adding time and procedural steps. Perforation risk rises with attempted passage of sharp objects through narrowed segments or around bends, which is why imaging before endoscopy helps map the position and decide the safest route of withdrawal. Understanding how endoscopy functions as both a diagnostic and treatment tool helps put foreign body removal in context alongside its other roles. Read more on role of endoscopy to see how the same flexible scope that retrieves foreign bodies also diagnoses and treats a wide range of GI conditions. Why Choose Dr. Vipulroy Rathod for Foreign Body Removal? Dr. Vipulroy Rathod has been performing therapeutic endoscopy at Fortis Hospital Mulund for over 30 years, including complex foreign body retrievals involving sharp objects, impacted dentures, batteries, and oesophageal food boluses. That experience means difficult cases, including those referred after failed attempts elsewhere, get handled with the technique and judgment the situation requires. Physicians from 35 countries have trained under his approach at Fortis. Book your consultation today with one of India’s most experienced specialists for endoscopic foreign body removal and therapeutic endoscopy. Book Appointment Call now Frequently Asked Questions How does endoscopic foreign body removal work? The endoscopist passes a flexible scope into the GI tract, locates the object under direct vision, and retrieves it using forceps, a snare, or a basket without any incision. Which foreign bodies need urgent removal? Button batteries and sharp objects in the oesophagus need removal within hours due to the risk of burns, perforation, and serious mucosal injury. Is endoscopic foreign body removal safe? Yes. It is minimally invasive, performed under sedation, and avoids surgery in the vast majority of cases, with complications being uncommon in experienced hands. What if the foreign body cannot be removed endoscopically? Surgical removal becomes necessary when the object is too large, too deeply embedded, or inaccessible, though this is needed in fewer than 5% of cases. Reference Overtube-Assisted Foreign Body Removal: A Review of Endoscopic Management — NCBI/PMC, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5707170/ Removal of Foreign Bodies in the Upper GI Tract: ESGE Clinical Guideline — Endoscopy/PubMed, https://pubmed.ncbi.nlm.nih.gov/26862844/

Colonoscopy reaches the colon and terminal ileum well, but a large stretch of small bowel between those two points stays largely invisible to it. The gap capsule endoscopy fills a camera the size of a pill that the patient swallows, which transmits images of the entire small bowel to a recorder worn around the waist. In IBD, particularly Crohn’s disease, it’s this segment that gets missed most often and investigated last, which is exactly where the capsule changes the clinical picture. According to Dr. Vipulroy Rathod, Gastroenterologist in Mumbai, “Capsule endoscopy picks up small bowel Crohn’s disease that colonoscopy and CT scans have both missed. Patients who’ve had unexplained anemia, weight loss, or abdominal pain for months with normal previous investigations often get a clear answer from a capsule study that nobody thought to do earlier.” When Is Capsule Endoscopy Used in IBD? Four situations in IBD practice consistently push the clinical decision toward a capsule study. Suspected small bowel Crohn’s with negative colonoscopy is the clearest indication. Up to 30% of Crohn’s patients have disease limited to the small bowel, and the capsule reaches those segments with a diagnostic yield that beats both CT and barium studies. Monitoring mucosal healing after treatment matters more now that deep remission is the target in Crohn’s management, and the capsule gives a direct mucosal view of segments that no external imaging assesses with enough resolution to count. Obscure GI bleeding in a patient with known IBD often points toward small bowel involvement, and when upper and lower endoscopy come back clean, the capsule is the next logical step rather than another round of cross-sectional imaging. Assessing post-operative recurrence after bowel resection in Crohn’s disease, particularly at the neo-terminal ileum, is a setting where the capsule adds detail that colonoscopy alone doesn’t provide for segments proximal to the anastomosis. These decisions sit within the broader framework of endoscopic IBD management, and a specialist in IBD management weighs which investigation fits the patient’s specific presentation. What Are the Limitations and Risks? Capsule endoscopy is powerful but not without conditions that limit its use. Capsule retention is the main risk. If the bowel is narrowed by a stricture, the capsule can get stuck, and a patency capsule or cross-sectional imaging beforehand checks whether the passage is clear enough to proceed safely. The capsule cannot take biopsies or treat what it finds, so any suspicious lesion it identifies still needs a follow-up procedure to sample tissue or deliver therapy. Bowel preparation affects image quality, and an inadequately prepared small bowel produces images that are harder to read and easier to misinterpret, making patient adherence to the prep protocol essential. Not every patient swallows it easily. Those with known oesophageal strictures or severe dysphagia sometimes need the capsule placed endoscopically rather than swallowed, which adds a step but doesn’t change the imaging itself. Understanding how colonoscopy fits alongside the capsule for IBD diagnosis helps clarify which tool does what. Read more on Crohn’s detection to understand what colonoscopy finds in Crohn’s disease and where it hands over to the capsule. Why Choose Dr. Vipulroy Rathod for Capsule Endoscopy? Dr. Vipulroy Rathod has been using capsule endoscopy as part of his IBD and small bowel practice at Fortis Hospital Mulund for over two decades, and the patients who reach him have often already had colonoscopy and CT without a clear answer. That experience means the clinical picture gets read correctly, the right preparatory steps are taken, and the capsule findings are interpreted in context rather than in isolation. Physicians from 35 countries have trained under his approach at Fortis. Book your consultation today with one of India’s most experienced specialists for capsule endoscopy and IBD assessment. Book Appointment Call now Frequently Asked Questions What is capsule endoscopy? A pill-sized camera swallowed by the patient that travels through the digestive tract and transmits small bowel images to a recorder worn around the waist. When is capsule endoscopy used for IBD? It is used when colonoscopy cannot reach suspected small bowel Crohn’s, when monitoring mucosal healing, or when obscure bleeding points to small bowel involvement. Can capsule endoscopy diagnose Crohn’s disease? Yes. It detects ulcers, erosions, and inflammatory changes in the small bowel that colonoscopy cannot reach, making it valuable for diagnosing and monitoring small bowel Crohn’s. What are the risks of capsule endoscopy? The main risk is capsule retention in a narrowed bowel segment, so patients with suspected strictures are assessed with a patency capsule or imaging first. Reference Capsule Endoscopy for Crohn’s Disease: Current Status of Diagnosis and Management — NCBI/PMC, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4706954/ Capsule Endoscopy Findings for the Diagnosis of Crohn’s Disease — NCBI/PMC, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6394710/

Jaundice, the yellowing of the skin and eyes, signals a build-up of bilirubin that the body isn’t clearing properly. The causes range from harmless and short-lived to genuinely dangerous, spanning bile duct stones, hepatitis, cirrhosis, and cancers of the pancreas or bile duct. What determines how worried to be is rarely the yellowing itself but what comes with it, particularly pain, fever, weight loss, or a change in the colour of urine and stool. According to Dr. Vipulroy Rathod, Gastroenterologist in Mumbai, “Jaundice always needs a cause identified, never just observation. Sometimes it’s a bile duct stone we can clear endoscopically in an afternoon, and sometimes it’s the first sign of pancreatic or bile duct cancer. The difference between those matters enormously, which is why painless jaundice in particular should never be waited out.” What Causes Jaundice in Adults? Jaundice in adults sits in one of three categories, and getting the right one matters because the investigation and treatment differ entirely. A stone sitting in the bile duct backs up into the bloodstream, turns the skin and eyes yellow, darkens the urine, and drains colour from the stool — and unlike most other causes, it can be cleared endoscopically in a single session once identified. What liver disease does to bilirubin depends on how badly the liver is damaged. Hepatitis, cirrhosis, and alcohol injury all reduce how efficiently the liver processes bilirubin, and the jaundice here often comes alongside fatigue, bruising, and other signs that the organ is struggling. Not every jaundice patient has a blocked duct or a damaged liver. Some have increased red cell breakdown, as seen in certain anaemias, which floods the system with more bilirubin than even a healthy liver can clear in time. Pancreatic, bile duct, or gallbladder cancers need naming separately because they block the bile duct silently, and painless jaundice accompanied by weight loss in someone over 50 is a cancer workup until a scan says otherwise. Sorting out which mechanism is behind the jaundice is where a biliary stone extraction specialist runs the right investigation rather than treating on assumption. When Is Jaundice Serious? The yellow skin is rarely what makes jaundice dangerous. It’s what else is happening at the same time. Painless jaundice with weight loss is the most important red flag in GI medicine. No pain does not mean no problem, and this combination belongs in a cancer workup immediately, not in a wait-and-watch queue. Cholangitis is what fever and severe pain alongside jaundice means until proven otherwise, and it’s an infected, obstructed bile duct that can turn life-threatening within hours without emergency drainage. If the urine has gone dark and the stools have turned pale, bile isn’t reaching the gut and something is blocking its passage, which needs urgent imaging rather than observation over a few days. Confusion or drowsiness coming on with the jaundice means bilirubin may be high enough to affect the brain or that liver failure is progressing, and this belongs in emergency care rather than an outpatient queue. Most obstructive causes can now be relieved endoscopically without surgery, often in the same procedure that diagnoses them. Read more on ERCP procedure to understand how bile duct obstruction causing jaundice is cleared endoscopically. Why Choose Dr. Vipulroy Rathod for Jaundice? Dr. Vipulroy Rathod has been diagnosing and treating the causes of jaundice at Fortis Hospital Mulund for over 30 years, with more than 20,000 EUS procedures and extensive ERCP experience behind him. That combination means an obstructing stone or tumour gets identified accurately and, in most cases, relieved endoscopically in the same session rather than through open surgery. Physicians from 35 countries have trained under his approach at Fortis. Book your consultation today with one of India’s most experienced specialists for jaundice assessment and endoscopic biliary treatment. Book Appointment Call now Frequently Asked Questions What causes jaundice in adults? Jaundice comes from raised bilirubin, caused by bile duct obstruction from stones or tumours, liver disease like hepatitis or cirrhosis, or increased red cell breakdown. When is jaundice serious? It is serious with fever, severe abdominal pain, weight loss, or dark urine and pale stools, as these can indicate obstruction, infection, or cancer. Can jaundice be a sign of cancer? Yes. Painless jaundice with weight loss can signal pancreatic, bile duct, or gallbladder cancer blocking the bile duct, which needs prompt investigation. How is jaundice treated? Treatment depends on the cause. Bile duct obstruction is often relieved endoscopically through ERCP, while liver-related jaundice is treated medically. Reference Endoscopic Retrograde Cholangiopancreatography for Choledocholithiasis and Obstructive Jaundice — NCBI/PMC, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12665873/ Evaluation of Jaundice in Adults — American Family Physician/NCBI, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5228380/

Difficulty swallowing, known medically as dysphagia, ranges from a harmless occasional sensation to an early warning of something serious. It can stem from acid reflux scarring, a muscle disorder like achalasia, inflammation, or in the cases that matter most, oesophageal cancer. What separates a benign cause from a dangerous one is often the pattern, particularly whether the difficulty is getting steadily worse and whether solid food is starting to stick. According to Dr. Vipulroy Rathod, Gastroenterologist in Mumbai, “Most patients treat swallowing difficulty as an inconvenience and wait it out, which is exactly the wrong instinct. Food sticking on the way down is never normal, and while the cause is often something treatable like a reflux stricture, it can also be the first sign of an oesophageal cancer that we’d much rather catch early.” What Causes Difficulty Swallowing? The cause behind dysphagia sets both how urgent it is and how it gets treated, and four stand out in clinical practice. Reflux strictures are the most common cause seen in the clinic. Years of acid exposure scar the lower oesophagus into a narrowing, and solid food begins catching where it never used to. Achalasia works differently. The lower oesophageal sphincter stops relaxing, food banks up above it, and patients describe a sensation of something lodged in the chest after nearly every meal. In younger patients with no reflux history, oesophageal inflammation from eosinophilic oesophagitis or infection is often the culprit, making swallowing both painful and difficult. The cause nobody can afford to miss is oesophageal cancer. A tumour narrowing the food pipe produces dysphagia that begins with solids and worsens steadily over weeks, which is exactly why progressive symptoms need a scope. Telling these apart is where an oesophageal cancer specialist directs the right investigation instead of treating on assumption. When Is Swallowing Difficulty Serious? Some patterns shift dysphagia from a nuisance into a red flag, and recognising them early is what changes the outcome. Progressive difficulty is the clearest warning sign. Trouble that starts with solids and marches on to soft foods and then liquids over a few weeks points hard toward a structural cause needing urgent evaluation. Weight loss alongside it changes everything. Dysphagia paired with unintended weight loss is one of the strongest signals of oesophageal cancer, and it should never be managed at home. Food genuinely getting stuck, not just moving slowly, is a mechanical sign of real narrowing, and whether the cause is a benign stricture or a tumour, only direct visualisation separates the two. Bleeding, anaemia, or new chest pain appearing with swallowing difficulty pushes the urgency higher still, and these belong in a timeline measured in days. Serious causes like achalasia now have minimally invasive endoscopic solutions that once required major surgery. Read more on POEM procedure to understand how achalasia and other swallowing disorders are treated endoscopically without open surgery. Why Choose Dr. Vipulroy Rathod for Swallowing Difficulty? Dr. Vipulroy Rathod has been evaluating and treating dysphagia at Fortis Hospital Mulund for over 30 years, across the full range of causes from reflux strictures and achalasia to early oesophageal cancer. His endoscopy and EUS practice means the cause is pinned down accurately and, where possible, treated in the same session rather than referred onward. Physicians from 35 countries have trained under his approach at Fortis. Book your consultation today with one of India’s most experienced specialists for swallowing difficulty assessment and endoscopic treatment. Book Appointment Call now Frequently Asked Questions What causes difficulty swallowing? Reflux strictures, achalasia, oesophageal inflammation, neurological conditions, and in serious cases oesophageal cancer can all cause it, so persistent symptoms need evaluation. When is difficulty swallowing serious? It is serious when progressive, when solid food sticks, or when it comes with weight loss or bleeding, as these can indicate a stricture or cancer. Can acid reflux cause swallowing difficulty? Yes. Long-standing reflux can scar and narrow the lower oesophagus into a stricture, causing food to stick, and can lead to Barrett’s oesophagus over time. How is difficulty swallowing diagnosed? Upper GI endoscopy is the main test, allowing direct visualisation and biopsy, with manometry or barium swallow added to assess motility disorders like achalasia. Reference Dysphagia: Evaluation and Diagnosis — American Family Physician/NCBI, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7233111/ Achalasia: Diagnosis and Management — NCBI/PMC, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6182129/

Diet is one of the few colorectal cancer risk factors a person can actually change, and over the years it adds up. Red and processed meat, low fibre, excess weight, and alcohol all push risk upward across study after study. Fibre-rich eating and a healthy weight pull it back down. None of this guarantees prevention, but among the things within a patient’s control, diet carries real weight. According to Dr. Vipulroy Rathod, Gastroenterologist in Mumbai, “Colorectal cancer isn’t just a screening problem, it’s partly a lifestyle problem, and the dietary patterns that drive it are the same ones driving metabolic disease more broadly. Patients who ask what they can do beyond getting scoped regularly are asking exactly the right question, and diet is one of the most actionable answers.” Which Foods Raise Colorectal Cancer Risk? Few areas of cancer research produce evidence this consistent, and a handful of dietary patterns turn up as risk-raisers again and again. Eating red meat daily raises risk through haem iron and the compounds formed when meat is cooked at high heat, and the link holds across studies from India, Europe, and North America alike. Processed meat is the clearer culprit. Bacon, sausages, salami, and deli meats carry the strongest evidence of all, and even modest regular intake nudges risk upward measurably. Alcohol matters at any level, with the risk climbing steadily the more regularly someone drinks rather than needing heavy consumption to register. Refined carbohydrates and ultra-processed food feed obesity and low-grade inflammation in the colon, and both of those conditions raise cancer risk on their own, which makes this increasingly relevant as Indian diets urbanise. Several of these habits running together over years is what lifts individual risk to a level worth acting on, and a colorectal cancer specialist can weigh that against the rest of a patient’s clinical picture. Which Dietary Habits Lower Colorectal Cancer Risk? The protective side of the evidence is just as solid, and more useful because it’s something patients can act on directly. Eat more fibre. Vegetables, legumes, whole grains, and fruit speed bowel transit and cut the time carcinogens spend in contact with the colon lining, and the association with lower risk is remarkably consistent. If weight is the one thing you change, change that. Central obesity creates the inflammatory conditions that drive polyp formation, and reducing it lowers risk independently of any single food. Keeping red meat to two or three portions a week rather than daily brings the exposure down to a level where the risk link weakens sharply. Adequate calcium and dairy show a modest protective link in several large studies, and building enough calcium into the diet is straightforward within a broadly sensible eating pattern. Diet and gut health overlap well beyond cancer risk, shaping how chronic GI conditions behave day to day. Read more on IBD and diet to understand how dietary choices influence gut inflammation and long-term bowel health. Why Choose Dr. Vipulroy Rathod for Colorectal Cancer? Dr. Vipulroy Rathod has been managing colorectal cancer and its risk factors at Fortis Hospital Mulund for over 30 years, watching the dietary and metabolic patterns behind late diagnoses play out across his referred patients. His colonoscopy and EUS practice means that when dietary risk turns into an actual finding, assessment and treatment happen in the same workup. Physicians from 35 countries have trained under his approach at Fortis. Book your consultation today with one of India’s most experienced specialists for colorectal cancer risk assessment and endoscopic screening. Book Appointment Call now Frequently Asked Questions How does diet affect colorectal cancer risk? Diets high in red and processed meat, low in fibre, and high in refined sugars raise colorectal cancer risk, while fibre-rich plant-based diets and healthy weight lower it. Which foods increase colorectal cancer risk? Red meat, processed meat, alcohol, refined carbohydrates, and ultra-processed foods are consistently linked to higher colorectal cancer risk across large population studies. Can a healthy diet prevent colorectal cancer? Diet alone cannot guarantee prevention, but a fibre-rich diet with limited red meat and no processed meat substantially reduces risk alongside healthy weight and regular screening. Is obesity linked to colorectal cancer? Yes. Excess body weight, particularly central obesity, is an independent risk factor for colorectal cancer through the inflammation it creates in the colon over time. Reference Diet, Nutrition, Physical Activity and Colorectal Cancer — World Cancer Research Fund/NCBI, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6326011/ Red Meat Consumption and Risk of Colorectal Cancer — NCBI/PMC, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4698595/

Balloon dilation widens a narrowed segment of the GI tract by inflating a balloon across the stricture through an endoscope, restoring normal passage without any incision. It’s used in the oesophagus, the small bowel, and the colon depending on where the narrowing sits, and in most cases the patient goes home the same day. What the procedure feels like, how many sessions it takes, and how durable the result is all depend on what caused the stricture in the first place. According to Dr. Vipulroy Rathod, Gastroenterologist in Mumbai, “Balloon dilation is one of those procedures that patients worry about far more than they need to. Done under sedation, it’s usually over in a few minutes and the improvement in swallowing or bowel passage is often immediate. The real clinical question isn’t the procedure itself but how often it needs repeating and whether the underlying cause is being addressed at the same time.” What Conditions Does Balloon Dilation Treat? The technique applies across several GI sites, with the balloon adapted in size to the stricture and the organ being treated. Peptic oesophageal strictures from years of acid reflux scarring the lower oesophageal lining are among the most common indications, and patients who’ve been managing progressive swallowing difficulty often notice improvement within days of the first dilation. In Crohn’s disease, short fibrotic strictures of the small bowel or colon that are causing obstructive symptoms respond well, and the procedure delays or avoids the bowel resection that would otherwise be the only alternative. After bowel or oesophageal surgery, anastomotic strictures at the joint site are a common complication and often need one or more dilation sessions before the narrowing stabilises and swallowing or passage returns to normal. Achalasia-related narrowing at the lower oesophageal sphincter can be opened with balloon dilation, though larger balloons and a slightly different technique apply here compared to a standard peptic stricture. Deciding which stricture needs dilation, how large the balloon should be, and whether the underlying condition needs addressing alongside it is where a specialist in IBD management shapes the whole approach. What Happens During and After the Procedure? Patients often arrive expecting something more uncomfortable than it turns out to be. Under sedation, the endoscope goes in first to visualise the stricture directly, and the balloon catheter is then passed through the scope and positioned across the narrowed segment. Inflating the balloon gradually opens the stricture by stretching it outward, held at target pressure for around a minute before deflation, with the degree of opening assessed through the scope immediately after. Most patients go home within a few hours, feeling mild discomfort or throat soreness after an oesophageal dilation that settles the same day, with diet restricted to liquids for 24 hours as a precaution. Follow-up depends on the cause. Some strictures hold well after one session; Crohn’s-related narrowings and refractory oesophageal strictures often need repeat dilation at planned intervals to maintain the result. Strictures from acid reflux are one of the clearest signs that GERD has gone beyond what medication alone can manage. Read more on GERD and endoscopy to understand when reflux complications like strictures need a scope rather than a prescription change. Why Choose Dr. Vipulroy Rathod for Balloon Dilation? Dr. Vipulroy Rathod has been performing balloon dilation for oesophageal, intestinal, and anastomotic strictures at Fortis Hospital Mulund for over 30 years, across the full range of causes including Crohn’s, peptic disease, post-surgical narrowing, and achalasia. That breadth means the balloon size, technique, and follow-up interval all get matched to the specific stricture rather than applied by rote. Physicians from 35 countries have trained under his approach at Fortis. Book your consultation today with one of India’s most experienced specialists for GI stricture assessment and balloon dilation. Book Appointment Call now Frequently Asked Questions What is balloon dilation for strictures? Balloon dilation widens a narrowed GI segment by inflating a balloon across it through an endoscope, restoring normal passage without surgery. What conditions require balloon dilation? It treats oesophageal strictures from reflux or surgery, Crohn’s intestinal strictures, anastomotic narrowing after bowel operations, and achalasia. How many sessions of balloon dilation are needed? Some patients need one session; others with Crohn’s or refractory strictures need repeat dilations at planned intervals over time. Is balloon dilation painful? Done under sedation, so no pain during the procedure. Mild throat discomfort after oesophageal dilation typically settles within a day. Reference Endoscopic Balloon Dilation for Crohn’s Disease-Associated Strictures — Korean Society of Gastrointestinal Endoscopy, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5642359/ Complex Refractory Oesophageal Stricture and Balloon Dilation — NCBI/PMC, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10305297/

TIPS, transjugular intrahepatic portosystemic shunt, creates a channel inside the liver between the portal and hepatic veins to lower the pressure that builds up in portal hypertension. It’s performed through the jugular vein under imaging guidance, with no open surgery and a recovery considerably shorter than a surgical shunt. The procedure is used when cirrhosis complications, most often variceal bleeding or refractory ascites, stop responding to medical treatment and need a more direct pressure-reduction approach. According to Dr. Vipulroy Rathod, Gastroenterologist in Mumbai, “TIPS isn’t a first-line treatment, but for patients where medical options have run out, it buys meaningful time. The key is selecting the right patient carefully, because TIPS can genuinely worsen liver function in someone whose hepatic reserve is already compromised, and that selection decision matters more than the procedure itself.” What Conditions Are TIPS Used For? TIPS targets the complications of portal hypertension that won’t settle with drugs or endoscopic management. Variceal bleeding that keeps recurring despite band ligation and pharmacotherapy is the clearest indication, where TIPS reduces the portal pressure driving the varices rather than repeatedly treating the varices themselves. Refractory ascites that require repeated paracentesis every few weeks is another strong indication, and TIPS relieves the pressure causing fluid accumulation and reduces the paracentesis burden substantially in suitable patients. Hepatic hydrothorax, fluid accumulating in the chest from portal hypertension, responds to TIPS in selected cases where thoracentesis has become the only management option. Hepatorenal syndrome can sometimes be reversed through TIPS when the pressure reduction restores enough renal perfusion, though this is reserved for carefully selected patients with sufficient residual liver function. Understanding how portal hypertension and liver decompensation interact is where a liver cirrhosis specialist decides whether TIPS is the right intervention or whether another route makes more clinical sense. What Are the Risks and Who Should Not Have TIPS? Patient selection is what separates a good TIPS outcome from a poor one, and the risks are real enough to make that selection non-negotiable. Hepatic encephalopathy is the most common complication, because TIPS diverts blood away from the liver and allows ammonia and other toxins to reach the brain rather than being cleared, which is why existing encephalopathy is a relative contraindication. Shunt stenosis or occlusion can develop over months and needs surveillance imaging to catch early, with covered stents now substantially reducing this problem compared to older bare metal designs. Patients with severe liver dysfunction are poor candidates because TIPS further reduces what little hepatic blood flow remains and can tip them into decompensation they can’t recover from. Heart failure and pulmonary hypertension push a significant volume of blood suddenly into the systemic circulation after TIPS, and an adequate cardiac workup before the procedure is essential in patients with any cardiac history. Managing the complications that lead patients to TIPS in the first place often involves a combination of endoscopic and medical treatment that endoscopy handles directly. Read more on pancreatic necrosis treatment to see how minimally invasive endoscopic approaches tackle other complex GI and hepatic complications without surgery. Why Choose Dr. Vipulroy Rathod for Liver Disease? Dr. Vipulroy Rathod has been managing cirrhosis complications and portal hypertension at Fortis Hospital Mulund for over 30 years, with endoscopic variceal management and EUS-guided assessment forming a core part of his practice. Patients approaching TIPS candidacy benefit from that depth of experience in identifying which complications can still be managed endoscopically and which genuinely need a shunt. Physicians from 35 countries have trained under his approach at Fortis. Book your consultation today with one of India’s most experienced specialists for liver cirrhosis and portal hypertension management. Book Appointment Call now Frequently Asked Questions What is the TIPS procedure? TIPS, or transjugular intrahepatic portosystemic shunt, is a procedure that creates a channel inside the liver between the portal and hepatic veins to reduce portal hypertension and its complications. What is TIPS used to treat? TIPS is used to treat portal hypertension complications including refractory variceal bleeding, recurrent ascites, hepatic hydrothorax, and in selected cases hepatorenal syndrome. Is TIPS a surgical procedure? No. TIPS is a minimally invasive interventional procedure performed through the jugular vein under imaging guidance, without open surgery and with significantly lower risk than a surgical shunt. What are the risks of the TIPS procedure? The main risks include hepatic encephalopathy, shunt stenosis or occlusion, and worsening liver function in patients with already compromised hepatic reserve, which is why careful patient selection is essential. Reference The Transjugular Intrahepatic Portosystemic Shunt in the Treatment of Portal Hypertension: Current Status — NCBI/PMC, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3408669/ Effects of TIPS Treatment in Patients with Liver Cirrhosis and Portal Hypertension — NCBI/PMC, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8270572/