Photo of Juan Gurria

Juan Gurria

861 timestamped statements across 11 topics — auto-found in recorded discussions, each timestamp jumps to the exact moment. Summaries Juan gave as host are listed separately below.

Islet Cell / TPIAT · guest expert Pancreatitis · guest expert Pediatric Robotic Surgery · guest expert Sarcoma (Ewing/Rhabdo) · guest expert

Featured statements

▶ Ep 9 · 4:23
If there's no other options and your endoscopic guy tells you, you know what, there's nothing for me to balloon dilate, open, drain, or anything. There's been a stent. Even with the stent, the patient keeps getting pancreatitis. There's no reason to keep going with ERCPs.
▶ Ep 10 · 2:29
Now, there's no reason to give antibiotics anymore at all for pancreatitis, even in the face of world of necrosis or necrotizing pancreatitis, unless there are signs of sepsis infected pancreatitis, which is a different beast
▶ Ep 6 · 3:23
There's a lot of factors that play into insulin independence uh on the, on the, on the, on the outcomes of this surgery, but right now, 50% chance if you hit 5000, 50% chance you're not going to require insulin.
▶ Ep 6 · 1:28
So, if you, most of the pancreatic parenchyma is in the head and the uncinate process. If you get rid of that head and there's a pancreatic, uh, uh, PRS1 mutation, this kid is gonna get uh recurrent attacks.
▶ Ep 9 · 15:32
PRSS one is the most common one, which is a trypsinogen activator. It activates trypsin inside the pancreas. So, you get auto-attacked by pancreatitis. It's the most aggressive one.
▶ Ep 1 · 2:06
Remember that pancreatitis is a state of, uh, hypoxia. You need to re-establish the intravascular flow to the pancreas to prevent hypoxia, necrosis, atrophic pancreas insufficiency.
quote · ALL

Nothing matches these filters — clear the search or widen the filters.

Juan's statements about Acute Pancreatitis 128 statements

Open the Acute Pancreatitis collection →

Update Course 2023 - Updates in Pancreatitis

▶ Ep 9 · 0:35
clinical Acute pancreatitis management has shifted from NPO and aggressive IV fluids causing pulmonary edema to early feeding and measured fluid resuscitation. ↗
▶ Ep 9 · 0:35
quote it is very important nowadays to feed the pancreas, even when there's pancreatitis ↗
▶ Ep 9 · 1:01
quote you cannot take care of a pancreas without a wonderful team ↗
▶ Ep 9 · 3:55
clinical For acute pancreatitis with tachycardia (HR 160) and hypotension in a 9-year-old, appropriate management is ICU admission with bolus ×2, maintenance IV fluids 1.5×, no antibiotics, and pain control. ↗
▶ Ep 9 · 4:03
quote Acute pancreatitis could be fatal ↗
▶ Ep 9 · 4:19
clinical Early fluid resuscitation is key to re-establish intravascular flow to the pancreas and prevent hypoxia, necrosis, and atrophic pancreatic insufficiency. ↗
▶ Ep 9 · 4:19
quote pancreatitis is a state of uh hypoxia. You need to re-establish the intravascular flow to the pancreas to prevent hypoxia, necrosis ↗
▶ Ep 9 · 4:39
clinical Excessive fluid resuscitation in pancreatitis leads to worse outcomes including fluid overload and multi-system organ failure. ↗
▶ Ep 9 · 4:42
guideline There is no indication for routine antibiotics in acute pancreatitis, even with necrosis or necrotizing pancreatitis, unless there are signs of sepsis or infected pancreatitis. ↗
▶ Ep 9 · 6:13
quote You cannot uh flow these lungs too much because the outcomes are worse ↗
▶ Ep 9 · 6:21
guideline Maintenance fluids should be 1.5 to 2 times normal maintenance, with reassessment at 12-24 hour mark to avoid fluid overload. ↗
▶ Ep 9 · 9:24
clinical Enteral nutrition as soon as the patient can tolerate PO is significantly better compared to TPN or NPO in acute pancreatitis. ↗
▶ Ep 9 · 10:19
clinical Some vomiting can be tolerated when feeding pancreatitis patients, similar to gastroschisis management, because feeding the gut produces dramatically better outcomes. ↗
▶ Ep 9 · 10:21
quote It's OK to tolerate some, some, some. Vomiting. If you can feed them, that's fine. ↗
▶ Ep 9 · 11:02
clinical No patient needs TPN in the first 7 days of acute illness. ↗
▶ Ep 9 · 11:02
quote nobody needs TPN the 1st 7 days of acute illness, right? ↗
▶ Ep 9 · 12:13
clinical The inflammatory head mass commonly seen in adult pancreatitis is rarely seen in children; pediatric patients typically have minimal duct change disease with small, usually non-dilated ducts. ↗
▶ Ep 9 · 14:38
clinical With every attack of pancreatitis, islet cells are lost, so repeated ERCPs that fail to prevent attacks result in progressive loss of beta-cell mass. ↗
▶ Ep 9 · 14:44
clinical ERCP does not change the islet yield available for transplantation, but pancreatitis attacks cause cell loss. ↗
▶ Ep 9 · 14:53
quote children get pancreatitis. We have a running list of 800 patients right now in Cin Children's. ↗
▶ Ep 9 · 14:59
epidemiological Cincinnati Children's has a running list of 800 pancreatitis patients and receives over 100 TPIAT referrals per year, but only performs 20-25 procedures annually because not all patients are candidates. ↗
▶ Ep 9 · 14:59
guideline Genetic testing is key in pediatric pancreatitis and should be obtained for all patients with chronic or recurrent pancreatitis, and even considered after a first severe attack. ↗
▶ Ep 9 · 15:23
quote The most common cause of pancreatitis in children is, is, is medicine induced. The most common risk factor for pancreatitis in children is, is genetic factors. ↗
▶ Ep 9 · 15:23
epidemiological The most common cause of pancreatitis in children is medication-induced, but the most common risk factor is genetic factors. ↗
▶ Ep 9 · 15:32
quote PRSS one is the most common one, which is a trypsinogen activator. It activates trypsin inside the pancreas. So, you get auto-attacked by pancreatitis. It's the most aggressive one. ↗
▶ Ep 9 · 15:32
clinical PRSS1 (trypsinogen activator) is the most common genetic mutation in pediatric pancreatitis and the most aggressive, causing auto-attack by activating trypsin inside the pancreas. ↗
▶ Ep 9 · 15:48
clinical Cincinnati Children's genetic panel tests 10 different genetic markers for pancreatitis including PRSS1, CTRC, CFTR, and CPA1. ↗
▶ Ep 9 · 16:06
opinion Genetics have fundamentally changed the approach to pediatric chronic pancreatitis treatment. ↗
▶ Ep 9 · 16:33
clinical In children with genetic mutations causing pancreatitis, conventional drainage procedures (Frey, Puestow) fail in up to 50% because the parenchyma continues to be attacked by the mutation despite duct drainage. ↗
▶ Ep 9 · 16:33
quote up to 50% of those children are gonna keep getting pancreatitis despite you opening the duct and draining it ↗
▶ Ep 9 · 16:49
quote you send half of your, the top of your pancreas to the trash ↗
▶ Ep 9 · 17:07
quote unfortunately we don't have that just yet. That's why I still have a job. ↗
▶ Ep 9 · 18:24
quote This patient most likely is gonna keep getting pancreatitis despite you draining the duct. The, the parenchyma is gonna keep getting attacked by the mutation. ↗
▶ Ep 9 · 19:02
quote TPIT, which is total pancreatectomy with eyelid autotransplantation. Uh, the main indication is, is for pain, chronic debilitating pain for children that are losing their lives. ↗
▶ Ep 9 · 19:08
clinical The main indication for TPIAT is chronic debilitating pain in children who have lost their quality of life—not attending school, withdrawn, unable to participate in activities. ↗
▶ Ep 9 · 19:19
quote There's no more ballerina dancers, right? ↗
▶ Ep 9 · 19:22
clinical The secondary goal of TPIAT is to prevent brittle diabetes by returning beta cells to the patient. ↗
▶ Ep 9 · 19:56
quote if you keep getting pancreatitis, you're losing time on that, right? The, the pancreas, we have 34 years old with like very atrophic pancreas ↗
▶ Ep 9 · 20:17
quote We don't offer. Uh, to take care of the pancreas unless you've maximize medical and endoscopic management. ↗
▶ Ep 9 · 20:59
clinical MRCP is the best non-invasive imaging study for the pancreas, superior to ultrasound and CT. ↗
▶ Ep 9 · 21:07
clinical ERCP is more therapeutic than diagnostic in chronic pancreatitis. ↗
▶ Ep 9 · 21:12
clinical Patients with chronic pancreatitis always have micronutrient and macronutrient deficiencies requiring nutritional support. ↗
▶ Ep 9 · 21:36
clinical Patients with chronic pancreatitis lose exocrine function first, then endocrine function, requiring screening and often pancreatic enzyme replacement therapy. ↗
▶ Ep 9 · 21:48
clinical Walled-off necrosis should be drained only if symptomatic (gastric outlet obstruction or pain) after the wall matures at 4-6 weeks; asymptomatic collections will self-resolve and do not require drainage or antibiotics. ↗
▶ Ep 9 · 22:08
epidemiological Chronic pancreatitis increases the risk of pancreatic cancer up to thirteenfold. ↗
▶ Ep 9 · 24:08
epidemiological Up to 50% of patients with chronic pancreatitis will eventually require surgery. ↗
▶ Ep 9 · 24:40
clinical TPIAT requires a multidisciplinary team including surgery, GI pancreatologists, social workers, geneticists, psychology, and pain management. ↗
▶ Ep 9 · 25:00
quote some families ask us like, so you're gonna get rid of the pain, right? 100%, and you cannot say that, right? ↗
▶ Ep 9 · 25:07
clinical Patients with chronic pain develop hyperalgesia and central sensitization—their brains learn to function in pain—so removing the organ may eliminate 90% of pain but 10% may linger, requiring behavioral therapy. ↗
▶ Ep 9 · 25:07
quote People that have chronic pain, their bodies, their brains learn how to be in pain, right? They can function in pain. That's called hyperalgesia and central sensitization. ↗
▶ Ep 9 · 25:18
quote when you take the, the, the organ part out, you maybe 90% of the pain is gone, but you cannot promise them that 10 that 10% is gonna linger for a little bit ↗
▶ Ep 9 · 26:32
clinical Islet equivalent per kilogram of body weight is used as a prognostic marker; at approximately 5000 islet equivalents/kg there is a 50% chance of insulin independence. ↗
▶ Ep 9 · 27:00
clinical TPIAT outcomes: 50% of patients achieve insulin independence, 20% require small insulin doses, and 30% remain diabetic. ↗
▶ Ep 9 · 27:05
quote I'm exchanging potentially disease for a disease, right? Chronic pancreatitis for potential diabetes. ↗
▶ Ep 9 · 27:05
clinical TPIAT exchanges chronic pancreatitis for potential diabetes, which must be clearly communicated to families. ↗
▶ Ep 9 · 27:23
quote My day starts the, the night before as I start going through the case. It's a long day. It's a long day. I reviewed this case in my head, uh, 30 times before I go in. ↗
▶ Ep 9 · 27:32
clinical TPIAT surgery takes an average of 8-10 hours: 3-4 hours for pancreatectomy, 4-4.5 hours for islet isolation in the lab, and 2 hours for reconstruction. ↗
▶ Ep 9 · 28:47
clinical Pylorus-preserving resection with pyloric Botox injection is performed during TPIAT reconstruction to address gastroparesis that all pancreatitis patients have; Roux-en-Y reconstruction also helps with gastroparesis. ↗
▶ Ep 9 · 29:33
clinical Routine splenectomy is performed with TPIAT because the pancreas and spleen share blood supply via tiny branches from the splenic vessels; preserving the spleen adds ischemia time and causes islet cell loss. ↗
▶ Ep 9 · 29:59
clinical There are four critical points where islet cells can be lost: (1) recurrent pancreatitis causing cell death, (2) ischemia during surgical dissection, (3) cell death during processing and injection, and (4) post-operative stress if glucose is not carefully managed. ↗
▶ Ep 9 · 30:20
clinical All TPIAT patients are kept on insulin in the ICU post-operatively to let the islet cells rest without working until they implant and establish new vascular supply from the liver. ↗
▶ Ep 9 · 31:10
clinical The liver is the best site for islet cell implantation via portal vein injection; extrahepatic sites (omentum, retroperitoneum, rectus muscle, gastric submucosa) have been tried but work less well. ↗
▶ Ep 9 · 31:58
clinical Portal vein thrombosis after islet injection occurs in less than 1% of cases; portal pressure is monitored during injection. ↗
▶ Ep 9 · 32:23
clinical The duodenum is resected at D1 post-pyloric during TPIAT because of shared blood supply with the pancreas; attempting to preserve it adds ischemia time. ↗

Update Course Rewind: Management of Acute Pancreatitis 2023

▶ Ep 10 · 1:56
quote Acute pancreatitis could be fatal. ↗
▶ Ep 10 · 1:56
clinical Acute pancreatitis could be fatal ↗
▶ Ep 10 · 1:58
clinical Bolus times 2 is adequate fluid resuscitation, with 1.5 times maintenance once past the early phase of acute resuscitation ↗
▶ Ep 10 · 2:06
quote Remember that pancreatitis is a state of, uh, hypoxia. You need to re-establish the intravascular flow to the pancreas to prevent hypoxia, necrosis, atrophic pancreas insufficiency. ↗
▶ Ep 10 · 2:06
clinical Pancreatitis is a state of hypoxia requiring re-establishment of intravascular flow to the pancreas to prevent hypoxia, necrosis, and atrophic pancreas insufficiency ↗
▶ Ep 10 · 2:22
clinical Early fluid resuscitation is key in pancreatitis management ↗
▶ Ep 10 · 2:26
clinical Excessive fluid administration worsens outcomes in pancreatitis ↗
▶ Ep 10 · 2:29
quote Now, there's no reason to give antibiotics anymore at all for pancreatitis, even in the face of world of necrosis or necrotizing pancreatitis, unless there are signs of sepsis infected pancreatitis, which is a different beast ↗
▶ Ep 10 · 2:29
guideline There is no reason to give antibiotics for pancreatitis, even in the face of necrosis or necrotizing pancreatitis, unless there are signs of sepsis or infected pancreatitis ↗
▶ Ep 10 · 2:57
guideline The North American Society of Pancreatitis, GI Pathology, and Nutrition published a position paper with guideline recommendations for pancreatitis management ↗
▶ Ep 10 · 3:07
clinical Early fluids lead to better outcomes in pancreatitis ↗
▶ Ep 10 · 3:11
guideline Recommended fluid bolus is 10 to 20 mL per kg, up to 3L in the first 24 hours, with reassessment at the 12-hour mark using urine output and vital signs ↗
▶ Ep 10 · 3:25
clinical Excessive fluid administration can flood the lungs and worsen outcomes ↗
▶ Ep 10 · 3:25
quote You cannot flow these lungs too much because the outcomes are worse. ↗
▶ Ep 10 · 3:45
quote It's been shown that LR. Decreases the incidence of inflammatory response and C, C-reactive protein at 24 hours compared to NS, right? ↗
▶ Ep 10 · 3:45
clinical Lactated Ringer's decreases the incidence of inflammatory response and C-reactive protein at 24 hours compared to normal saline in pancreatitis ↗
▶ Ep 10 · 3:54
clinical If albumin is low in pancreatitis patients, albumin should be given ↗
▶ Ep 10 · 3:58
clinical Enrique de Madaria conducted a multi-center worldwide RCT called the Waterfall trial comparing moderate versus aggressive fluid resuscitation in pancreatitis ↗
▶ Ep 10 · 4:18
clinical The Waterfall trial was stopped early because patients receiving too much fluid were developing organ failure ↗
▶ Ep 10 · 4:27
clinical A follow-up Waterland trial is underway to determine whether lactated Ringer's is better than normal saline, expected to be published in one to two years ↗
▶ Ep 10 · 4:47
clinical Patients with pancreatitis should be fed as soon as they are able to tolerate oral intake ↗
▶ Ep 10 · 4:51
clinical Enteral nutrition is significantly better compared to TPN or NPO in pancreatitis ↗
▶ Ep 10 · 4:57
clinical Gastric feeding is preferred over post-pyloric feeding in pancreatitis if the patient can tolerate it ↗
▶ Ep 10 · 5:19
opinion Some vomiting is tolerable during refeeding in pancreatitis, similar to gastroschisis management ↗
▶ Ep 10 · 5:19
quote If they cannot tolerate it, it's OK. I mean, but it's like gastroschisis, it's OK to tolerate some, some, some vomiting. ↗
▶ Ep 10 · 5:26
quote If you're losing nutrition and you're losing ground, the patient's gonna have a worse outcome. Their albumin is gonna drop, inflammatory reaction is gonna be worse. ↗
▶ Ep 10 · 5:26
clinical If nutrition is lost and the patient loses ground, outcomes will be worse, with dropping albumin and worse inflammatory reaction ↗
▶ Ep 10 · 5:34
clinical Outcomes are dramatically better when the gut is fed in pancreatitis patients ↗

Overview of the Surgical Management of Acute and Chronic Pancreatitis in Children with Dr. Juan Gurria

▶ Ep 11 · 5:44
guideline Diagnosis of acute pancreatitis requires serum lipase at least 3 times the upper limit of normal, plus imaging findings (ultrasound, MRI/MRCP, or CT). ↗
▶ Ep 11 · 7:23
epidemiological In the Cincinnati Children's cohort of 1000 pediatric pancreatitis patients, 85% have genetic mutations. ↗
▶ Ep 11 · 8:01
clinical PRSS1 mutation causes very aggressive attacks very early in life (ages 1–3 years) because it autoactivates trypsinogen inside the pancreas. ↗
▶ Ep 11 · 8:37
clinical Medications including L-asparaginase, steroids, valproic acid, and diuretics (Lasix) can cause pancreatitis in children. ↗
▶ Ep 11 · 9:32
clinical Hereditary pancreatitis increases the risk of pancreatic cancer by a huge fold, which is a major concern in children diagnosed at age 5–6 who may live 95 more years. ↗
▶ Ep 11 · 10:15
clinical Most fluid collections in pediatric acute pancreatitis are self-limited and should not be touched unless absolutely necessary. ↗
▶ Ep 11 · 18:08
quote Please do not touch these collections ever unless you absolutely have to. ↗
▶ Ep 11 · 18:40
clinical Early necrosectomies (before 4 weeks) usually increase mortality. ↗
▶ Ep 11 · 19:49
clinical Following lipase levels tells you nothing about how the pancreas is behaving in acute pancreatitis; cross-sectional imaging is required. ↗
▶ Ep 11 · 21:36
clinical Asymptomatic pseudocysts, regardless of size, do not require intervention. ↗
▶ Ep 11 · 23:29
clinical Patients with acute pancreatitis should be fed as soon as possible (orally or via NG/NJ tube) because bacterial translocation from NPO status will complicate the disease. ↗
▶ Ep 11 · 23:29
quote Please feed your patients as soon as you can, all right? If they're vomiting and they're gonna puke it, well, that doesn't make any sense. You, if you have to throw out an NG or an NG tube, feed the god because bacterial translocation from NPL will complicate acute pancreatitis. ↗
▶ Ep 11 · 25:13
epidemiological In pediatric patients with hereditary pancreatitis or hereditary plus anatomic abnormalities, half will develop chronic pancreatitis. ↗
▶ Ep 11 · 25:38
clinical Cincinnati Children's evaluates over 100 patients per year for chronic pancreatitis but only operates on 25–30, because medical and endoscopic options should be exhausted first. ↗
▶ Ep 11 · 26:50
clinical Chronic pain in pancreatitis involves brain plasticity, hypertrophic nerve reactions, and peripheral nerve hypersensitization, not just organic retroperitoneal pain. ↗
▶ Ep 11 · 27:43
clinical After total pancreatectomy, 95% of pain is resolved, but 5% may persist due to central sensitization and requires behavioral medicine and psychiatric support. ↗
▶ Ep 11 · 27:43
quote I'm gonna take your pancreas out if it's uh indicated, and I'm gonna take care of 95% of your pain. But that 5, 5% that is left. We need to work with psych, behavioral med, uh, and eventually reteach their brains how to live not in pain. ↗
▶ Ep 11 · 28:37
clinical Pediatric chronic pancreatitis usually presents with minimal ductal changes, not the dilated ducts seen in adults, so drainage procedures are often not applicable. ↗
▶ Ep 11 · 28:57
clinical In patients with genetic mutations, partial pancreatectomy (Whipple, distal pancreatectomy) discards islet mass and does not address the underlying defect, so the remaining pancreas continues to be affected. ↗
▶ Ep 11 · 28:57
quote If you have a genetic mutation and you chop off a piece of the pancreas, throw it in the trash. You can maybe relieve some of the pain. If you do whipple, have the pancreas drain better, do a piece so, I'm gonna touch base on that in a sec, drain the pancreatic duct better. But I put a piece of paper in the trash. And the genetic mutations will keep affecting the rest of the pancreas. ↗
▶ Ep 11 · 37:44
quote We're doing this for, for chronic pain and that should be the, the, the major thing in our head. ↗
▶ Ep 11 · 37:54
guideline TPIAT is indicated when patients have chronic pancreatitis findings, at least 6 months of disease, exocrine or endocrine insufficiency, and impaired quality of life despite maximal medical and endoscopic therapy. ↗
▶ Ep 11 · 39:00
clinical The goal of islet autotransplantation is to replace beta cell mass and insulin secretory capacity, not to cure diabetes—pain control is the primary indication. ↗
▶ Ep 11 · 40:28
clinical TPIAT used to be a 20-hour operation but is now down to an average of 8–9 hours at Cincinnati Children's. ↗
▶ Ep 11 · 43:15
clinical Spleen-sparing TPIAT has equal glycemic outcomes to splenectomy TPIAT when islet equivalent per kilogram transplanted is matched. ↗
▶ Ep 11 · 43:42
clinical Spleen-sparing TPIAT is now performed in 80% of cases (over the last 5 years), compared to none in the first 8 years of the program. ↗
▶ Ep 11 · 45:16
clinical Intraoperative pyloric Botox injection reduces gastroparesis, decreases length of stay, and improves time to full oral intake and glycemic control after TPIAT. ↗
▶ Ep 11 · 46:27
clinical Islet isolation takes about 3–3.5 hours, sometimes 4 hours depending on the degree of pancreatic injury. ↗
▶ Ep 11 · 47:39
clinical TPIAT is performed under anticoagulation (heparin) to prevent portal vein thrombosis during islet infusion. ↗
▶ Ep 11 · 48:11
clinical Portal vein thrombosis rate at Cincinnati Children's is less than 1% for TPIAT. ↗
▶ Ep 11 · 48:26
clinical Cincinnati Children's has performed close to 200 TPIAT cases with no anastomotic leaks. ↗
▶ Ep 11 · 50:07
clinical Patients are extubated in the operating room after TPIAT. ↗
▶ Ep 11 · 51:32
clinical Younger children are more likely to achieve insulin independence and opioid independence after TPIAT. ↗
▶ Ep 11 · 52:25
clinical Islet yield (IEQ/kg) is inversely related to pancreatic calcification, ductal dilation, fibrosis, duration of symptoms, and prior resections or drainage procedures. ↗
▶ Ep 11 · 54:59
clinical Predictors of insulin independence after TPIAT include younger age at surgery, smaller body surface area, no pre-existing insulin dependence, and higher IEQ/kg transplanted. ↗
▶ Ep 11 · 56:09
clinical TPIAT dramatically improves quality of life in appropriately selected children, with families reporting they have 'never met this kid before'—new person, happy, playing, eating normally. ↗
Juan's statements about Acute Recurrent Pancreatitis 48 statements

Open the Acute Recurrent Pancreatitis collection →

Update Course Rewind: Management of Recurrent Pancreatitis

▶ Ep 9 · 1:40
quote Every time you get an, an ERCP you have a risk of getting post-E ERCP pancreatitis. It's low, right? But it's still a risk, and you lose eyelet cells with every attack. ↗
▶ Ep 9 · 1:40
clinical Every ERCP carries a risk of post-ERCP pancreatitis, and with every pancreatitis attack, islet cells are lost. ↗
▶ Ep 9 · 1:57
clinical PRSS1 is the most common genetic mutation in recurrent pancreatitis and is a trypsinogen activator that activates trypsin inside the pancreas. ↗
▶ Ep 9 · 1:57
quote PRSS1 is the most common one, which is a trypsinogen activator. It activates trypsin inside the pancreas. ↗
▶ Ep 9 · 2:06
clinical The genetic panel at Cincinnati Children's tests 10 different genetic markers for pancreatitis (including PRSS1, CTRC, CFTR, CPA1). ↗
▶ Ep 9 · 2:17
quote That's how we're changing the approach to pediatric pancreatitis, chronic pan pancreatitis treatment because of the genetic factors. ↗
▶ Ep 9 · 2:17
opinion Genetic factors are changing the approach to pediatric chronic pancreatitis treatment. ↗
▶ Ep 9 · 2:48
quote No, no, there's no, unfortunately we don't have that just yet. That's why I still have a job, but, uh, I hope, I hope some Monday we have, you know. ↗
▶ Ep 9 · 2:48
clinical There is currently no medication to mitigate trypsin activation in genetic pancreatitis mutations. ↗
▶ Ep 9 · 3:09
clinical In a Frey procedure (partial head pancreatectomy with pancreaticojejunostomy), the top half of the pancreas is removed to open the duct, which results in loss of islet cells. ↗
▶ Ep 9 · 3:19
clinical In patients with PRSS1 mutation, draining the duct (e.g., via Frey) temporizes attacks but does not fix the problem, as the parenchyma continues to be attacked by the mutation and pancreatitis will likely recur. ↗
▶ Ep 9 · 3:19
quote This patient most likely is gonna keep getting pancreatitis despite you draining the duct. The, the parenchyma is gonna keep getting attacked by the mutation. So, you're temporizing um the attack by draining the duct, uh, but you're not fixing the problem. ↗
▶ Ep 9 · 4:09
opinion There is no set number of ERCPs that defines when to escalate care; the sooner the referral for evaluation, the better. ↗
▶ Ep 9 · 4:16
quote We don't offer, uh, to take care of the pancreas unless you've. Maximize medical and endoscopic management. ↗
▶ Ep 9 · 4:16
guideline Surgical management of the pancreas is not offered unless medical and endoscopic management have been maximized. ↗
▶ Ep 9 · 4:23
clinical If the endoscopist has no further options (nothing to balloon dilate, open, or drain) and the patient continues to have pancreatitis despite stenting, there is no reason to continue ERCPs. ↗
▶ Ep 9 · 4:23
quote If there's no other options and your endoscopic guy tells you, you know what, there's nothing for me to balloon dilate, open, drain, or anything. There's been a stent. Even with the stent, the patient keeps getting pancreatitis. There's no reason to keep going with ERCPs. ↗
▶ Ep 9 · 4:58
clinical MRCP is the best non-invasive imaging study for the pancreas, particularly with T2 sequences. ↗
▶ Ep 9 · 4:58
quote MRCP is the best non-invasive study for pancreas by far, uh, with different uh uh T2 sequences. ↗
▶ Ep 9 · 5:07
clinical ERCP is more therapeutic than diagnostic. ↗
▶ Ep 9 · 5:22
quote Once the, the wall is mature in 4 to 6 weeks, uh, if there's symptoms, drain it. If there's no symptoms, don't drain it. ↗
▶ Ep 9 · 5:22
clinical Pancreatic fluid collections should be drained once the wall is mature (4 to 6 weeks) only if the patient is symptomatic (e.g., gastric outlet obstruction or pain); asymptomatic collections will self-resolve and do not require drainage or antibiotics. ↗

Total pancreatectomy with islet autotransplantation (TPIAT) - Cincinnati Children's Pancreas Care Center

▶ Ep 10 · 0:48
quote TPIAT is clearly one of the most complex abdominal surgical procedures we perform in children. ↗
▶ Ep 10 · 0:48
opinion TPIAT is one of the most complex abdominal surgical procedures performed in children. ↗
▶ Ep 10 · 0:54
clinical Surgical indications for TPIAT are for patients with either chronic or acute recurrent pancreatitis. ↗
▶ Ep 10 · 1:02
quote These patients are candidates for TPAT when all medical and endoscopic therapy has failed. ↗
▶ Ep 10 · 1:02
guideline Patients are candidates for TPIAT when all medical and endoscopic therapy has failed. ↗
▶ Ep 10 · 1:23
clinical The Pancreas Care Center team includes GI, social worker, endocrine, surgery, radiology, genetics, behavioral health, physical therapy, anesthesia, and pain team. ↗
▶ Ep 10 · 1:45
clinical The entire team reviews and votes patients in for surgery to determine if they are candidates for TPIAT. ↗
▶ Ep 10 · 1:45
clinical Patients are prepared with vaccinations for potential splenectomy before TPIAT surgery. ↗
▶ Ep 10 · 2:40
clinical Pain catheters are placed in the transversus abdominis muscle by pain specialists. ↗
▶ Ep 10 · 3:14
quote Remember, this, this pancreas has been injured for sometimes years, which makes this procedure quite challenging. ↗
▶ Ep 10 · 3:14
clinical The pancreas in TPIAT patients has been injured for sometimes years, which makes the procedure quite challenging. ↗
▶ Ep 10 · 3:29
clinical On the right side, the small intestine (duodenum) and liver hilum are mobilized, with careful identification of bile ducts and blood supply to the liver. ↗
▶ Ep 10 · 4:06
clinical Blood supply to the head and entire body of the pancreas is preserved very carefully until the very last moment to avoid hypoxia of islet cells. ↗
▶ Ep 10 · 4:06
quote We preserve very carefully the blood supply to the head and the entire body until the pancreas, until the very last moment because we cannot risk hypoxying these cells. ↗
▶ Ep 10 · 6:33
clinical During islet processing, the surgical team performs reconstruction of the gastrointestinal tract by bringing a loop of duodenum up to the bile duct and reconnecting another loop of intestine to the duodenum past the pyloric muscle. ↗
▶ Ep 10 · 6:53
clinical A feeding tube is placed to allow patients to be fed while important connections heal. ↗
▶ Ep 10 · 7:02
clinical Drains are left where the spleen was removed and on top of the connection with the biliary tract. ↗
▶ Ep 10 · 7:15
clinical Islet cells are transfused into the portal vein with the hope that they will implant in the liver and start producing insulin. ↗
▶ Ep 10 · 7:25
quote While we infuse the eyelid itself, we're constantly checking the pressures in the portal vein to make sure we don't risk any thrombosis in the portal vein, which could cause a lot of morbidity to the patient. ↗
▶ Ep 10 · 7:25
clinical Portal vein pressures are constantly checked during islet infusion to prevent portal vein thrombosis, which could cause significant morbidity. ↗
▶ Ep 10 · 8:01
clinical Patients are placed in the intensive care unit post-operatively to control hemodynamics and fluid shift balance. ↗
▶ Ep 10 · 8:08
clinical Islet cells need to heal in a very homeostatic environment, requiring close monitoring of vital signs. ↗
▶ Ep 10 · 8:18
clinical Glucose and insulin are controlled via exogenous infusions post-operatively. ↗
▶ Ep 10 · 8:22
clinical Close attention to nutrition is key in the healing of connections between the bile tract and gastrointestinal tract. ↗
▶ Ep 10 · 8:39
clinical Patients are deemed ready for discharge when pain is well controlled, they are on full feeds (via tube or by mouth), glucose is well controlled via continuous glucose monitoring, and they have received full education. ↗
▶ Ep 10 · 8:47
clinical After discharge, local GI physicians continue to follow patients along with the Cincinnati Children's team. ↗
Juan's statements about ALL 28 statements

Open the ALL collection →

Update Course Rewind: Management of Acute Pancreatitis 2023

▶ Ep 1 · 1:56
clinical Acute pancreatitis could be fatal ↗
▶ Ep 1 · 1:56
quote Acute pancreatitis could be fatal. ↗
▶ Ep 1 · 1:58
clinical Bolus times 2 is adequate fluid resuscitation, with 1.5 times maintenance once past the early phase of acute resuscitation ↗
▶ Ep 1 · 2:06
quote Remember that pancreatitis is a state of, uh, hypoxia. You need to re-establish the intravascular flow to the pancreas to prevent hypoxia, necrosis, atrophic pancreas insufficiency. ↗
▶ Ep 1 · 2:06
clinical Pancreatitis is a state of hypoxia requiring re-establishment of intravascular flow to the pancreas to prevent hypoxia, necrosis, and atrophic pancreas insufficiency ↗
▶ Ep 1 · 2:22
clinical Early fluid resuscitation is key in pancreatitis management ↗
▶ Ep 1 · 2:26
clinical Excessive fluid administration worsens outcomes in pancreatitis ↗
▶ Ep 1 · 2:29
guideline There is no reason to give antibiotics for pancreatitis, even in the face of necrosis or necrotizing pancreatitis, unless there are signs of sepsis or infected pancreatitis ↗
▶ Ep 1 · 2:29
quote Now, there's no reason to give antibiotics anymore at all for pancreatitis, even in the face of world of necrosis or necrotizing pancreatitis, unless there are signs of sepsis infected pancreatitis, which is a different beast ↗
▶ Ep 1 · 2:57
guideline The North American Society of Pancreatitis, GI Pathology, and Nutrition published a position paper with guideline recommendations for pancreatitis management ↗
▶ Ep 1 · 3:07
clinical Early fluids lead to better outcomes in pancreatitis ↗
▶ Ep 1 · 3:11
guideline Recommended fluid bolus is 10 to 20 mL per kg, up to 3L in the first 24 hours, with reassessment at the 12-hour mark using urine output and vital signs ↗
▶ Ep 1 · 3:25
quote You cannot flow these lungs too much because the outcomes are worse. ↗
▶ Ep 1 · 3:25
clinical Excessive fluid administration can flood the lungs and worsen outcomes ↗
▶ Ep 1 · 3:45
clinical Lactated Ringer's decreases the incidence of inflammatory response and C-reactive protein at 24 hours compared to normal saline in pancreatitis ↗
▶ Ep 1 · 3:45
quote It's been shown that LR. Decreases the incidence of inflammatory response and C, C-reactive protein at 24 hours compared to NS, right? ↗
▶ Ep 1 · 3:54
clinical If albumin is low in pancreatitis patients, albumin should be given ↗
▶ Ep 1 · 3:58
clinical Enrique de Madaria conducted a multi-center worldwide RCT called the Waterfall trial comparing moderate versus aggressive fluid resuscitation in pancreatitis ↗
▶ Ep 1 · 4:18
clinical The Waterfall trial was stopped early because patients receiving too much fluid were developing organ failure ↗
▶ Ep 1 · 4:27
clinical A follow-up Waterland trial is underway to determine whether lactated Ringer's is better than normal saline, expected to be published in one to two years ↗
▶ Ep 1 · 4:47
clinical Patients with pancreatitis should be fed as soon as they are able to tolerate oral intake ↗
▶ Ep 1 · 4:51
clinical Enteral nutrition is significantly better compared to TPN or NPO in pancreatitis ↗
▶ Ep 1 · 4:57
clinical Gastric feeding is preferred over post-pyloric feeding in pancreatitis if the patient can tolerate it ↗
▶ Ep 1 · 5:19
quote If they cannot tolerate it, it's OK. I mean, but it's like gastroschisis, it's OK to tolerate some, some, some vomiting. ↗
▶ Ep 1 · 5:19
opinion Some vomiting is tolerable during refeeding in pancreatitis, similar to gastroschisis management ↗
▶ Ep 1 · 5:26
clinical If nutrition is lost and the patient loses ground, outcomes will be worse, with dropping albumin and worse inflammatory reaction ↗
▶ Ep 1 · 5:26
quote If you're losing nutrition and you're losing ground, the patient's gonna have a worse outcome. Their albumin is gonna drop, inflammatory reaction is gonna be worse. ↗
▶ Ep 1 · 5:34
clinical Outcomes are dramatically better when the gut is fed in pancreatitis patients ↗
Juan's statements about Choledochal Cyst 21 statements

Open the Choledochal Cyst collection →

2025 Pediatric Surgery Update Course - Robotics in Pediatric Surgery: Which indications benefit the most?

▶ Ep 5 · 0:24
epidemiological Four out of approximately 30 attendees perform robotic surgery; another 12 have robot access but do not use it ↗
▶ Ep 5 · 0:24
opinion Choledochal cyst is a perfect case for robotic surgery ↗
▶ Ep 5 · 0:24
clinical Robotic instruments have seven degrees of freedom compared to six for the human hand ↗
▶ Ep 5 · 0:24
opinion Adrenalectomy for neuroblastoma confined to the adrenal is a perfect robotic case ↗
▶ Ep 5 · 0:24
quote Who is a robotic surgery here in the audience? The ones who are not lifting up their hands, who has a robot available? ↗
▶ Ep 5 · 2:51
clinical Room turnover time for robotic cases can be reduced to 30 minutes with trained personnel ↗
▶ Ep 5 · 2:51
clinical Robotic surgery shows lower conversion to open rates compared to laparoscopy in colorectal cases ↗
▶ Ep 5 · 2:51
clinical Learning curve for basic proficiency is 20-30 cases for laparoscopy versus 10-15 cases for robotics ↗
▶ Ep 5 · 2:51
clinical Initial cost premium for robotic surgery is approximately $4000 per case in most institutions ↗
▶ Ep 5 · 2:51
clinical Each additional 15 minutes of operative time costs the same for robotic and laparoscopic surgery ↗
▶ Ep 5 · 2:51
epidemiological All pediatric surgery fellowships are integrating robotic training ↗
▶ Ep 5 · 3:15
opinion Median arcuate ligament release should not be performed laparoscopically or open anymore due to difficulty accessing the angle near the celiac trunk ↗
▶ Ep 5 · 3:38
guideline There is no FDA approval for robotic systems in pediatric surgery ↗
▶ Ep 5 · 3:38
quote Are there FDA indications for the robot for pediatric surgery? Great question. Great question. No. ↗
▶ Ep 5 · 7:16
opinion Robotic surgery is not recommended for appendectomy ↗
▶ Ep 5 · 7:16
clinical ICG fluorescence allows visualization of adrenal arteries supplied by renal, diaphragmatic, and aortic vessels ↗
▶ Ep 5 · 12:55
opinion Robotic surgery is not a standard of care but a tool to aid efficiency and access to difficult angles ↗
▶ Ep 5 · 14:05
quote This is not about being cool. It's about efficiency and outcomes. Less cases to prove it now. Less cases to proficiency. ↗
▶ Ep 5 · 15:59
opinion Surgeons trained primarily in robotics cannot tie, sew, or work with 3mm instruments effectively ↗
▶ Ep 5 · 17:14
clinical ICG fluorescence in choledochal cyst surgery allows visualization far back to the head of the pancreas to achieve proper tapering, decreasing future cancer risk ↗
▶ Ep 5 · 17:14
clinical New robotic systems with tactile sensors reduce force application by 83% ↗
Juan's statements about Chronic Pancreatitis 193 statements

Open the Chronic Pancreatitis collection →

Update Course 2023 - Updates in Pancreatitis

▶ Ep 5 · 0:35
quote it is very important nowadays to feed the pancreas, even when there's pancreatitis ↗
▶ Ep 5 · 0:35
clinical Acute pancreatitis management has shifted from NPO and aggressive IV fluids causing pulmonary edema to early feeding and measured fluid resuscitation. ↗
▶ Ep 5 · 1:01
quote you cannot take care of a pancreas without a wonderful team ↗
▶ Ep 5 · 3:55
clinical For acute pancreatitis with tachycardia (HR 160) and hypotension in a 9-year-old, appropriate management is ICU admission with bolus ×2, maintenance IV fluids 1.5×, no antibiotics, and pain control. ↗
▶ Ep 5 · 4:03
quote Acute pancreatitis could be fatal ↗
▶ Ep 5 · 4:19
quote pancreatitis is a state of uh hypoxia. You need to re-establish the intravascular flow to the pancreas to prevent hypoxia, necrosis ↗
▶ Ep 5 · 4:19
clinical Early fluid resuscitation is key to re-establish intravascular flow to the pancreas and prevent hypoxia, necrosis, and atrophic pancreatic insufficiency. ↗
▶ Ep 5 · 4:39
clinical Excessive fluid resuscitation in pancreatitis leads to worse outcomes including fluid overload and multi-system organ failure. ↗
▶ Ep 5 · 4:42
guideline There is no indication for routine antibiotics in acute pancreatitis, even with necrosis or necrotizing pancreatitis, unless there are signs of sepsis or infected pancreatitis. ↗
▶ Ep 5 · 6:13
quote You cannot uh flow these lungs too much because the outcomes are worse ↗
▶ Ep 5 · 6:21
guideline Maintenance fluids should be 1.5 to 2 times normal maintenance, with reassessment at 12-24 hour mark to avoid fluid overload. ↗
▶ Ep 5 · 9:24
clinical Enteral nutrition as soon as the patient can tolerate PO is significantly better compared to TPN or NPO in acute pancreatitis. ↗
▶ Ep 5 · 10:19
clinical Some vomiting can be tolerated when feeding pancreatitis patients, similar to gastroschisis management, because feeding the gut produces dramatically better outcomes. ↗
▶ Ep 5 · 10:21
quote It's OK to tolerate some, some, some. Vomiting. If you can feed them, that's fine. ↗
▶ Ep 5 · 11:02
quote nobody needs TPN the 1st 7 days of acute illness, right? ↗
▶ Ep 5 · 11:02
clinical No patient needs TPN in the first 7 days of acute illness. ↗
▶ Ep 5 · 12:13
clinical The inflammatory head mass commonly seen in adult pancreatitis is rarely seen in children; pediatric patients typically have minimal duct change disease with small, usually non-dilated ducts. ↗
▶ Ep 5 · 14:38
clinical With every attack of pancreatitis, islet cells are lost, so repeated ERCPs that fail to prevent attacks result in progressive loss of beta-cell mass. ↗
▶ Ep 5 · 14:44
clinical ERCP does not change the islet yield available for transplantation, but pancreatitis attacks cause cell loss. ↗
▶ Ep 5 · 14:53
quote children get pancreatitis. We have a running list of 800 patients right now in Cin Children's. ↗
▶ Ep 5 · 14:59
guideline Genetic testing is key in pediatric pancreatitis and should be obtained for all patients with chronic or recurrent pancreatitis, and even considered after a first severe attack. ↗
▶ Ep 5 · 14:59
epidemiological Cincinnati Children's has a running list of 800 pancreatitis patients and receives over 100 TPIAT referrals per year, but only performs 20-25 procedures annually because not all patients are candidates. ↗
▶ Ep 5 · 15:23
epidemiological The most common cause of pancreatitis in children is medication-induced, but the most common risk factor is genetic factors. ↗
▶ Ep 5 · 15:23
quote The most common cause of pancreatitis in children is, is, is medicine induced. The most common risk factor for pancreatitis in children is, is genetic factors. ↗
▶ Ep 5 · 15:32
quote PRSS one is the most common one, which is a trypsinogen activator. It activates trypsin inside the pancreas. So, you get auto-attacked by pancreatitis. It's the most aggressive one. ↗
▶ Ep 5 · 15:32
clinical PRSS1 (trypsinogen activator) is the most common genetic mutation in pediatric pancreatitis and the most aggressive, causing auto-attack by activating trypsin inside the pancreas. ↗
▶ Ep 5 · 15:48
clinical Cincinnati Children's genetic panel tests 10 different genetic markers for pancreatitis including PRSS1, CTRC, CFTR, and CPA1. ↗
▶ Ep 5 · 16:06
opinion Genetics have fundamentally changed the approach to pediatric chronic pancreatitis treatment. ↗
▶ Ep 5 · 16:33
clinical In children with genetic mutations causing pancreatitis, conventional drainage procedures (Frey, Puestow) fail in up to 50% because the parenchyma continues to be attacked by the mutation despite duct drainage. ↗
▶ Ep 5 · 16:33
quote up to 50% of those children are gonna keep getting pancreatitis despite you opening the duct and draining it ↗
▶ Ep 5 · 16:49
quote you send half of your, the top of your pancreas to the trash ↗
▶ Ep 5 · 17:07
quote unfortunately we don't have that just yet. That's why I still have a job. ↗
▶ Ep 5 · 18:24
quote This patient most likely is gonna keep getting pancreatitis despite you draining the duct. The, the parenchyma is gonna keep getting attacked by the mutation. ↗
▶ Ep 5 · 19:02
quote TPIT, which is total pancreatectomy with eyelid autotransplantation. Uh, the main indication is, is for pain, chronic debilitating pain for children that are losing their lives. ↗
▶ Ep 5 · 19:08
clinical The main indication for TPIAT is chronic debilitating pain in children who have lost their quality of life—not attending school, withdrawn, unable to participate in activities. ↗
▶ Ep 5 · 19:19
quote There's no more ballerina dancers, right? ↗
▶ Ep 5 · 19:22
clinical The secondary goal of TPIAT is to prevent brittle diabetes by returning beta cells to the patient. ↗
▶ Ep 5 · 19:56
quote if you keep getting pancreatitis, you're losing time on that, right? The, the pancreas, we have 34 years old with like very atrophic pancreas ↗
▶ Ep 5 · 20:17
quote We don't offer. Uh, to take care of the pancreas unless you've maximize medical and endoscopic management. ↗
▶ Ep 5 · 20:59
clinical MRCP is the best non-invasive imaging study for the pancreas, superior to ultrasound and CT. ↗
▶ Ep 5 · 21:07
clinical ERCP is more therapeutic than diagnostic in chronic pancreatitis. ↗
▶ Ep 5 · 21:12
clinical Patients with chronic pancreatitis always have micronutrient and macronutrient deficiencies requiring nutritional support. ↗
▶ Ep 5 · 21:36
clinical Patients with chronic pancreatitis lose exocrine function first, then endocrine function, requiring screening and often pancreatic enzyme replacement therapy. ↗
▶ Ep 5 · 21:48
clinical Walled-off necrosis should be drained only if symptomatic (gastric outlet obstruction or pain) after the wall matures at 4-6 weeks; asymptomatic collections will self-resolve and do not require drainage or antibiotics. ↗
▶ Ep 5 · 22:08
epidemiological Chronic pancreatitis increases the risk of pancreatic cancer up to thirteenfold. ↗
▶ Ep 5 · 24:08
epidemiological Up to 50% of patients with chronic pancreatitis will eventually require surgery. ↗
▶ Ep 5 · 24:40
clinical TPIAT requires a multidisciplinary team including surgery, GI pancreatologists, social workers, geneticists, psychology, and pain management. ↗
▶ Ep 5 · 25:00
quote some families ask us like, so you're gonna get rid of the pain, right? 100%, and you cannot say that, right? ↗
▶ Ep 5 · 25:07
clinical Patients with chronic pain develop hyperalgesia and central sensitization—their brains learn to function in pain—so removing the organ may eliminate 90% of pain but 10% may linger, requiring behavioral therapy. ↗
▶ Ep 5 · 25:07
quote People that have chronic pain, their bodies, their brains learn how to be in pain, right? They can function in pain. That's called hyperalgesia and central sensitization. ↗
▶ Ep 5 · 25:18
quote when you take the, the, the organ part out, you maybe 90% of the pain is gone, but you cannot promise them that 10 that 10% is gonna linger for a little bit ↗
▶ Ep 5 · 26:32
clinical Islet equivalent per kilogram of body weight is used as a prognostic marker; at approximately 5000 islet equivalents/kg there is a 50% chance of insulin independence. ↗
▶ Ep 5 · 27:00
clinical TPIAT outcomes: 50% of patients achieve insulin independence, 20% require small insulin doses, and 30% remain diabetic. ↗
▶ Ep 5 · 27:05
quote I'm exchanging potentially disease for a disease, right? Chronic pancreatitis for potential diabetes. ↗
▶ Ep 5 · 27:05
clinical TPIAT exchanges chronic pancreatitis for potential diabetes, which must be clearly communicated to families. ↗
▶ Ep 5 · 27:23
quote My day starts the, the night before as I start going through the case. It's a long day. It's a long day. I reviewed this case in my head, uh, 30 times before I go in. ↗
▶ Ep 5 · 27:32
clinical TPIAT surgery takes an average of 8-10 hours: 3-4 hours for pancreatectomy, 4-4.5 hours for islet isolation in the lab, and 2 hours for reconstruction. ↗
▶ Ep 5 · 28:47
clinical Pylorus-preserving resection with pyloric Botox injection is performed during TPIAT reconstruction to address gastroparesis that all pancreatitis patients have; Roux-en-Y reconstruction also helps with gastroparesis. ↗
▶ Ep 5 · 29:33
clinical Routine splenectomy is performed with TPIAT because the pancreas and spleen share blood supply via tiny branches from the splenic vessels; preserving the spleen adds ischemia time and causes islet cell loss. ↗
▶ Ep 5 · 29:59
clinical There are four critical points where islet cells can be lost: (1) recurrent pancreatitis causing cell death, (2) ischemia during surgical dissection, (3) cell death during processing and injection, and (4) post-operative stress if glucose is not carefully managed. ↗
▶ Ep 5 · 30:20
clinical All TPIAT patients are kept on insulin in the ICU post-operatively to let the islet cells rest without working until they implant and establish new vascular supply from the liver. ↗
▶ Ep 5 · 31:10
clinical The liver is the best site for islet cell implantation via portal vein injection; extrahepatic sites (omentum, retroperitoneum, rectus muscle, gastric submucosa) have been tried but work less well. ↗
▶ Ep 5 · 31:58
clinical Portal vein thrombosis after islet injection occurs in less than 1% of cases; portal pressure is monitored during injection. ↗
▶ Ep 5 · 32:23
clinical The duodenum is resected at D1 post-pyloric during TPIAT because of shared blood supply with the pancreas; attempting to preserve it adds ischemia time. ↗

Update Course Rewind: Management of Chronic Pancreatitis 2023

▶ Ep 6 · 0:43
quote OK, we have a 5-year-old, chronic pancreatitis, debilitating abdominal pain, multiple hospital admission admissions in the last 2 years, fell behind on milestones, Dilaudid 3 times per week. ↗
▶ Ep 6 · 1:28
quote So, if you, most of the pancreatic parenchyma is in the head and the uncinate process. If you get rid of that head and there's a pancreatic, uh, uh, PRS1 mutation, this kid is gonna get uh recurrent attacks. ↗
▶ Ep 6 · 1:28
clinical If a patient has a PRSS1 mutation and only the pancreatic head is removed, recurrent attacks will occur. ↗
▶ Ep 6 · 1:28
clinical Most of the pancreatic parenchyma is in the head and the uncinate process. ↗
▶ Ep 6 · 1:40
quote So, up to 50% of patients with chronic pancreatitis will eventually require surgery. ↗
▶ Ep 6 · 1:40
epidemiological Up to 50% of patients with chronic pancreatitis will eventually require surgery. ↗
▶ Ep 6 · 2:01
quote Not everybody is, is a candidate for, they need support, they need social support, right? ↗
▶ Ep 6 · 2:10
guideline TPIAT requires a multidisciplinary team including surgery, GI pancreatologists, social worker, geneticists, psychiatry, and pain control. ↗
▶ Ep 6 · 2:18
quote So remember, patients with chronic pancreatitis are, are always having micro and macronutrient deficiencies, so we need to pay a lot of attention to this. ↗
▶ Ep 6 · 2:18
clinical Patients with chronic pancreatitis always have micro and macronutrient deficiencies. ↗
▶ Ep 6 · 2:33
clinical Chronic pancreatitis patients sometimes need pancreatic enzyme replacement therapy. ↗
▶ Ep 6 · 2:40
quote Um, you lose first your exocrine and then your endocrine function, so you need to keep screening for it. ↗
▶ Ep 6 · 2:40
clinical In chronic pancreatitis, exocrine function is lost first, then endocrine function. ↗
▶ Ep 6 · 2:49
quote The goals is to bring this kid back to their life, right? These kids are like totally withdrawn, they dropped their milestones dramatically, so it's important to bring, bring them back to their society. ↗
▶ Ep 6 · 2:49
clinical The primary goal of TPIAT is to restore the child's quality of life and return them to normal activities. ↗
▶ Ep 6 · 2:59
clinical The secondary goal of TPIAT is to prevent brittle diabetes by preserving beta cell function. ↗
▶ Ep 6 · 2:59
quote And as a secondary goal is to try to prevent the brittle diabetes that happens once your pancreas is out. ↗
▶ Ep 6 · 3:06
clinical All TPIAT patients require enzyme replacement therapy post-operatively. ↗
▶ Ep 6 · 3:23
quote There's a lot of factors that play into insulin independence uh on the, on the, on the, on the outcomes of this surgery, but right now, 50% chance if you hit 5000, 50% chance you're not going to require insulin. ↗
▶ Ep 6 · 3:23
clinical With an islet cell count of 5000, there is a 50% chance of not requiring insulin post-TPIAT. ↗
▶ Ep 6 · 3:36
clinical With an islet cell count of 5000, there is a 20% chance of requiring a small dose of insulin post-TPIAT. ↗
▶ Ep 6 · 3:40
clinical With an islet cell count of 5000, 30% of patients remain diabetic post-TPIAT. ↗
▶ Ep 6 · 3:42
clinical TPIAT potentially exchanges chronic pancreatitis for diabetes, and families must be counseled about this trade-off. ↗
▶ Ep 6 · 3:42
quote So we need to tell the families they're, I'm exchanging potentially disease for a disease, right? Chronic pancreatitis for potential diabetes. ↗
▶ Ep 6 · 4:25
clinical TPIAT surgery takes an average of 8 to 10 hours. ↗
▶ Ep 6 · 4:34
clinical The pancreas is cemented in the retroperitoneum with neovascularization and collateralization, making removal the most problematic part of TPIAT. ↗
▶ Ep 6 · 4:34
clinical Some chronic pancreatitis patients have thrombosis in the portal vein or splenic vein. ↗
▶ Ep 6 · 4:51
clinical Pancreatectomy during TPIAT takes 3 to 4 hours. ↗
▶ Ep 6 · 5:09
clinical During TPIAT, biliary and intestinal reconstruction is performed using a Roux-en-Y technique while islet isolation is occurring. ↗
▶ Ep 6 · 5:28
clinical The spleen is removed along with the pancreas during TPIAT. ↗
▶ Ep 6 · 5:35
clinical Islet cell isolation takes 4 to 4.5 hours. ↗
▶ Ep 6 · 5:39
clinical Islet cells are injected into the portal vein inside the liver. ↗
▶ Ep 6 · 6:05
clinical In the acute post-operative period, glucose must be managed externally to prevent stress on transplanted islet cells. ↗
▶ Ep 6 · 6:09
quote If you put them under stress, the cells die. ↗
▶ Ep 6 · 6:12
clinical All TPIAT patients are on insulin in the ICU to allow islet cells to implant without stress. ↗
▶ Ep 6 · 6:14
clinical Islet cells need to find new vessels from the liver to survive after transplantation. ↗
▶ Ep 6 · 6:14
quote I want the cells to be like just chilling, not doing any work until they implant and find new vessels from the liver to survive. ↗
▶ Ep 6 · 6:27
clinical Islet cells implant in the end branches of the portal vein inside the liver. ↗
▶ Ep 6 · 6:34
clinical Extrahepatic islet cell reimplantation does not work as well as intrahepatic placement. ↗
▶ Ep 6 · 6:43
clinical Extrahepatic islet cells produce a better glucagon response for hypoglycemia compared to intrahepatic cells. ↗
▶ Ep 6 · 6:51
clinical The liver is the best site for islet cell transplantation. ↗
▶ Ep 6 · 6:54
clinical The risk of portal vein thrombosis after intrahepatic islet injection is less than 1%. ↗
▶ Ep 6 · 6:54
clinical Portal pressure is monitored during islet cell injection to prevent complications. ↗
▶ Ep 6 · 7:05
clinical During TPIAT, the duodenum is removed at D1 post-pyloric level along with the pancreas. ↗
▶ Ep 6 · 7:10
clinical The duodenum and pancreas share blood supply, making duodenal preservation difficult during TPIAT. ↗

Update Course Rewind: Management of Recurrent Pancreatitis

▶ Ep 7 · 1:40
quote Every time you get an, an ERCP you have a risk of getting post-E ERCP pancreatitis. It's low, right? But it's still a risk, and you lose eyelet cells with every attack. ↗
▶ Ep 7 · 1:40
clinical Every ERCP carries a risk of post-ERCP pancreatitis, and with every pancreatitis attack, islet cells are lost. ↗
▶ Ep 7 · 1:57
quote PRSS1 is the most common one, which is a trypsinogen activator. It activates trypsin inside the pancreas. ↗
▶ Ep 7 · 1:57
clinical PRSS1 is the most common genetic mutation in recurrent pancreatitis and is a trypsinogen activator that activates trypsin inside the pancreas. ↗
▶ Ep 7 · 2:06
clinical The genetic panel at Cincinnati Children's tests 10 different genetic markers for pancreatitis (including PRSS1, CTRC, CFTR, CPA1). ↗
▶ Ep 7 · 2:17
quote That's how we're changing the approach to pediatric pancreatitis, chronic pan pancreatitis treatment because of the genetic factors. ↗
▶ Ep 7 · 2:17
opinion Genetic factors are changing the approach to pediatric chronic pancreatitis treatment. ↗
▶ Ep 7 · 2:48
quote No, no, there's no, unfortunately we don't have that just yet. That's why I still have a job, but, uh, I hope, I hope some Monday we have, you know. ↗
▶ Ep 7 · 2:48
clinical There is currently no medication to mitigate trypsin activation in genetic pancreatitis mutations. ↗
▶ Ep 7 · 3:09
clinical In a Frey procedure (partial head pancreatectomy with pancreaticojejunostomy), the top half of the pancreas is removed to open the duct, which results in loss of islet cells. ↗
▶ Ep 7 · 3:19
quote This patient most likely is gonna keep getting pancreatitis despite you draining the duct. The, the parenchyma is gonna keep getting attacked by the mutation. So, you're temporizing um the attack by draining the duct, uh, but you're not fixing the problem. ↗
▶ Ep 7 · 3:19
clinical In patients with PRSS1 mutation, draining the duct (e.g., via Frey) temporizes attacks but does not fix the problem, as the parenchyma continues to be attacked by the mutation and pancreatitis will likely recur. ↗
▶ Ep 7 · 4:09
opinion There is no set number of ERCPs that defines when to escalate care; the sooner the referral for evaluation, the better. ↗
▶ Ep 7 · 4:16
guideline Surgical management of the pancreas is not offered unless medical and endoscopic management have been maximized. ↗
▶ Ep 7 · 4:16
quote We don't offer, uh, to take care of the pancreas unless you've. Maximize medical and endoscopic management. ↗
▶ Ep 7 · 4:23
quote If there's no other options and your endoscopic guy tells you, you know what, there's nothing for me to balloon dilate, open, drain, or anything. There's been a stent. Even with the stent, the patient keeps getting pancreatitis. There's no reason to keep going with ERCPs. ↗
▶ Ep 7 · 4:23
clinical If the endoscopist has no further options (nothing to balloon dilate, open, or drain) and the patient continues to have pancreatitis despite stenting, there is no reason to continue ERCPs. ↗
▶ Ep 7 · 4:58
quote MRCP is the best non-invasive study for pancreas by far, uh, with different uh uh T2 sequences. ↗
▶ Ep 7 · 4:58
clinical MRCP is the best non-invasive imaging study for the pancreas, particularly with T2 sequences. ↗
▶ Ep 7 · 5:07
clinical ERCP is more therapeutic than diagnostic. ↗
▶ Ep 7 · 5:22
quote Once the, the wall is mature in 4 to 6 weeks, uh, if there's symptoms, drain it. If there's no symptoms, don't drain it. ↗
▶ Ep 7 · 5:22
clinical Pancreatic fluid collections should be drained once the wall is mature (4 to 6 weeks) only if the patient is symptomatic (e.g., gastric outlet obstruction or pain); asymptomatic collections will self-resolve and do not require drainage or antibiotics. ↗

Total pancreatectomy with islet autotransplantation (TPIAT) - Cincinnati Children's Pancreas Care Center

▶ Ep 9 · 0:48
opinion TPIAT is one of the most complex abdominal surgical procedures performed in children. ↗
▶ Ep 9 · 0:48
quote TPIAT is clearly one of the most complex abdominal surgical procedures we perform in children. ↗
▶ Ep 9 · 0:54
clinical Surgical indications for TPIAT are for patients with either chronic or acute recurrent pancreatitis. ↗
▶ Ep 9 · 1:02
guideline Patients are candidates for TPIAT when all medical and endoscopic therapy has failed. ↗
▶ Ep 9 · 1:02
quote These patients are candidates for TPAT when all medical and endoscopic therapy has failed. ↗
▶ Ep 9 · 1:23
clinical The Pancreas Care Center team includes GI, social worker, endocrine, surgery, radiology, genetics, behavioral health, physical therapy, anesthesia, and pain team. ↗
▶ Ep 9 · 1:45
clinical The entire team reviews and votes patients in for surgery to determine if they are candidates for TPIAT. ↗
▶ Ep 9 · 1:45
clinical Patients are prepared with vaccinations for potential splenectomy before TPIAT surgery. ↗
▶ Ep 9 · 2:40
clinical Pain catheters are placed in the transversus abdominis muscle by pain specialists. ↗
▶ Ep 9 · 3:14
clinical The pancreas in TPIAT patients has been injured for sometimes years, which makes the procedure quite challenging. ↗
▶ Ep 9 · 3:14
quote Remember, this, this pancreas has been injured for sometimes years, which makes this procedure quite challenging. ↗
▶ Ep 9 · 3:29
clinical On the right side, the small intestine (duodenum) and liver hilum are mobilized, with careful identification of bile ducts and blood supply to the liver. ↗
▶ Ep 9 · 4:06
clinical Blood supply to the head and entire body of the pancreas is preserved very carefully until the very last moment to avoid hypoxia of islet cells. ↗
▶ Ep 9 · 4:06
quote We preserve very carefully the blood supply to the head and the entire body until the pancreas, until the very last moment because we cannot risk hypoxying these cells. ↗
▶ Ep 9 · 6:33
clinical During islet processing, the surgical team performs reconstruction of the gastrointestinal tract by bringing a loop of duodenum up to the bile duct and reconnecting another loop of intestine to the duodenum past the pyloric muscle. ↗
▶ Ep 9 · 6:53
clinical A feeding tube is placed to allow patients to be fed while important connections heal. ↗
▶ Ep 9 · 7:02
clinical Drains are left where the spleen was removed and on top of the connection with the biliary tract. ↗
▶ Ep 9 · 7:15
clinical Islet cells are transfused into the portal vein with the hope that they will implant in the liver and start producing insulin. ↗
▶ Ep 9 · 7:25
clinical Portal vein pressures are constantly checked during islet infusion to prevent portal vein thrombosis, which could cause significant morbidity. ↗
▶ Ep 9 · 7:25
quote While we infuse the eyelid itself, we're constantly checking the pressures in the portal vein to make sure we don't risk any thrombosis in the portal vein, which could cause a lot of morbidity to the patient. ↗
▶ Ep 9 · 8:01
clinical Patients are placed in the intensive care unit post-operatively to control hemodynamics and fluid shift balance. ↗
▶ Ep 9 · 8:08
clinical Islet cells need to heal in a very homeostatic environment, requiring close monitoring of vital signs. ↗
▶ Ep 9 · 8:18
clinical Glucose and insulin are controlled via exogenous infusions post-operatively. ↗
▶ Ep 9 · 8:22
clinical Close attention to nutrition is key in the healing of connections between the bile tract and gastrointestinal tract. ↗
▶ Ep 9 · 8:39
clinical Patients are deemed ready for discharge when pain is well controlled, they are on full feeds (via tube or by mouth), glucose is well controlled via continuous glucose monitoring, and they have received full education. ↗
▶ Ep 9 · 8:47
clinical After discharge, local GI physicians continue to follow patients along with the Cincinnati Children's team. ↗

Overview of the Surgical Management of Acute and Chronic Pancreatitis in Children with Dr. Juan Gurria

▶ Ep 11 · 5:44
guideline Diagnosis of acute pancreatitis requires serum lipase at least 3 times the upper limit of normal, plus imaging findings (ultrasound, MRI/MRCP, or CT). ↗
▶ Ep 11 · 7:23
epidemiological In the Cincinnati Children's cohort of 1000 pediatric pancreatitis patients, 85% have genetic mutations. ↗
▶ Ep 11 · 8:01
clinical PRSS1 mutation causes very aggressive attacks very early in life (ages 1–3 years) because it autoactivates trypsinogen inside the pancreas. ↗
▶ Ep 11 · 8:37
clinical Medications including L-asparaginase, steroids, valproic acid, and diuretics (Lasix) can cause pancreatitis in children. ↗
▶ Ep 11 · 9:32
clinical Hereditary pancreatitis increases the risk of pancreatic cancer by a huge fold, which is a major concern in children diagnosed at age 5–6 who may live 95 more years. ↗
▶ Ep 11 · 10:15
clinical Most fluid collections in pediatric acute pancreatitis are self-limited and should not be touched unless absolutely necessary. ↗
▶ Ep 11 · 18:08
quote Please do not touch these collections ever unless you absolutely have to. ↗
▶ Ep 11 · 18:40
clinical Early necrosectomies (before 4 weeks) usually increase mortality. ↗
▶ Ep 11 · 19:49
clinical Following lipase levels tells you nothing about how the pancreas is behaving in acute pancreatitis; cross-sectional imaging is required. ↗
▶ Ep 11 · 21:36
clinical Asymptomatic pseudocysts, regardless of size, do not require intervention. ↗
▶ Ep 11 · 23:29
clinical Patients with acute pancreatitis should be fed as soon as possible (orally or via NG/NJ tube) because bacterial translocation from NPO status will complicate the disease. ↗
▶ Ep 11 · 23:29
quote Please feed your patients as soon as you can, all right? If they're vomiting and they're gonna puke it, well, that doesn't make any sense. You, if you have to throw out an NG or an NG tube, feed the god because bacterial translocation from NPL will complicate acute pancreatitis. ↗
▶ Ep 11 · 25:13
epidemiological In pediatric patients with hereditary pancreatitis or hereditary plus anatomic abnormalities, half will develop chronic pancreatitis. ↗
▶ Ep 11 · 25:38
clinical Cincinnati Children's evaluates over 100 patients per year for chronic pancreatitis but only operates on 25–30, because medical and endoscopic options should be exhausted first. ↗
▶ Ep 11 · 26:50
clinical Chronic pain in pancreatitis involves brain plasticity, hypertrophic nerve reactions, and peripheral nerve hypersensitization, not just organic retroperitoneal pain. ↗
▶ Ep 11 · 27:43
clinical After total pancreatectomy, 95% of pain is resolved, but 5% may persist due to central sensitization and requires behavioral medicine and psychiatric support. ↗
▶ Ep 11 · 27:43
quote I'm gonna take your pancreas out if it's uh indicated, and I'm gonna take care of 95% of your pain. But that 5, 5% that is left. We need to work with psych, behavioral med, uh, and eventually reteach their brains how to live not in pain. ↗
▶ Ep 11 · 28:37
clinical Pediatric chronic pancreatitis usually presents with minimal ductal changes, not the dilated ducts seen in adults, so drainage procedures are often not applicable. ↗
▶ Ep 11 · 28:57
clinical In patients with genetic mutations, partial pancreatectomy (Whipple, distal pancreatectomy) discards islet mass and does not address the underlying defect, so the remaining pancreas continues to be affected. ↗
▶ Ep 11 · 28:57
quote If you have a genetic mutation and you chop off a piece of the pancreas, throw it in the trash. You can maybe relieve some of the pain. If you do whipple, have the pancreas drain better, do a piece so, I'm gonna touch base on that in a sec, drain the pancreatic duct better. But I put a piece of paper in the trash. And the genetic mutations will keep affecting the rest of the pancreas. ↗
▶ Ep 11 · 37:44
quote We're doing this for, for chronic pain and that should be the, the, the major thing in our head. ↗
▶ Ep 11 · 37:54
guideline TPIAT is indicated when patients have chronic pancreatitis findings, at least 6 months of disease, exocrine or endocrine insufficiency, and impaired quality of life despite maximal medical and endoscopic therapy. ↗
▶ Ep 11 · 39:00
clinical The goal of islet autotransplantation is to replace beta cell mass and insulin secretory capacity, not to cure diabetes—pain control is the primary indication. ↗
▶ Ep 11 · 40:28
clinical TPIAT used to be a 20-hour operation but is now down to an average of 8–9 hours at Cincinnati Children's. ↗
▶ Ep 11 · 43:15
clinical Spleen-sparing TPIAT has equal glycemic outcomes to splenectomy TPIAT when islet equivalent per kilogram transplanted is matched. ↗
▶ Ep 11 · 43:42
clinical Spleen-sparing TPIAT is now performed in 80% of cases (over the last 5 years), compared to none in the first 8 years of the program. ↗
▶ Ep 11 · 45:16
clinical Intraoperative pyloric Botox injection reduces gastroparesis, decreases length of stay, and improves time to full oral intake and glycemic control after TPIAT. ↗
▶ Ep 11 · 46:27
clinical Islet isolation takes about 3–3.5 hours, sometimes 4 hours depending on the degree of pancreatic injury. ↗
▶ Ep 11 · 47:39
clinical TPIAT is performed under anticoagulation (heparin) to prevent portal vein thrombosis during islet infusion. ↗
▶ Ep 11 · 48:11
clinical Portal vein thrombosis rate at Cincinnati Children's is less than 1% for TPIAT. ↗
▶ Ep 11 · 48:26
clinical Cincinnati Children's has performed close to 200 TPIAT cases with no anastomotic leaks. ↗
▶ Ep 11 · 50:07
clinical Patients are extubated in the operating room after TPIAT. ↗
▶ Ep 11 · 51:32
clinical Younger children are more likely to achieve insulin independence and opioid independence after TPIAT. ↗
▶ Ep 11 · 52:25
clinical Islet yield (IEQ/kg) is inversely related to pancreatic calcification, ductal dilation, fibrosis, duration of symptoms, and prior resections or drainage procedures. ↗
▶ Ep 11 · 54:59
clinical Predictors of insulin independence after TPIAT include younger age at surgery, smaller body surface area, no pre-existing insulin dependence, and higher IEQ/kg transplanted. ↗
▶ Ep 11 · 56:09
clinical TPIAT dramatically improves quality of life in appropriately selected children, with families reporting they have 'never met this kid before'—new person, happy, playing, eating normally. ↗
Juan's statements about Islet Cell / TPIAT 26 statements

Open the Islet Cell / TPIAT collection →

Total pancreatectomy with islet autotransplantation (TPIAT) - Cincinnati Children's Pancreas Care Center

▶ Ep 3 · 0:48
quote TPIAT is clearly one of the most complex abdominal surgical procedures we perform in children. ↗
▶ Ep 3 · 0:48
opinion TPIAT is one of the most complex abdominal surgical procedures performed in children. ↗
▶ Ep 3 · 0:54
clinical Surgical indications for TPIAT are for patients with either chronic or acute recurrent pancreatitis. ↗
▶ Ep 3 · 1:02
guideline Patients are candidates for TPIAT when all medical and endoscopic therapy has failed. ↗
▶ Ep 3 · 1:02
quote These patients are candidates for TPAT when all medical and endoscopic therapy has failed. ↗
▶ Ep 3 · 1:23
clinical The Pancreas Care Center team includes GI, social worker, endocrine, surgery, radiology, genetics, behavioral health, physical therapy, anesthesia, and pain team. ↗
▶ Ep 3 · 1:45
clinical Patients are prepared with vaccinations for potential splenectomy before TPIAT surgery. ↗
▶ Ep 3 · 1:45
clinical The entire team reviews and votes patients in for surgery to determine if they are candidates for TPIAT. ↗
▶ Ep 3 · 2:40
clinical Pain catheters are placed in the transversus abdominis muscle by pain specialists. ↗
▶ Ep 3 · 3:14
clinical The pancreas in TPIAT patients has been injured for sometimes years, which makes the procedure quite challenging. ↗
▶ Ep 3 · 3:14
quote Remember, this, this pancreas has been injured for sometimes years, which makes this procedure quite challenging. ↗
▶ Ep 3 · 3:29
clinical On the right side, the small intestine (duodenum) and liver hilum are mobilized, with careful identification of bile ducts and blood supply to the liver. ↗
▶ Ep 3 · 4:06
clinical Blood supply to the head and entire body of the pancreas is preserved very carefully until the very last moment to avoid hypoxia of islet cells. ↗
▶ Ep 3 · 4:06
quote We preserve very carefully the blood supply to the head and the entire body until the pancreas, until the very last moment because we cannot risk hypoxying these cells. ↗
▶ Ep 3 · 6:33
clinical During islet processing, the surgical team performs reconstruction of the gastrointestinal tract by bringing a loop of duodenum up to the bile duct and reconnecting another loop of intestine to the duodenum past the pyloric muscle. ↗
▶ Ep 3 · 6:53
clinical A feeding tube is placed to allow patients to be fed while important connections heal. ↗
▶ Ep 3 · 7:02
clinical Drains are left where the spleen was removed and on top of the connection with the biliary tract. ↗
▶ Ep 3 · 7:15
clinical Islet cells are transfused into the portal vein with the hope that they will implant in the liver and start producing insulin. ↗
▶ Ep 3 · 7:25
clinical Portal vein pressures are constantly checked during islet infusion to prevent portal vein thrombosis, which could cause significant morbidity. ↗
▶ Ep 3 · 7:25
quote While we infuse the eyelid itself, we're constantly checking the pressures in the portal vein to make sure we don't risk any thrombosis in the portal vein, which could cause a lot of morbidity to the patient. ↗
▶ Ep 3 · 8:01
clinical Patients are placed in the intensive care unit post-operatively to control hemodynamics and fluid shift balance. ↗
▶ Ep 3 · 8:08
clinical Islet cells need to heal in a very homeostatic environment, requiring close monitoring of vital signs. ↗
▶ Ep 3 · 8:18
clinical Glucose and insulin are controlled via exogenous infusions post-operatively. ↗
▶ Ep 3 · 8:22
clinical Close attention to nutrition is key in the healing of connections between the bile tract and gastrointestinal tract. ↗
▶ Ep 3 · 8:39
clinical Patients are deemed ready for discharge when pain is well controlled, they are on full feeds (via tube or by mouth), glucose is well controlled via continuous glucose monitoring, and they have received full education. ↗
▶ Ep 3 · 8:47
clinical After discharge, local GI physicians continue to follow patients along with the Cincinnati Children's team. ↗
Juan's statements about Pancreatic Surgery & Critical Care 64 statements

Open the Pancreatic Surgery & Critical Care collection →

Update Course 2023 - Updates in Pancreatitis

▶ Ep 1 · 0:35
clinical Acute pancreatitis management has shifted from NPO and aggressive IV fluids causing pulmonary edema to early feeding and measured fluid resuscitation. ↗
▶ Ep 1 · 0:35
quote it is very important nowadays to feed the pancreas, even when there's pancreatitis ↗
▶ Ep 1 · 1:01
quote you cannot take care of a pancreas without a wonderful team ↗
▶ Ep 1 · 3:55
clinical For acute pancreatitis with tachycardia (HR 160) and hypotension in a 9-year-old, appropriate management is ICU admission with bolus ×2, maintenance IV fluids 1.5×, no antibiotics, and pain control. ↗
▶ Ep 1 · 4:03
quote Acute pancreatitis could be fatal ↗
▶ Ep 1 · 4:19
quote pancreatitis is a state of uh hypoxia. You need to re-establish the intravascular flow to the pancreas to prevent hypoxia, necrosis ↗
▶ Ep 1 · 4:19
clinical Early fluid resuscitation is key to re-establish intravascular flow to the pancreas and prevent hypoxia, necrosis, and atrophic pancreatic insufficiency. ↗
▶ Ep 1 · 4:39
clinical Excessive fluid resuscitation in pancreatitis leads to worse outcomes including fluid overload and multi-system organ failure. ↗
▶ Ep 1 · 4:42
guideline There is no indication for routine antibiotics in acute pancreatitis, even with necrosis or necrotizing pancreatitis, unless there are signs of sepsis or infected pancreatitis. ↗
▶ Ep 1 · 6:13
quote You cannot uh flow these lungs too much because the outcomes are worse ↗
▶ Ep 1 · 6:21
guideline Maintenance fluids should be 1.5 to 2 times normal maintenance, with reassessment at 12-24 hour mark to avoid fluid overload. ↗
▶ Ep 1 · 9:24
clinical Enteral nutrition as soon as the patient can tolerate PO is significantly better compared to TPN or NPO in acute pancreatitis. ↗
▶ Ep 1 · 10:19
clinical Some vomiting can be tolerated when feeding pancreatitis patients, similar to gastroschisis management, because feeding the gut produces dramatically better outcomes. ↗
▶ Ep 1 · 10:21
quote It's OK to tolerate some, some, some. Vomiting. If you can feed them, that's fine. ↗
▶ Ep 1 · 11:02
quote nobody needs TPN the 1st 7 days of acute illness, right? ↗
▶ Ep 1 · 11:02
clinical No patient needs TPN in the first 7 days of acute illness. ↗
▶ Ep 1 · 12:13
clinical The inflammatory head mass commonly seen in adult pancreatitis is rarely seen in children; pediatric patients typically have minimal duct change disease with small, usually non-dilated ducts. ↗
▶ Ep 1 · 14:38
clinical With every attack of pancreatitis, islet cells are lost, so repeated ERCPs that fail to prevent attacks result in progressive loss of beta-cell mass. ↗
▶ Ep 1 · 14:44
clinical ERCP does not change the islet yield available for transplantation, but pancreatitis attacks cause cell loss. ↗
▶ Ep 1 · 14:53
quote children get pancreatitis. We have a running list of 800 patients right now in Cin Children's. ↗
▶ Ep 1 · 14:59
guideline Genetic testing is key in pediatric pancreatitis and should be obtained for all patients with chronic or recurrent pancreatitis, and even considered after a first severe attack. ↗
▶ Ep 1 · 14:59
epidemiological Cincinnati Children's has a running list of 800 pancreatitis patients and receives over 100 TPIAT referrals per year, but only performs 20-25 procedures annually because not all patients are candidates. ↗
▶ Ep 1 · 15:23
epidemiological The most common cause of pancreatitis in children is medication-induced, but the most common risk factor is genetic factors. ↗
▶ Ep 1 · 15:23
quote The most common cause of pancreatitis in children is, is, is medicine induced. The most common risk factor for pancreatitis in children is, is genetic factors. ↗
▶ Ep 1 · 15:32
quote PRSS one is the most common one, which is a trypsinogen activator. It activates trypsin inside the pancreas. So, you get auto-attacked by pancreatitis. It's the most aggressive one. ↗
▶ Ep 1 · 15:32
clinical PRSS1 (trypsinogen activator) is the most common genetic mutation in pediatric pancreatitis and the most aggressive, causing auto-attack by activating trypsin inside the pancreas. ↗
▶ Ep 1 · 15:48
clinical Cincinnati Children's genetic panel tests 10 different genetic markers for pancreatitis including PRSS1, CTRC, CFTR, and CPA1. ↗
▶ Ep 1 · 16:06
opinion Genetics have fundamentally changed the approach to pediatric chronic pancreatitis treatment. ↗
▶ Ep 1 · 16:33
quote up to 50% of those children are gonna keep getting pancreatitis despite you opening the duct and draining it ↗
▶ Ep 1 · 16:33
clinical In children with genetic mutations causing pancreatitis, conventional drainage procedures (Frey, Puestow) fail in up to 50% because the parenchyma continues to be attacked by the mutation despite duct drainage. ↗
▶ Ep 1 · 16:49
quote you send half of your, the top of your pancreas to the trash ↗
▶ Ep 1 · 17:07
quote unfortunately we don't have that just yet. That's why I still have a job. ↗
▶ Ep 1 · 18:24
quote This patient most likely is gonna keep getting pancreatitis despite you draining the duct. The, the parenchyma is gonna keep getting attacked by the mutation. ↗
▶ Ep 1 · 19:02
quote TPIT, which is total pancreatectomy with eyelid autotransplantation. Uh, the main indication is, is for pain, chronic debilitating pain for children that are losing their lives. ↗
▶ Ep 1 · 19:08
clinical The main indication for TPIAT is chronic debilitating pain in children who have lost their quality of life—not attending school, withdrawn, unable to participate in activities. ↗
▶ Ep 1 · 19:19
quote There's no more ballerina dancers, right? ↗
▶ Ep 1 · 19:22
clinical The secondary goal of TPIAT is to prevent brittle diabetes by returning beta cells to the patient. ↗
▶ Ep 1 · 19:56
quote if you keep getting pancreatitis, you're losing time on that, right? The, the pancreas, we have 34 years old with like very atrophic pancreas ↗
▶ Ep 1 · 20:17
quote We don't offer. Uh, to take care of the pancreas unless you've maximize medical and endoscopic management. ↗
▶ Ep 1 · 20:59
clinical MRCP is the best non-invasive imaging study for the pancreas, superior to ultrasound and CT. ↗
▶ Ep 1 · 21:07
clinical ERCP is more therapeutic than diagnostic in chronic pancreatitis. ↗
▶ Ep 1 · 21:12
clinical Patients with chronic pancreatitis always have micronutrient and macronutrient deficiencies requiring nutritional support. ↗
▶ Ep 1 · 21:36
clinical Patients with chronic pancreatitis lose exocrine function first, then endocrine function, requiring screening and often pancreatic enzyme replacement therapy. ↗
▶ Ep 1 · 21:48
clinical Walled-off necrosis should be drained only if symptomatic (gastric outlet obstruction or pain) after the wall matures at 4-6 weeks; asymptomatic collections will self-resolve and do not require drainage or antibiotics. ↗
▶ Ep 1 · 22:08
epidemiological Chronic pancreatitis increases the risk of pancreatic cancer up to thirteenfold. ↗
▶ Ep 1 · 24:08
epidemiological Up to 50% of patients with chronic pancreatitis will eventually require surgery. ↗
▶ Ep 1 · 24:40
clinical TPIAT requires a multidisciplinary team including surgery, GI pancreatologists, social workers, geneticists, psychology, and pain management. ↗
▶ Ep 1 · 25:00
quote some families ask us like, so you're gonna get rid of the pain, right? 100%, and you cannot say that, right? ↗
▶ Ep 1 · 25:07
clinical Patients with chronic pain develop hyperalgesia and central sensitization—their brains learn to function in pain—so removing the organ may eliminate 90% of pain but 10% may linger, requiring behavioral therapy. ↗
▶ Ep 1 · 25:07
quote People that have chronic pain, their bodies, their brains learn how to be in pain, right? They can function in pain. That's called hyperalgesia and central sensitization. ↗
▶ Ep 1 · 25:18
quote when you take the, the, the organ part out, you maybe 90% of the pain is gone, but you cannot promise them that 10 that 10% is gonna linger for a little bit ↗
▶ Ep 1 · 26:32
clinical Islet equivalent per kilogram of body weight is used as a prognostic marker; at approximately 5000 islet equivalents/kg there is a 50% chance of insulin independence. ↗
▶ Ep 1 · 27:00
clinical TPIAT outcomes: 50% of patients achieve insulin independence, 20% require small insulin doses, and 30% remain diabetic. ↗
▶ Ep 1 · 27:05
quote I'm exchanging potentially disease for a disease, right? Chronic pancreatitis for potential diabetes. ↗
▶ Ep 1 · 27:05
clinical TPIAT exchanges chronic pancreatitis for potential diabetes, which must be clearly communicated to families. ↗
▶ Ep 1 · 27:23
quote My day starts the, the night before as I start going through the case. It's a long day. It's a long day. I reviewed this case in my head, uh, 30 times before I go in. ↗
▶ Ep 1 · 27:32
clinical TPIAT surgery takes an average of 8-10 hours: 3-4 hours for pancreatectomy, 4-4.5 hours for islet isolation in the lab, and 2 hours for reconstruction. ↗
▶ Ep 1 · 28:47
clinical Pylorus-preserving resection with pyloric Botox injection is performed during TPIAT reconstruction to address gastroparesis that all pancreatitis patients have; Roux-en-Y reconstruction also helps with gastroparesis. ↗
▶ Ep 1 · 29:33
clinical Routine splenectomy is performed with TPIAT because the pancreas and spleen share blood supply via tiny branches from the splenic vessels; preserving the spleen adds ischemia time and causes islet cell loss. ↗
▶ Ep 1 · 29:59
clinical There are four critical points where islet cells can be lost: (1) recurrent pancreatitis causing cell death, (2) ischemia during surgical dissection, (3) cell death during processing and injection, and (4) post-operative stress if glucose is not carefully managed. ↗
▶ Ep 1 · 30:20
clinical All TPIAT patients are kept on insulin in the ICU post-operatively to let the islet cells rest without working until they implant and establish new vascular supply from the liver. ↗
▶ Ep 1 · 31:10
clinical The liver is the best site for islet cell implantation via portal vein injection; extrahepatic sites (omentum, retroperitoneum, rectus muscle, gastric submucosa) have been tried but work less well. ↗
▶ Ep 1 · 31:58
clinical Portal vein thrombosis after islet injection occurs in less than 1% of cases; portal pressure is monitored during injection. ↗
▶ Ep 1 · 32:23
clinical The duodenum is resected at D1 post-pyloric during TPIAT because of shared blood supply with the pancreas; attempting to preserve it adds ischemia time. ↗
Juan's statements about Pancreatitis 266 statements

Open the Pancreatitis collection →

Update Course 2023 - Updates in Pancreatitis

▶ Ep 13 · 0:35
quote it is very important nowadays to feed the pancreas, even when there's pancreatitis ↗
▶ Ep 13 · 0:35
clinical Acute pancreatitis management has shifted from NPO and aggressive IV fluids causing pulmonary edema to early feeding and measured fluid resuscitation. ↗
▶ Ep 13 · 1:01
quote you cannot take care of a pancreas without a wonderful team ↗
▶ Ep 13 · 3:55
clinical For acute pancreatitis with tachycardia (HR 160) and hypotension in a 9-year-old, appropriate management is ICU admission with bolus ×2, maintenance IV fluids 1.5×, no antibiotics, and pain control. ↗
▶ Ep 13 · 4:03
quote Acute pancreatitis could be fatal ↗
▶ Ep 13 · 4:19
clinical Early fluid resuscitation is key to re-establish intravascular flow to the pancreas and prevent hypoxia, necrosis, and atrophic pancreatic insufficiency. ↗
▶ Ep 13 · 4:19
quote pancreatitis is a state of uh hypoxia. You need to re-establish the intravascular flow to the pancreas to prevent hypoxia, necrosis ↗
▶ Ep 13 · 4:39
clinical Excessive fluid resuscitation in pancreatitis leads to worse outcomes including fluid overload and multi-system organ failure. ↗
▶ Ep 13 · 4:42
guideline There is no indication for routine antibiotics in acute pancreatitis, even with necrosis or necrotizing pancreatitis, unless there are signs of sepsis or infected pancreatitis. ↗
▶ Ep 13 · 6:13
quote You cannot uh flow these lungs too much because the outcomes are worse ↗
▶ Ep 13 · 6:21
guideline Maintenance fluids should be 1.5 to 2 times normal maintenance, with reassessment at 12-24 hour mark to avoid fluid overload. ↗
▶ Ep 13 · 9:24
clinical Enteral nutrition as soon as the patient can tolerate PO is significantly better compared to TPN or NPO in acute pancreatitis. ↗
▶ Ep 13 · 10:19
clinical Some vomiting can be tolerated when feeding pancreatitis patients, similar to gastroschisis management, because feeding the gut produces dramatically better outcomes. ↗
▶ Ep 13 · 10:21
quote It's OK to tolerate some, some, some. Vomiting. If you can feed them, that's fine. ↗
▶ Ep 13 · 11:02
clinical No patient needs TPN in the first 7 days of acute illness. ↗
▶ Ep 13 · 11:02
quote nobody needs TPN the 1st 7 days of acute illness, right? ↗
▶ Ep 13 · 12:13
clinical The inflammatory head mass commonly seen in adult pancreatitis is rarely seen in children; pediatric patients typically have minimal duct change disease with small, usually non-dilated ducts. ↗
▶ Ep 13 · 14:38
clinical With every attack of pancreatitis, islet cells are lost, so repeated ERCPs that fail to prevent attacks result in progressive loss of beta-cell mass. ↗
▶ Ep 13 · 14:44
clinical ERCP does not change the islet yield available for transplantation, but pancreatitis attacks cause cell loss. ↗
▶ Ep 13 · 14:53
quote children get pancreatitis. We have a running list of 800 patients right now in Cin Children's. ↗
▶ Ep 13 · 14:59
guideline Genetic testing is key in pediatric pancreatitis and should be obtained for all patients with chronic or recurrent pancreatitis, and even considered after a first severe attack. ↗
▶ Ep 13 · 14:59
epidemiological Cincinnati Children's has a running list of 800 pancreatitis patients and receives over 100 TPIAT referrals per year, but only performs 20-25 procedures annually because not all patients are candidates. ↗
▶ Ep 13 · 15:23
epidemiological The most common cause of pancreatitis in children is medication-induced, but the most common risk factor is genetic factors. ↗
▶ Ep 13 · 15:23
quote The most common cause of pancreatitis in children is, is, is medicine induced. The most common risk factor for pancreatitis in children is, is genetic factors. ↗
▶ Ep 13 · 15:32
quote PRSS one is the most common one, which is a trypsinogen activator. It activates trypsin inside the pancreas. So, you get auto-attacked by pancreatitis. It's the most aggressive one. ↗
▶ Ep 13 · 15:32
clinical PRSS1 (trypsinogen activator) is the most common genetic mutation in pediatric pancreatitis and the most aggressive, causing auto-attack by activating trypsin inside the pancreas. ↗
▶ Ep 13 · 15:48
clinical Cincinnati Children's genetic panel tests 10 different genetic markers for pancreatitis including PRSS1, CTRC, CFTR, and CPA1. ↗
▶ Ep 13 · 16:06
opinion Genetics have fundamentally changed the approach to pediatric chronic pancreatitis treatment. ↗
▶ Ep 13 · 16:33
quote up to 50% of those children are gonna keep getting pancreatitis despite you opening the duct and draining it ↗
▶ Ep 13 · 16:33
clinical In children with genetic mutations causing pancreatitis, conventional drainage procedures (Frey, Puestow) fail in up to 50% because the parenchyma continues to be attacked by the mutation despite duct drainage. ↗
▶ Ep 13 · 16:49
quote you send half of your, the top of your pancreas to the trash ↗
▶ Ep 13 · 17:07
quote unfortunately we don't have that just yet. That's why I still have a job. ↗
▶ Ep 13 · 18:24
quote This patient most likely is gonna keep getting pancreatitis despite you draining the duct. The, the parenchyma is gonna keep getting attacked by the mutation. ↗
▶ Ep 13 · 19:02
quote TPIT, which is total pancreatectomy with eyelid autotransplantation. Uh, the main indication is, is for pain, chronic debilitating pain for children that are losing their lives. ↗
▶ Ep 13 · 19:08
clinical The main indication for TPIAT is chronic debilitating pain in children who have lost their quality of life—not attending school, withdrawn, unable to participate in activities. ↗
▶ Ep 13 · 19:19
quote There's no more ballerina dancers, right? ↗
▶ Ep 13 · 19:22
clinical The secondary goal of TPIAT is to prevent brittle diabetes by returning beta cells to the patient. ↗
▶ Ep 13 · 19:56
quote if you keep getting pancreatitis, you're losing time on that, right? The, the pancreas, we have 34 years old with like very atrophic pancreas ↗
▶ Ep 13 · 20:17
quote We don't offer. Uh, to take care of the pancreas unless you've maximize medical and endoscopic management. ↗
▶ Ep 13 · 20:59
clinical MRCP is the best non-invasive imaging study for the pancreas, superior to ultrasound and CT. ↗
▶ Ep 13 · 21:07
clinical ERCP is more therapeutic than diagnostic in chronic pancreatitis. ↗
▶ Ep 13 · 21:12
clinical Patients with chronic pancreatitis always have micronutrient and macronutrient deficiencies requiring nutritional support. ↗
▶ Ep 13 · 21:36
clinical Patients with chronic pancreatitis lose exocrine function first, then endocrine function, requiring screening and often pancreatic enzyme replacement therapy. ↗
▶ Ep 13 · 21:48
clinical Walled-off necrosis should be drained only if symptomatic (gastric outlet obstruction or pain) after the wall matures at 4-6 weeks; asymptomatic collections will self-resolve and do not require drainage or antibiotics. ↗
▶ Ep 13 · 22:08
epidemiological Chronic pancreatitis increases the risk of pancreatic cancer up to thirteenfold. ↗
▶ Ep 13 · 24:08
epidemiological Up to 50% of patients with chronic pancreatitis will eventually require surgery. ↗
▶ Ep 13 · 24:40
clinical TPIAT requires a multidisciplinary team including surgery, GI pancreatologists, social workers, geneticists, psychology, and pain management. ↗
▶ Ep 13 · 25:00
quote some families ask us like, so you're gonna get rid of the pain, right? 100%, and you cannot say that, right? ↗
▶ Ep 13 · 25:07
quote People that have chronic pain, their bodies, their brains learn how to be in pain, right? They can function in pain. That's called hyperalgesia and central sensitization. ↗
▶ Ep 13 · 25:07
clinical Patients with chronic pain develop hyperalgesia and central sensitization—their brains learn to function in pain—so removing the organ may eliminate 90% of pain but 10% may linger, requiring behavioral therapy. ↗
▶ Ep 13 · 25:18
quote when you take the, the, the organ part out, you maybe 90% of the pain is gone, but you cannot promise them that 10 that 10% is gonna linger for a little bit ↗
▶ Ep 13 · 26:32
clinical Islet equivalent per kilogram of body weight is used as a prognostic marker; at approximately 5000 islet equivalents/kg there is a 50% chance of insulin independence. ↗
▶ Ep 13 · 27:00
clinical TPIAT outcomes: 50% of patients achieve insulin independence, 20% require small insulin doses, and 30% remain diabetic. ↗
▶ Ep 13 · 27:05
quote I'm exchanging potentially disease for a disease, right? Chronic pancreatitis for potential diabetes. ↗
▶ Ep 13 · 27:05
clinical TPIAT exchanges chronic pancreatitis for potential diabetes, which must be clearly communicated to families. ↗
▶ Ep 13 · 27:23
quote My day starts the, the night before as I start going through the case. It's a long day. It's a long day. I reviewed this case in my head, uh, 30 times before I go in. ↗
▶ Ep 13 · 27:32
clinical TPIAT surgery takes an average of 8-10 hours: 3-4 hours for pancreatectomy, 4-4.5 hours for islet isolation in the lab, and 2 hours for reconstruction. ↗
▶ Ep 13 · 28:47
clinical Pylorus-preserving resection with pyloric Botox injection is performed during TPIAT reconstruction to address gastroparesis that all pancreatitis patients have; Roux-en-Y reconstruction also helps with gastroparesis. ↗
▶ Ep 13 · 29:33
clinical Routine splenectomy is performed with TPIAT because the pancreas and spleen share blood supply via tiny branches from the splenic vessels; preserving the spleen adds ischemia time and causes islet cell loss. ↗
▶ Ep 13 · 29:59
clinical There are four critical points where islet cells can be lost: (1) recurrent pancreatitis causing cell death, (2) ischemia during surgical dissection, (3) cell death during processing and injection, and (4) post-operative stress if glucose is not carefully managed. ↗
▶ Ep 13 · 30:20
clinical All TPIAT patients are kept on insulin in the ICU post-operatively to let the islet cells rest without working until they implant and establish new vascular supply from the liver. ↗
▶ Ep 13 · 31:10
clinical The liver is the best site for islet cell implantation via portal vein injection; extrahepatic sites (omentum, retroperitoneum, rectus muscle, gastric submucosa) have been tried but work less well. ↗
▶ Ep 13 · 31:58
clinical Portal vein thrombosis after islet injection occurs in less than 1% of cases; portal pressure is monitored during injection. ↗
▶ Ep 13 · 32:23
clinical The duodenum is resected at D1 post-pyloric during TPIAT because of shared blood supply with the pancreas; attempting to preserve it adds ischemia time. ↗

Update Course Rewind: Management of Acute Pancreatitis 2023

▶ Ep 14 · 1:56
quote Acute pancreatitis could be fatal. ↗
▶ Ep 14 · 1:56
clinical Acute pancreatitis could be fatal ↗
▶ Ep 14 · 1:58
clinical Bolus times 2 is adequate fluid resuscitation, with 1.5 times maintenance once past the early phase of acute resuscitation ↗
▶ Ep 14 · 2:06
clinical Pancreatitis is a state of hypoxia requiring re-establishment of intravascular flow to the pancreas to prevent hypoxia, necrosis, and atrophic pancreas insufficiency ↗
▶ Ep 14 · 2:06
quote Remember that pancreatitis is a state of, uh, hypoxia. You need to re-establish the intravascular flow to the pancreas to prevent hypoxia, necrosis, atrophic pancreas insufficiency. ↗
▶ Ep 14 · 2:22
clinical Early fluid resuscitation is key in pancreatitis management ↗
▶ Ep 14 · 2:26
clinical Excessive fluid administration worsens outcomes in pancreatitis ↗
▶ Ep 14 · 2:29
guideline There is no reason to give antibiotics for pancreatitis, even in the face of necrosis or necrotizing pancreatitis, unless there are signs of sepsis or infected pancreatitis ↗
▶ Ep 14 · 2:29
quote Now, there's no reason to give antibiotics anymore at all for pancreatitis, even in the face of world of necrosis or necrotizing pancreatitis, unless there are signs of sepsis infected pancreatitis, which is a different beast ↗
▶ Ep 14 · 2:57
guideline The North American Society of Pancreatitis, GI Pathology, and Nutrition published a position paper with guideline recommendations for pancreatitis management ↗
▶ Ep 14 · 3:07
clinical Early fluids lead to better outcomes in pancreatitis ↗
▶ Ep 14 · 3:11
guideline Recommended fluid bolus is 10 to 20 mL per kg, up to 3L in the first 24 hours, with reassessment at the 12-hour mark using urine output and vital signs ↗
▶ Ep 14 · 3:25
clinical Excessive fluid administration can flood the lungs and worsen outcomes ↗
▶ Ep 14 · 3:25
quote You cannot flow these lungs too much because the outcomes are worse. ↗
▶ Ep 14 · 3:45
quote It's been shown that LR. Decreases the incidence of inflammatory response and C, C-reactive protein at 24 hours compared to NS, right? ↗
▶ Ep 14 · 3:45
clinical Lactated Ringer's decreases the incidence of inflammatory response and C-reactive protein at 24 hours compared to normal saline in pancreatitis ↗
▶ Ep 14 · 3:54
clinical If albumin is low in pancreatitis patients, albumin should be given ↗
▶ Ep 14 · 3:58
clinical Enrique de Madaria conducted a multi-center worldwide RCT called the Waterfall trial comparing moderate versus aggressive fluid resuscitation in pancreatitis ↗
▶ Ep 14 · 4:18
clinical The Waterfall trial was stopped early because patients receiving too much fluid were developing organ failure ↗
▶ Ep 14 · 4:27
clinical A follow-up Waterland trial is underway to determine whether lactated Ringer's is better than normal saline, expected to be published in one to two years ↗
▶ Ep 14 · 4:47
clinical Patients with pancreatitis should be fed as soon as they are able to tolerate oral intake ↗
▶ Ep 14 · 4:51
clinical Enteral nutrition is significantly better compared to TPN or NPO in pancreatitis ↗
▶ Ep 14 · 4:57
clinical Gastric feeding is preferred over post-pyloric feeding in pancreatitis if the patient can tolerate it ↗
▶ Ep 14 · 5:19
opinion Some vomiting is tolerable during refeeding in pancreatitis, similar to gastroschisis management ↗
▶ Ep 14 · 5:19
quote If they cannot tolerate it, it's OK. I mean, but it's like gastroschisis, it's OK to tolerate some, some, some vomiting. ↗
▶ Ep 14 · 5:26
quote If you're losing nutrition and you're losing ground, the patient's gonna have a worse outcome. Their albumin is gonna drop, inflammatory reaction is gonna be worse. ↗
▶ Ep 14 · 5:26
clinical If nutrition is lost and the patient loses ground, outcomes will be worse, with dropping albumin and worse inflammatory reaction ↗
▶ Ep 14 · 5:34
clinical Outcomes are dramatically better when the gut is fed in pancreatitis patients ↗

Update Course Rewind: Management of Chronic Pancreatitis 2023

▶ Ep 15 · 0:43
quote OK, we have a 5-year-old, chronic pancreatitis, debilitating abdominal pain, multiple hospital admission admissions in the last 2 years, fell behind on milestones, Dilaudid 3 times per week. ↗
▶ Ep 15 · 0:43
quote OK, we have a 5-year-old, chronic pancreatitis, debilitating abdominal pain, multiple hospital admission admissions in the last 2 years, fell behind on milestones, Dilaudid 3 times per week. ↗
▶ Ep 15 · 1:28
quote So, if you, most of the pancreatic parenchyma is in the head and the uncinate process. If you get rid of that head and there's a pancreatic, uh, uh, PRS1 mutation, this kid is gonna get uh recurrent attacks. ↗
▶ Ep 15 · 1:28
quote So, if you, most of the pancreatic parenchyma is in the head and the uncinate process. If you get rid of that head and there's a pancreatic, uh, uh, PRS1 mutation, this kid is gonna get uh recurrent attacks. ↗
▶ Ep 15 · 1:28
clinical If a patient has a PRSS1 mutation and only the pancreatic head is removed, recurrent attacks will occur. ↗
▶ Ep 15 · 1:28
clinical Most of the pancreatic parenchyma is in the head and the uncinate process. ↗
▶ Ep 15 · 1:28
clinical Most of the pancreatic parenchyma is in the head and the uncinate process. ↗
▶ Ep 15 · 1:28
clinical If a patient has a PRSS1 mutation and only the pancreatic head is removed, recurrent attacks will occur. ↗
▶ Ep 15 · 1:40
epidemiological Up to 50% of patients with chronic pancreatitis will eventually require surgery. ↗
▶ Ep 15 · 1:40
epidemiological Up to 50% of patients with chronic pancreatitis will eventually require surgery. ↗
▶ Ep 15 · 1:40
quote So, up to 50% of patients with chronic pancreatitis will eventually require surgery. ↗
▶ Ep 15 · 1:40
quote So, up to 50% of patients with chronic pancreatitis will eventually require surgery. ↗
▶ Ep 15 · 2:01
quote Not everybody is, is a candidate for, they need support, they need social support, right? ↗
▶ Ep 15 · 2:01
quote Not everybody is, is a candidate for, they need support, they need social support, right? ↗
▶ Ep 15 · 2:10
guideline TPIAT requires a multidisciplinary team including surgery, GI pancreatologists, social worker, geneticists, psychiatry, and pain control. ↗
▶ Ep 15 · 2:10
guideline TPIAT requires a multidisciplinary team including surgery, GI pancreatologists, social worker, geneticists, psychiatry, and pain control. ↗
▶ Ep 15 · 2:18
clinical Patients with chronic pancreatitis always have micro and macronutrient deficiencies. ↗
▶ Ep 15 · 2:18
clinical Patients with chronic pancreatitis always have micro and macronutrient deficiencies. ↗
▶ Ep 15 · 2:18
quote So remember, patients with chronic pancreatitis are, are always having micro and macronutrient deficiencies, so we need to pay a lot of attention to this. ↗
▶ Ep 15 · 2:18
quote So remember, patients with chronic pancreatitis are, are always having micro and macronutrient deficiencies, so we need to pay a lot of attention to this. ↗
▶ Ep 15 · 2:33
clinical Chronic pancreatitis patients sometimes need pancreatic enzyme replacement therapy. ↗
▶ Ep 15 · 2:33
clinical Chronic pancreatitis patients sometimes need pancreatic enzyme replacement therapy. ↗
▶ Ep 15 · 2:40
quote Um, you lose first your exocrine and then your endocrine function, so you need to keep screening for it. ↗
▶ Ep 15 · 2:40
clinical In chronic pancreatitis, exocrine function is lost first, then endocrine function. ↗
▶ Ep 15 · 2:40
clinical In chronic pancreatitis, exocrine function is lost first, then endocrine function. ↗
▶ Ep 15 · 2:40
quote Um, you lose first your exocrine and then your endocrine function, so you need to keep screening for it. ↗
▶ Ep 15 · 2:49
quote The goals is to bring this kid back to their life, right? These kids are like totally withdrawn, they dropped their milestones dramatically, so it's important to bring, bring them back to their society. ↗
▶ Ep 15 · 2:49
quote The goals is to bring this kid back to their life, right? These kids are like totally withdrawn, they dropped their milestones dramatically, so it's important to bring, bring them back to their society. ↗
▶ Ep 15 · 2:49
clinical The primary goal of TPIAT is to restore the child's quality of life and return them to normal activities. ↗
▶ Ep 15 · 2:49
clinical The primary goal of TPIAT is to restore the child's quality of life and return them to normal activities. ↗
▶ Ep 15 · 2:59
clinical The secondary goal of TPIAT is to prevent brittle diabetes by preserving beta cell function. ↗
▶ Ep 15 · 2:59
clinical The secondary goal of TPIAT is to prevent brittle diabetes by preserving beta cell function. ↗
▶ Ep 15 · 2:59
quote And as a secondary goal is to try to prevent the brittle diabetes that happens once your pancreas is out. ↗
▶ Ep 15 · 2:59
quote And as a secondary goal is to try to prevent the brittle diabetes that happens once your pancreas is out. ↗
▶ Ep 15 · 3:06
clinical All TPIAT patients require enzyme replacement therapy post-operatively. ↗
▶ Ep 15 · 3:06
clinical All TPIAT patients require enzyme replacement therapy post-operatively. ↗
▶ Ep 15 · 3:23
clinical With an islet cell count of 5000, there is a 50% chance of not requiring insulin post-TPIAT. ↗
▶ Ep 15 · 3:23
quote There's a lot of factors that play into insulin independence uh on the, on the, on the, on the outcomes of this surgery, but right now, 50% chance if you hit 5000, 50% chance you're not going to require insulin. ↗
▶ Ep 15 · 3:23
clinical With an islet cell count of 5000, there is a 50% chance of not requiring insulin post-TPIAT. ↗
▶ Ep 15 · 3:23
quote There's a lot of factors that play into insulin independence uh on the, on the, on the, on the outcomes of this surgery, but right now, 50% chance if you hit 5000, 50% chance you're not going to require insulin. ↗
▶ Ep 15 · 3:36
clinical With an islet cell count of 5000, there is a 20% chance of requiring a small dose of insulin post-TPIAT. ↗
▶ Ep 15 · 3:36
clinical With an islet cell count of 5000, there is a 20% chance of requiring a small dose of insulin post-TPIAT. ↗
▶ Ep 15 · 3:40
clinical With an islet cell count of 5000, 30% of patients remain diabetic post-TPIAT. ↗
▶ Ep 15 · 3:40
clinical With an islet cell count of 5000, 30% of patients remain diabetic post-TPIAT. ↗
▶ Ep 15 · 3:42
clinical TPIAT potentially exchanges chronic pancreatitis for diabetes, and families must be counseled about this trade-off. ↗
▶ Ep 15 · 3:42
quote So we need to tell the families they're, I'm exchanging potentially disease for a disease, right? Chronic pancreatitis for potential diabetes. ↗
▶ Ep 15 · 3:42
clinical TPIAT potentially exchanges chronic pancreatitis for diabetes, and families must be counseled about this trade-off. ↗
▶ Ep 15 · 3:42
quote So we need to tell the families they're, I'm exchanging potentially disease for a disease, right? Chronic pancreatitis for potential diabetes. ↗
▶ Ep 15 · 4:25
clinical TPIAT surgery takes an average of 8 to 10 hours. ↗
▶ Ep 15 · 4:25
clinical TPIAT surgery takes an average of 8 to 10 hours. ↗
▶ Ep 15 · 4:34
clinical Some chronic pancreatitis patients have thrombosis in the portal vein or splenic vein. ↗
▶ Ep 15 · 4:34
clinical The pancreas is cemented in the retroperitoneum with neovascularization and collateralization, making removal the most problematic part of TPIAT. ↗
▶ Ep 15 · 4:34
clinical Some chronic pancreatitis patients have thrombosis in the portal vein or splenic vein. ↗
▶ Ep 15 · 4:34
clinical The pancreas is cemented in the retroperitoneum with neovascularization and collateralization, making removal the most problematic part of TPIAT. ↗
▶ Ep 15 · 4:51
clinical Pancreatectomy during TPIAT takes 3 to 4 hours. ↗
▶ Ep 15 · 4:51
clinical Pancreatectomy during TPIAT takes 3 to 4 hours. ↗
▶ Ep 15 · 5:09
clinical During TPIAT, biliary and intestinal reconstruction is performed using a Roux-en-Y technique while islet isolation is occurring. ↗
▶ Ep 15 · 5:09
clinical During TPIAT, biliary and intestinal reconstruction is performed using a Roux-en-Y technique while islet isolation is occurring. ↗
▶ Ep 15 · 5:28
clinical The spleen is removed along with the pancreas during TPIAT. ↗
▶ Ep 15 · 5:28
clinical The spleen is removed along with the pancreas during TPIAT. ↗
▶ Ep 15 · 5:35
clinical Islet cell isolation takes 4 to 4.5 hours. ↗
▶ Ep 15 · 5:35
clinical Islet cell isolation takes 4 to 4.5 hours. ↗
▶ Ep 15 · 5:39
clinical Islet cells are injected into the portal vein inside the liver. ↗
▶ Ep 15 · 5:39
clinical Islet cells are injected into the portal vein inside the liver. ↗
▶ Ep 15 · 6:05
clinical In the acute post-operative period, glucose must be managed externally to prevent stress on transplanted islet cells. ↗
▶ Ep 15 · 6:05
clinical In the acute post-operative period, glucose must be managed externally to prevent stress on transplanted islet cells. ↗
▶ Ep 15 · 6:09
quote If you put them under stress, the cells die. ↗
▶ Ep 15 · 6:09
quote If you put them under stress, the cells die. ↗
▶ Ep 15 · 6:12
clinical All TPIAT patients are on insulin in the ICU to allow islet cells to implant without stress. ↗
▶ Ep 15 · 6:12
clinical All TPIAT patients are on insulin in the ICU to allow islet cells to implant without stress. ↗
▶ Ep 15 · 6:14
quote I want the cells to be like just chilling, not doing any work until they implant and find new vessels from the liver to survive. ↗
▶ Ep 15 · 6:14
clinical Islet cells need to find new vessels from the liver to survive after transplantation. ↗
▶ Ep 15 · 6:14
clinical Islet cells need to find new vessels from the liver to survive after transplantation. ↗
▶ Ep 15 · 6:14
quote I want the cells to be like just chilling, not doing any work until they implant and find new vessels from the liver to survive. ↗
▶ Ep 15 · 6:27
clinical Islet cells implant in the end branches of the portal vein inside the liver. ↗
▶ Ep 15 · 6:27
clinical Islet cells implant in the end branches of the portal vein inside the liver. ↗
▶ Ep 15 · 6:34
clinical Extrahepatic islet cell reimplantation does not work as well as intrahepatic placement. ↗
▶ Ep 15 · 6:34
clinical Extrahepatic islet cell reimplantation does not work as well as intrahepatic placement. ↗
▶ Ep 15 · 6:43
clinical Extrahepatic islet cells produce a better glucagon response for hypoglycemia compared to intrahepatic cells. ↗
▶ Ep 15 · 6:43
clinical Extrahepatic islet cells produce a better glucagon response for hypoglycemia compared to intrahepatic cells. ↗
▶ Ep 15 · 6:51
clinical The liver is the best site for islet cell transplantation. ↗
▶ Ep 15 · 6:51
clinical The liver is the best site for islet cell transplantation. ↗
▶ Ep 15 · 6:54
clinical Portal pressure is monitored during islet cell injection to prevent complications. ↗
▶ Ep 15 · 6:54
clinical The risk of portal vein thrombosis after intrahepatic islet injection is less than 1%. ↗
▶ Ep 15 · 6:54
clinical Portal pressure is monitored during islet cell injection to prevent complications. ↗
▶ Ep 15 · 6:54
clinical The risk of portal vein thrombosis after intrahepatic islet injection is less than 1%. ↗
▶ Ep 15 · 7:05
clinical During TPIAT, the duodenum is removed at D1 post-pyloric level along with the pancreas. ↗
▶ Ep 15 · 7:05
clinical During TPIAT, the duodenum is removed at D1 post-pyloric level along with the pancreas. ↗
▶ Ep 15 · 7:10
clinical The duodenum and pancreas share blood supply, making duodenal preservation difficult during TPIAT. ↗
▶ Ep 15 · 7:10
clinical The duodenum and pancreas share blood supply, making duodenal preservation difficult during TPIAT. ↗

Update Course Rewind: Management of Recurrent Pancreatitis

▶ Ep 17 · 1:40
clinical Every ERCP carries a risk of post-ERCP pancreatitis, and with every pancreatitis attack, islet cells are lost. ↗
▶ Ep 17 · 1:40
quote Every time you get an, an ERCP you have a risk of getting post-E ERCP pancreatitis. It's low, right? But it's still a risk, and you lose eyelet cells with every attack. ↗
▶ Ep 17 · 1:57
quote PRSS1 is the most common one, which is a trypsinogen activator. It activates trypsin inside the pancreas. ↗
▶ Ep 17 · 1:57
clinical PRSS1 is the most common genetic mutation in recurrent pancreatitis and is a trypsinogen activator that activates trypsin inside the pancreas. ↗
▶ Ep 17 · 2:06
clinical The genetic panel at Cincinnati Children's tests 10 different genetic markers for pancreatitis (including PRSS1, CTRC, CFTR, CPA1). ↗
▶ Ep 17 · 2:17
opinion Genetic factors are changing the approach to pediatric chronic pancreatitis treatment. ↗
▶ Ep 17 · 2:17
quote That's how we're changing the approach to pediatric pancreatitis, chronic pan pancreatitis treatment because of the genetic factors. ↗
▶ Ep 17 · 2:48
quote No, no, there's no, unfortunately we don't have that just yet. That's why I still have a job, but, uh, I hope, I hope some Monday we have, you know. ↗
▶ Ep 17 · 2:48
clinical There is currently no medication to mitigate trypsin activation in genetic pancreatitis mutations. ↗
▶ Ep 17 · 3:09
clinical In a Frey procedure (partial head pancreatectomy with pancreaticojejunostomy), the top half of the pancreas is removed to open the duct, which results in loss of islet cells. ↗
▶ Ep 17 · 3:19
quote This patient most likely is gonna keep getting pancreatitis despite you draining the duct. The, the parenchyma is gonna keep getting attacked by the mutation. So, you're temporizing um the attack by draining the duct, uh, but you're not fixing the problem. ↗
▶ Ep 17 · 3:19
clinical In patients with PRSS1 mutation, draining the duct (e.g., via Frey) temporizes attacks but does not fix the problem, as the parenchyma continues to be attacked by the mutation and pancreatitis will likely recur. ↗
▶ Ep 17 · 4:09
opinion There is no set number of ERCPs that defines when to escalate care; the sooner the referral for evaluation, the better. ↗
▶ Ep 17 · 4:16
guideline Surgical management of the pancreas is not offered unless medical and endoscopic management have been maximized. ↗
▶ Ep 17 · 4:16
quote We don't offer, uh, to take care of the pancreas unless you've. Maximize medical and endoscopic management. ↗
▶ Ep 17 · 4:23
clinical If the endoscopist has no further options (nothing to balloon dilate, open, or drain) and the patient continues to have pancreatitis despite stenting, there is no reason to continue ERCPs. ↗
▶ Ep 17 · 4:23
quote If there's no other options and your endoscopic guy tells you, you know what, there's nothing for me to balloon dilate, open, drain, or anything. There's been a stent. Even with the stent, the patient keeps getting pancreatitis. There's no reason to keep going with ERCPs. ↗
▶ Ep 17 · 4:58
quote MRCP is the best non-invasive study for pancreas by far, uh, with different uh uh T2 sequences. ↗
▶ Ep 17 · 4:58
clinical MRCP is the best non-invasive imaging study for the pancreas, particularly with T2 sequences. ↗
▶ Ep 17 · 5:07
clinical ERCP is more therapeutic than diagnostic. ↗
▶ Ep 17 · 5:22
quote Once the, the wall is mature in 4 to 6 weeks, uh, if there's symptoms, drain it. If there's no symptoms, don't drain it. ↗
▶ Ep 17 · 5:22
clinical Pancreatic fluid collections should be drained once the wall is mature (4 to 6 weeks) only if the patient is symptomatic (e.g., gastric outlet obstruction or pain); asymptomatic collections will self-resolve and do not require drainage or antibiotics. ↗

Total pancreatectomy with islet autotransplantation (TPIAT) - Cincinnati Children's Pancreas Care Center

▶ Ep 21 · 0:48
opinion TPIAT is one of the most complex abdominal surgical procedures performed in children. ↗
▶ Ep 21 · 0:48
quote TPIAT is clearly one of the most complex abdominal surgical procedures we perform in children. ↗
▶ Ep 21 · 0:54
clinical Surgical indications for TPIAT are for patients with either chronic or acute recurrent pancreatitis. ↗
▶ Ep 21 · 1:02
guideline Patients are candidates for TPIAT when all medical and endoscopic therapy has failed. ↗
▶ Ep 21 · 1:02
quote These patients are candidates for TPAT when all medical and endoscopic therapy has failed. ↗
▶ Ep 21 · 1:23
clinical The Pancreas Care Center team includes GI, social worker, endocrine, surgery, radiology, genetics, behavioral health, physical therapy, anesthesia, and pain team. ↗
▶ Ep 21 · 1:45
clinical The entire team reviews and votes patients in for surgery to determine if they are candidates for TPIAT. ↗
▶ Ep 21 · 1:45
clinical Patients are prepared with vaccinations for potential splenectomy before TPIAT surgery. ↗
▶ Ep 21 · 2:40
clinical Pain catheters are placed in the transversus abdominis muscle by pain specialists. ↗
▶ Ep 21 · 3:14
clinical The pancreas in TPIAT patients has been injured for sometimes years, which makes the procedure quite challenging. ↗
▶ Ep 21 · 3:14
quote Remember, this, this pancreas has been injured for sometimes years, which makes this procedure quite challenging. ↗
▶ Ep 21 · 3:29
clinical On the right side, the small intestine (duodenum) and liver hilum are mobilized, with careful identification of bile ducts and blood supply to the liver. ↗
▶ Ep 21 · 4:06
clinical Blood supply to the head and entire body of the pancreas is preserved very carefully until the very last moment to avoid hypoxia of islet cells. ↗
▶ Ep 21 · 4:06
quote We preserve very carefully the blood supply to the head and the entire body until the pancreas, until the very last moment because we cannot risk hypoxying these cells. ↗
▶ Ep 21 · 6:33
clinical During islet processing, the surgical team performs reconstruction of the gastrointestinal tract by bringing a loop of duodenum up to the bile duct and reconnecting another loop of intestine to the duodenum past the pyloric muscle. ↗
▶ Ep 21 · 6:53
clinical A feeding tube is placed to allow patients to be fed while important connections heal. ↗
▶ Ep 21 · 7:02
clinical Drains are left where the spleen was removed and on top of the connection with the biliary tract. ↗
▶ Ep 21 · 7:15
clinical Islet cells are transfused into the portal vein with the hope that they will implant in the liver and start producing insulin. ↗
▶ Ep 21 · 7:25
clinical Portal vein pressures are constantly checked during islet infusion to prevent portal vein thrombosis, which could cause significant morbidity. ↗
▶ Ep 21 · 7:25
quote While we infuse the eyelid itself, we're constantly checking the pressures in the portal vein to make sure we don't risk any thrombosis in the portal vein, which could cause a lot of morbidity to the patient. ↗
▶ Ep 21 · 8:01
clinical Patients are placed in the intensive care unit post-operatively to control hemodynamics and fluid shift balance. ↗
▶ Ep 21 · 8:08
clinical Islet cells need to heal in a very homeostatic environment, requiring close monitoring of vital signs. ↗
▶ Ep 21 · 8:18
clinical Glucose and insulin are controlled via exogenous infusions post-operatively. ↗
▶ Ep 21 · 8:22
clinical Close attention to nutrition is key in the healing of connections between the bile tract and gastrointestinal tract. ↗
▶ Ep 21 · 8:39
clinical Patients are deemed ready for discharge when pain is well controlled, they are on full feeds (via tube or by mouth), glucose is well controlled via continuous glucose monitoring, and they have received full education. ↗
▶ Ep 21 · 8:47
clinical After discharge, local GI physicians continue to follow patients along with the Cincinnati Children's team. ↗

Overview of the Surgical Management of Acute and Chronic Pancreatitis in Children with Dr. Juan Gurria

▶ Ep 26 · 5:44
guideline Diagnosis of acute pancreatitis requires serum lipase at least 3 times the upper limit of normal, plus imaging findings (ultrasound, MRI/MRCP, or CT). ↗
▶ Ep 26 · 7:23
epidemiological In the Cincinnati Children's cohort of 1000 pediatric pancreatitis patients, 85% have genetic mutations. ↗
▶ Ep 26 · 8:01
clinical PRSS1 mutation causes very aggressive attacks very early in life (ages 1–3 years) because it autoactivates trypsinogen inside the pancreas. ↗
▶ Ep 26 · 8:37
clinical Medications including L-asparaginase, steroids, valproic acid, and diuretics (Lasix) can cause pancreatitis in children. ↗
▶ Ep 26 · 9:32
clinical Hereditary pancreatitis increases the risk of pancreatic cancer by a huge fold, which is a major concern in children diagnosed at age 5–6 who may live 95 more years. ↗
▶ Ep 26 · 10:15
clinical Most fluid collections in pediatric acute pancreatitis are self-limited and should not be touched unless absolutely necessary. ↗
▶ Ep 26 · 18:08
quote Please do not touch these collections ever unless you absolutely have to. ↗
▶ Ep 26 · 18:40
clinical Early necrosectomies (before 4 weeks) usually increase mortality. ↗
▶ Ep 26 · 19:49
clinical Following lipase levels tells you nothing about how the pancreas is behaving in acute pancreatitis; cross-sectional imaging is required. ↗
▶ Ep 26 · 21:36
clinical Asymptomatic pseudocysts, regardless of size, do not require intervention. ↗
▶ Ep 26 · 23:29
clinical Patients with acute pancreatitis should be fed as soon as possible (orally or via NG/NJ tube) because bacterial translocation from NPO status will complicate the disease. ↗
▶ Ep 26 · 23:29
quote Please feed your patients as soon as you can, all right? If they're vomiting and they're gonna puke it, well, that doesn't make any sense. You, if you have to throw out an NG or an NG tube, feed the god because bacterial translocation from NPL will complicate acute pancreatitis. ↗
▶ Ep 26 · 25:13
epidemiological In pediatric patients with hereditary pancreatitis or hereditary plus anatomic abnormalities, half will develop chronic pancreatitis. ↗
▶ Ep 26 · 25:38
clinical Cincinnati Children's evaluates over 100 patients per year for chronic pancreatitis but only operates on 25–30, because medical and endoscopic options should be exhausted first. ↗
▶ Ep 26 · 26:50
clinical Chronic pain in pancreatitis involves brain plasticity, hypertrophic nerve reactions, and peripheral nerve hypersensitization, not just organic retroperitoneal pain. ↗
▶ Ep 26 · 27:43
clinical After total pancreatectomy, 95% of pain is resolved, but 5% may persist due to central sensitization and requires behavioral medicine and psychiatric support. ↗
▶ Ep 26 · 27:43
quote I'm gonna take your pancreas out if it's uh indicated, and I'm gonna take care of 95% of your pain. But that 5, 5% that is left. We need to work with psych, behavioral med, uh, and eventually reteach their brains how to live not in pain. ↗
▶ Ep 26 · 28:37
clinical Pediatric chronic pancreatitis usually presents with minimal ductal changes, not the dilated ducts seen in adults, so drainage procedures are often not applicable. ↗
▶ Ep 26 · 28:57
quote If you have a genetic mutation and you chop off a piece of the pancreas, throw it in the trash. You can maybe relieve some of the pain. If you do whipple, have the pancreas drain better, do a piece so, I'm gonna touch base on that in a sec, drain the pancreatic duct better. But I put a piece of paper in the trash. And the genetic mutations will keep affecting the rest of the pancreas. ↗
▶ Ep 26 · 28:57
clinical In patients with genetic mutations, partial pancreatectomy (Whipple, distal pancreatectomy) discards islet mass and does not address the underlying defect, so the remaining pancreas continues to be affected. ↗
▶ Ep 26 · 37:44
quote We're doing this for, for chronic pain and that should be the, the, the major thing in our head. ↗
▶ Ep 26 · 37:54
guideline TPIAT is indicated when patients have chronic pancreatitis findings, at least 6 months of disease, exocrine or endocrine insufficiency, and impaired quality of life despite maximal medical and endoscopic therapy. ↗
▶ Ep 26 · 39:00
clinical The goal of islet autotransplantation is to replace beta cell mass and insulin secretory capacity, not to cure diabetes—pain control is the primary indication. ↗
▶ Ep 26 · 40:28
clinical TPIAT used to be a 20-hour operation but is now down to an average of 8–9 hours at Cincinnati Children's. ↗
▶ Ep 26 · 43:15
clinical Spleen-sparing TPIAT has equal glycemic outcomes to splenectomy TPIAT when islet equivalent per kilogram transplanted is matched. ↗
▶ Ep 26 · 43:42
clinical Spleen-sparing TPIAT is now performed in 80% of cases (over the last 5 years), compared to none in the first 8 years of the program. ↗
▶ Ep 26 · 45:16
clinical Intraoperative pyloric Botox injection reduces gastroparesis, decreases length of stay, and improves time to full oral intake and glycemic control after TPIAT. ↗
▶ Ep 26 · 46:27
clinical Islet isolation takes about 3–3.5 hours, sometimes 4 hours depending on the degree of pancreatic injury. ↗
▶ Ep 26 · 47:39
clinical TPIAT is performed under anticoagulation (heparin) to prevent portal vein thrombosis during islet infusion. ↗
▶ Ep 26 · 48:11
clinical Portal vein thrombosis rate at Cincinnati Children's is less than 1% for TPIAT. ↗
▶ Ep 26 · 48:26
clinical Cincinnati Children's has performed close to 200 TPIAT cases with no anastomotic leaks. ↗
▶ Ep 26 · 50:07
clinical Patients are extubated in the operating room after TPIAT. ↗
▶ Ep 26 · 51:32
clinical Younger children are more likely to achieve insulin independence and opioid independence after TPIAT. ↗
▶ Ep 26 · 52:25
clinical Islet yield (IEQ/kg) is inversely related to pancreatic calcification, ductal dilation, fibrosis, duration of symptoms, and prior resections or drainage procedures. ↗
▶ Ep 26 · 54:59
clinical Predictors of insulin independence after TPIAT include younger age at surgery, smaller body surface area, no pre-existing insulin dependence, and higher IEQ/kg transplanted. ↗
▶ Ep 26 · 56:09
clinical TPIAT dramatically improves quality of life in appropriately selected children, with families reporting they have 'never met this kid before'—new person, happy, playing, eating normally. ↗
Juan's statements about Pediatric Oncology 21 statements

Open the Pediatric Oncology collection →

2025 Pediatric Surgery Update Course - Robotics in Pediatric Surgery: Which indications benefit the most?

▶ Ep 591 · 0:24
quote Who is a robotic surgery here in the audience? The ones who are not lifting up their hands, who has a robot available? ↗
▶ Ep 591 · 0:24
opinion Choledochal cyst is a perfect case for robotic surgery ↗
▶ Ep 591 · 0:24
clinical Robotic instruments have seven degrees of freedom compared to six for the human hand ↗
▶ Ep 591 · 0:24
opinion Adrenalectomy for neuroblastoma confined to the adrenal is a perfect robotic case ↗
▶ Ep 591 · 0:24
epidemiological Four out of approximately 30 attendees perform robotic surgery; another 12 have robot access but do not use it ↗
▶ Ep 591 · 2:51
epidemiological All pediatric surgery fellowships are integrating robotic training ↗
▶ Ep 591 · 2:51
clinical Room turnover time for robotic cases can be reduced to 30 minutes with trained personnel ↗
▶ Ep 591 · 2:51
clinical Each additional 15 minutes of operative time costs the same for robotic and laparoscopic surgery ↗
▶ Ep 591 · 2:51
clinical Initial cost premium for robotic surgery is approximately $4000 per case in most institutions ↗
▶ Ep 591 · 2:51
clinical Learning curve for basic proficiency is 20-30 cases for laparoscopy versus 10-15 cases for robotics ↗
▶ Ep 591 · 2:51
clinical Robotic surgery shows lower conversion to open rates compared to laparoscopy in colorectal cases ↗
▶ Ep 591 · 3:15
opinion Median arcuate ligament release should not be performed laparoscopically or open anymore due to difficulty accessing the angle near the celiac trunk ↗
▶ Ep 591 · 3:38
guideline There is no FDA approval for robotic systems in pediatric surgery ↗
▶ Ep 591 · 3:38
quote Are there FDA indications for the robot for pediatric surgery? Great question. Great question. No. ↗
▶ Ep 591 · 7:16
clinical ICG fluorescence allows visualization of adrenal arteries supplied by renal, diaphragmatic, and aortic vessels ↗
▶ Ep 591 · 7:16
opinion Robotic surgery is not recommended for appendectomy ↗
▶ Ep 591 · 12:55
opinion Robotic surgery is not a standard of care but a tool to aid efficiency and access to difficult angles ↗
▶ Ep 591 · 14:05
quote This is not about being cool. It's about efficiency and outcomes. Less cases to prove it now. Less cases to proficiency. ↗
▶ Ep 591 · 15:59
opinion Surgeons trained primarily in robotics cannot tie, sew, or work with 3mm instruments effectively ↗
▶ Ep 591 · 17:14
clinical New robotic systems with tactile sensors reduce force application by 83% ↗
▶ Ep 591 · 17:14
clinical ICG fluorescence in choledochal cyst surgery allows visualization far back to the head of the pancreas to achieve proper tapering, decreasing future cancer risk ↗
Juan's statements about Pediatric Robotic Surgery 22 statements

Open the Pediatric Robotic Surgery collection →

Update Course Rewind 2025: Robotics in Pediatric Surgery: Which indications benefit the most?

▶ Ep 7 · 0:41
quote the hand has 6 degrees of freedom for mobility, robotic has 7. ↗
▶ Ep 7 · 0:41
clinical Robotic surgery provides 7 degrees of freedom for mobility compared to the human hand's 6 degrees. ↗
▶ Ep 7 · 0:49
quote That's unimaginable angles that you can reach with a robot up there near the diaphragm, back near the cave. ↗
▶ Ep 7 · 1:21
clinical The learning curve for robotic surgery is better than laparoscopic surgery. ↗
▶ Ep 7 · 1:21
quote If we look at laparoscopic versus robotic, the learning curve is better. ↗
▶ Ep 7 · 1:26
quote Time to reduce your operative times is way faster than laparoscopic after a few cases. ↗
▶ Ep 7 · 1:26
clinical Time to reduce operative times is way faster for robotic surgery than laparoscopic after a few cases. ↗
▶ Ep 7 · 1:42
quote No, there's no FDA approval for it for pediatrics, but it should be coming soon. ↗
▶ Ep 7 · 1:42
guideline There is no FDA approval for robotic surgery in pediatrics, but it should be coming soon. ↗
▶ Ep 7 · 1:53
clinical After a few cases, robotic surgery decreases operative time, which reduces costs in the long run. ↗
▶ Ep 7 · 1:53
quote After a few cases, you're decreasing your operative time. ↗
▶ Ep 7 · 2:05
clinical New robotic systems allow surgeons to detect when suture is about to rupture. ↗
▶ Ep 7 · 2:05
quote New systems in the current system, you can tell when the suture is about to rupture. ↗
▶ Ep 7 · 2:17
quote You get your feedback from your eyes. You get used to it. It takes, it takes only a few cases to do that. ↗
▶ Ep 7 · 2:17
clinical Surgeons get tactile feedback from visual cues in robotic surgery, and it takes only a few cases to adapt. ↗
▶ Ep 7 · 2:37
clinical With trained personnel, room turnover time for robotic surgery equals that of laparoscopic surgery. ↗
▶ Ep 7 · 2:37
quote If you train your personnel, it will take the same amount of time to turn over the the the room for robot than for a lab. ↗
▶ Ep 7 · 2:51
quote Cases needed for basic proficiency, 20 to 30 laparoscopy. Robotic, 10 to 15. ↗
▶ Ep 7 · 2:51
clinical Basic proficiency in laparoscopy requires 20 to 30 cases. ↗
▶ Ep 7 · 2:55
clinical Basic proficiency in robotic surgery requires 10 to 15 cases. ↗
▶ Ep 7 · 3:07
clinical Robotic surgery does not impair outcomes in oncologic surgeries. ↗
▶ Ep 7 · 3:07
quote That initial cost is about efficiency and outcomes because it does not impair outcomes in oncologic surgeries either. ↗
Juan's statements about Pediatric Surgery Essentials 44 statements

Open the Pediatric Surgery Essentials collection →

Update Course Rewind 2025: Robotics in Pediatric Surgery: Which indications benefit the most?

▶ Ep 2 · 0:41
quote the hand has 6 degrees of freedom for mobility, robotic has 7. ↗
▶ Ep 2 · 0:41
clinical Robotic surgery provides 7 degrees of freedom for mobility compared to the human hand's 6 degrees. ↗
▶ Ep 2 · 0:49
quote That's unimaginable angles that you can reach with a robot up there near the diaphragm, back near the cave. ↗
▶ Ep 2 · 1:21
quote If we look at laparoscopic versus robotic, the learning curve is better. ↗
▶ Ep 2 · 1:21
clinical The learning curve for robotic surgery is better than laparoscopic surgery. ↗
▶ Ep 2 · 1:26
clinical Time to reduce operative times is way faster for robotic surgery than laparoscopic after a few cases. ↗
▶ Ep 2 · 1:26
quote Time to reduce your operative times is way faster than laparoscopic after a few cases. ↗
▶ Ep 2 · 1:42
quote No, there's no FDA approval for it for pediatrics, but it should be coming soon. ↗
▶ Ep 2 · 1:42
guideline There is no FDA approval for robotic surgery in pediatrics, but it should be coming soon. ↗
▶ Ep 2 · 1:53
clinical After a few cases, robotic surgery decreases operative time, which reduces costs in the long run. ↗
▶ Ep 2 · 1:53
quote After a few cases, you're decreasing your operative time. ↗
▶ Ep 2 · 2:05
quote New systems in the current system, you can tell when the suture is about to rupture. ↗
▶ Ep 2 · 2:05
clinical New robotic systems allow surgeons to detect when suture is about to rupture. ↗
▶ Ep 2 · 2:17
quote You get your feedback from your eyes. You get used to it. It takes, it takes only a few cases to do that. ↗
▶ Ep 2 · 2:17
clinical Surgeons get tactile feedback from visual cues in robotic surgery, and it takes only a few cases to adapt. ↗
▶ Ep 2 · 2:37
quote If you train your personnel, it will take the same amount of time to turn over the the the room for robot than for a lab. ↗
▶ Ep 2 · 2:37
clinical With trained personnel, room turnover time for robotic surgery equals that of laparoscopic surgery. ↗
▶ Ep 2 · 2:51
clinical Basic proficiency in laparoscopy requires 20 to 30 cases. ↗
▶ Ep 2 · 2:51
quote Cases needed for basic proficiency, 20 to 30 laparoscopy. Robotic, 10 to 15. ↗
▶ Ep 2 · 2:55
clinical Basic proficiency in robotic surgery requires 10 to 15 cases. ↗
▶ Ep 2 · 3:07
quote That initial cost is about efficiency and outcomes because it does not impair outcomes in oncologic surgeries either. ↗
▶ Ep 2 · 3:07
clinical Robotic surgery does not impair outcomes in oncologic surgeries. ↗

Update Course Rewind 2025: Robotics in Pediatric Surgery: Which indications benefit the most?

▶ Ep 3 · 0:41
quote Perfect visualization, tiny incisions, the hand has 6 degrees of freedom for mobility, robotic has 7. ↗
▶ Ep 3 · 0:41
clinical Robotic instruments have 7 degrees of freedom compared to 6 for the human hand. ↗
▶ Ep 3 · 0:49
quote That's unimaginable angles that you can reach with a robot up there near the diaphragm, back near the cave. ↗
▶ Ep 3 · 1:21
clinical The learning curve for robotic surgery is better than laparoscopic surgery. ↗
▶ Ep 3 · 1:21
quote If we look at laparoscopic versus robotic, the learning curve is better. ↗
▶ Ep 3 · 1:27
clinical Time to reduce operative times is way faster for robotic than laparoscopic after a few cases. ↗
▶ Ep 3 · 1:27
quote Time to reduce your operative times is way faster than laparoscopic after a few cases. ↗
▶ Ep 3 · 1:42
guideline There is currently no FDA approval for robotic surgery in pediatrics, but it should be coming soon. ↗
▶ Ep 3 · 1:42
quote Right now, there's no FDA approval for it for pediatrics, but it should be coming soon. ↗
▶ Ep 3 · 1:53
quote After a few cases, you're decreasing your operative time. ↗
▶ Ep 3 · 1:53
clinical After a few cases, robotic surgery decreases operative time, which reduces costs in the long run. ↗
▶ Ep 3 · 2:05
quote New systems in the current system, you can tell when the suture is about to rupture. ↗
▶ Ep 3 · 2:05
clinical New robotic systems allow surgeons to detect when suture is about to rupture. ↗
▶ Ep 3 · 2:17
quote You get your feedback from your eyes. You get used to it. It takes, it takes only a few cases to do that. ↗
▶ Ep 3 · 2:37
clinical With trained personnel, room turnover time for robotic surgery equals that of laparoscopic surgery. ↗
▶ Ep 3 · 2:37
quote If you train your personnel, it will take the same amount of time to turn over the the the room for robot than for a lab. ↗
▶ Ep 3 · 2:51
clinical Basic proficiency in laparoscopy requires 20 to 30 cases. ↗
▶ Ep 3 · 2:51
quote Cases needed for basic proficiency, 20 to 30 laparoscopy. Robotic, 10 to 15. ↗
▶ Ep 3 · 2:55
clinical Basic proficiency in robotic surgery requires 10 to 15 cases. ↗
▶ Ep 3 · 3:03
quote So that is going to decrease your operative times, decrease the cost of the robot. ↗
▶ Ep 3 · 3:07
clinical Robotic surgery does not impair outcomes in oncologic surgeries. ↗
▶ Ep 3 · 3:07
quote That initial cost is about efficiency and outcomes because it does not impair outcomes in oncologic surgeries either. ↗

Summaries Juan gave as host · 49 summaries

Recaps of what the experts said, with Juan as narrator — not Juan's own clinical position, and never cited in answers.

Summaries Juan gave as host · Acute Pancreatitis 14 summaries

Open the Acute Pancreatitis collection →

Update Course 2023 - Updates in Pancreatitis

▶ Ep 9 · 0:44
host summary Juan Gurria summarizing a resource: remember they, they used to tell you, put the patient NPO, throw him in the ICU and, and fluid his lungs, right? So we don't do that anymore. ↗
▶ Ep 9 · 5:45
host summary Juan Gurria summarizing a resource: The North American Society of Pancreatitis, GI Pathology and Nutrition recommends bolus 10-20 mL/kg up to 3 L in the first 24 hours, with reassessment at 12 hours preferred. ↗
▶ Ep 9 · 6:32
host summary Juan Gurria summarizing a resource: Lactated Ringer's decreases the incidence of inflammatory response and C-reactive protein at 24 hours compared to normal saline in pancreatitis. ↗
▶ Ep 9 · 8:33
host summary Juan Gurria summarizing a resource: The WATERFALL trial by Enrique de Madaria is a multi-center, multi-country RCT comparing lactated Ringer's versus normal saline in pancreatitis, with results expected in 1-2 years. ↗
▶ Ep 9 · 9:07
host summary Juan Gurria summarizing a resource: Aggressive fluid resuscitation in the first 24 hours (better in first 12) is associated with shorter length of stay, less severe complications, and fewer ICU admissions. ↗
▶ Ep 9 · 9:47
host summary Juan Gurria summarizing a resource: Gastric feeding is preferred over jejunal feeding in pancreatitis when the patient can tolerate it. ↗
▶ Ep 9 · 13:13
host summary Juan Gurria summarizing a resource: Children don't get pancreatitis ↗

Overview of the Surgical Management of Acute and Chronic Pancreatitis in Children with Dr. Juan Gurria

▶ Ep 11 · 5:03
host summary Juan Gurria summarizing a resource: do not mess with the pancreas ↗
▶ Ep 11 · 18:17
host summary Juan Gurria summarizing a resource: Position papers from the European Pancreas Club and American Pancreas Association state there is no role for early pancreatectomies or early drainage procedures in acute pancreatitis. ↗
▶ Ep 11 · 20:06
host summary Juan Gurria summarizing a resource: The step-up approach for necrotizing pancreatitis—starting with transgastric endoscopic necrosectomy—reduces major complications compared to open surgery. ↗
▶ Ep 11 · 23:48
host summary Juan Gurria summarizing a resource: Lactated Ringer solution for initial resuscitation in acute pancreatitis is better than normal saline, per a paper from Cincinnati Children's by Dr. Farrell. ↗
▶ Ep 11 · 28:01
host summary Juan Gurria summarizing a resource: These families come back and say, listen, I've never met this kid in my life. It's a new kid, happy playing. ↗
▶ Ep 11 · 50:58
host summary Juan Gurria summarizing a resource: TPIAT results in over 80% reduction in opioid use at 1–2 months, with sustained effect for years. ↗
▶ Ep 11 · 53:03
host summary Juan Gurria summarizing a resource: Transplanting ≥5000 islet equivalents per kilogram into the portal vein predicts 92% insulin independence at 36 months (Minnesota data); Cincinnati Children's currently achieves 70% insulin independence. ↗
Summaries Juan gave as host · Chronic Pancreatitis 14 summaries

Open the Chronic Pancreatitis collection →

Update Course 2023 - Updates in Pancreatitis

▶ Ep 5 · 0:44
host summary Juan Gurria summarizing a resource: remember they, they used to tell you, put the patient NPO, throw him in the ICU and, and fluid his lungs, right? So we don't do that anymore. ↗
▶ Ep 5 · 5:45
host summary Juan Gurria summarizing a resource: The North American Society of Pancreatitis, GI Pathology and Nutrition recommends bolus 10-20 mL/kg up to 3 L in the first 24 hours, with reassessment at 12 hours preferred. ↗
▶ Ep 5 · 6:32
host summary Juan Gurria summarizing a resource: Lactated Ringer's decreases the incidence of inflammatory response and C-reactive protein at 24 hours compared to normal saline in pancreatitis. ↗
▶ Ep 5 · 8:33
host summary Juan Gurria summarizing a resource: The WATERFALL trial by Enrique de Madaria is a multi-center, multi-country RCT comparing lactated Ringer's versus normal saline in pancreatitis, with results expected in 1-2 years. ↗
▶ Ep 5 · 9:07
host summary Juan Gurria summarizing a resource: Aggressive fluid resuscitation in the first 24 hours (better in first 12) is associated with shorter length of stay, less severe complications, and fewer ICU admissions. ↗
▶ Ep 5 · 9:47
host summary Juan Gurria summarizing a resource: Gastric feeding is preferred over jejunal feeding in pancreatitis when the patient can tolerate it. ↗
▶ Ep 5 · 13:13
host summary Juan Gurria summarizing a resource: Children don't get pancreatitis ↗

Overview of the Surgical Management of Acute and Chronic Pancreatitis in Children with Dr. Juan Gurria

▶ Ep 11 · 5:03
host summary Juan Gurria summarizing a resource: do not mess with the pancreas ↗
▶ Ep 11 · 18:17
host summary Juan Gurria summarizing a resource: Position papers from the European Pancreas Club and American Pancreas Association state there is no role for early pancreatectomies or early drainage procedures in acute pancreatitis. ↗
▶ Ep 11 · 20:06
host summary Juan Gurria summarizing a resource: The step-up approach for necrotizing pancreatitis—starting with transgastric endoscopic necrosectomy—reduces major complications compared to open surgery. ↗
▶ Ep 11 · 23:48
host summary Juan Gurria summarizing a resource: Lactated Ringer solution for initial resuscitation in acute pancreatitis is better than normal saline, per a paper from Cincinnati Children's by Dr. Farrell. ↗
▶ Ep 11 · 28:01
host summary Juan Gurria summarizing a resource: These families come back and say, listen, I've never met this kid in my life. It's a new kid, happy playing. ↗
▶ Ep 11 · 50:58
host summary Juan Gurria summarizing a resource: TPIAT results in over 80% reduction in opioid use at 1–2 months, with sustained effect for years. ↗
▶ Ep 11 · 53:03
host summary Juan Gurria summarizing a resource: Transplanting ≥5000 islet equivalents per kilogram into the portal vein predicts 92% insulin independence at 36 months (Minnesota data); Cincinnati Children's currently achieves 70% insulin independence. ↗
Summaries Juan gave as host · Pancreatic Surgery & Critical Care 7 summaries

Open the Pancreatic Surgery & Critical Care collection →

Update Course 2023 - Updates in Pancreatitis

▶ Ep 1 · 0:44
host summary Juan Gurria summarizing a resource: remember they, they used to tell you, put the patient NPO, throw him in the ICU and, and fluid his lungs, right? So we don't do that anymore. ↗
▶ Ep 1 · 5:45
host summary Juan Gurria summarizing a resource: The North American Society of Pancreatitis, GI Pathology and Nutrition recommends bolus 10-20 mL/kg up to 3 L in the first 24 hours, with reassessment at 12 hours preferred. ↗
▶ Ep 1 · 6:32
host summary Juan Gurria summarizing a resource: Lactated Ringer's decreases the incidence of inflammatory response and C-reactive protein at 24 hours compared to normal saline in pancreatitis. ↗
▶ Ep 1 · 8:33
host summary Juan Gurria summarizing a resource: The WATERFALL trial by Enrique de Madaria is a multi-center, multi-country RCT comparing lactated Ringer's versus normal saline in pancreatitis, with results expected in 1-2 years. ↗
▶ Ep 1 · 9:07
host summary Juan Gurria summarizing a resource: Aggressive fluid resuscitation in the first 24 hours (better in first 12) is associated with shorter length of stay, less severe complications, and fewer ICU admissions. ↗
▶ Ep 1 · 9:47
host summary Juan Gurria summarizing a resource: Gastric feeding is preferred over jejunal feeding in pancreatitis when the patient can tolerate it. ↗
▶ Ep 1 · 13:13
host summary Juan Gurria summarizing a resource: Children don't get pancreatitis ↗
Summaries Juan gave as host · Pancreatitis 14 summaries

Open the Pancreatitis collection →

Update Course 2023 - Updates in Pancreatitis

▶ Ep 13 · 0:44
host summary Juan Gurria summarizing a resource: remember they, they used to tell you, put the patient NPO, throw him in the ICU and, and fluid his lungs, right? So we don't do that anymore. ↗
▶ Ep 13 · 5:45
host summary Juan Gurria summarizing a resource: The North American Society of Pancreatitis, GI Pathology and Nutrition recommends bolus 10-20 mL/kg up to 3 L in the first 24 hours, with reassessment at 12 hours preferred. ↗
▶ Ep 13 · 6:32
host summary Juan Gurria summarizing a resource: Lactated Ringer's decreases the incidence of inflammatory response and C-reactive protein at 24 hours compared to normal saline in pancreatitis. ↗
▶ Ep 13 · 8:33
host summary Juan Gurria summarizing a resource: The WATERFALL trial by Enrique de Madaria is a multi-center, multi-country RCT comparing lactated Ringer's versus normal saline in pancreatitis, with results expected in 1-2 years. ↗
▶ Ep 13 · 9:07
host summary Juan Gurria summarizing a resource: Aggressive fluid resuscitation in the first 24 hours (better in first 12) is associated with shorter length of stay, less severe complications, and fewer ICU admissions. ↗
▶ Ep 13 · 9:47
host summary Juan Gurria summarizing a resource: Gastric feeding is preferred over jejunal feeding in pancreatitis when the patient can tolerate it. ↗
▶ Ep 13 · 13:13
host summary Juan Gurria summarizing a resource: Children don't get pancreatitis ↗

Overview of the Surgical Management of Acute and Chronic Pancreatitis in Children with Dr. Juan Gurria

▶ Ep 26 · 5:03
host summary Juan Gurria summarizing a resource: do not mess with the pancreas ↗
▶ Ep 26 · 18:17
host summary Juan Gurria summarizing a resource: Position papers from the European Pancreas Club and American Pancreas Association state there is no role for early pancreatectomies or early drainage procedures in acute pancreatitis. ↗
▶ Ep 26 · 20:06
host summary Juan Gurria summarizing a resource: The step-up approach for necrotizing pancreatitis—starting with transgastric endoscopic necrosectomy—reduces major complications compared to open surgery. ↗
▶ Ep 26 · 23:48
host summary Juan Gurria summarizing a resource: Lactated Ringer solution for initial resuscitation in acute pancreatitis is better than normal saline, per a paper from Cincinnati Children's by Dr. Farrell. ↗
▶ Ep 26 · 28:01
host summary Juan Gurria summarizing a resource: These families come back and say, listen, I've never met this kid in my life. It's a new kid, happy playing. ↗
▶ Ep 26 · 50:58
host summary Juan Gurria summarizing a resource: TPIAT results in over 80% reduction in opioid use at 1–2 months, with sustained effect for years. ↗
▶ Ep 26 · 53:03
host summary Juan Gurria summarizing a resource: Transplanting ≥5000 islet equivalents per kilogram into the portal vein predicts 92% insulin independence at 36 months (Minnesota data); Cincinnati Children's currently achieves 70% insulin independence. ↗