MTC 6/21: When stones have the gall to attack

This morning, Dr. Lainey Flatow-Trujillo, one of our amazing R2s, shared with us the case of a young woman with a history of biliary colic who presented with 5 days of epigastric pain radiating to the back and an initial lipase > 3000. The group quickly arrived at the diagnosis of gallstone pancreatitis.

We then spent some time delving into the management of acute pancreatitis. Because gallstones are the most common cause, an abdominal US is required. Patients in whom the diagnosis is unclear or whose symptoms persist may benefit from a CT with contrast. In patients without gallstones or heavy alcohol use, other etiologies, such as hypertriglyceridemia, hypercalcemia, and medications, should be investigated. Other less common causes include post-ERCP, traumatic, infectious, and autoimmune pancreatitis.

The key to management is aggressive hydration (e.g., 4 liters in the first 24 hours). Patients are often volume-depleted, so a bolus followed by a continuous infusion (e.g., 2 L up front followed by 100 mL/hr for 20 hr) is reasonable. IV analgesics are indicated. Oral (or at least parenteral) feeding should be started as soon as the patient is able to tolerate it, as this has been shown to decrease the risk of complications such as infection.

ERCP, a therapeutic procedure, is indicated when there is concern for ascending cholangitis or persistent obstruction. Otherwise, MRCP or EUS can be considered (not required for mild episodes). Laparoscopic cholecystectomy is recommended during the same admission to reduce the risk of recurrence for mild cases of gallstone pancreatitis. Debridement of necrosis, if present, should be avoided unless the patient is unstable.

Thank you to Dr. Wilson Kwong, our expert discussant, for offering his clinical pearls!

Medical Spanish Word of the Day: la piedra (colloquial), el cálculo (formal) = stone

VA Morning Report 4/22: Ischemic Colitis

This morning, Jerry Lipinski, one of our stellar R2s presented an interesting patient he recently took care of at the VA: a 53-year-old woman with a history of Rheumatoid Arthritis who presented with acute bloody diarrhea. Her initial presentation was notable for sinus tachycardia, LLQ tenderness, leukocytosis. We used the opportunity to work through our differential diagnosis and discuss the work-up to obtain. 

A CT scan of the abdomen showed non-specific inflammation of the colon in the splenic flexure and adjacent bowel. We highlighted some of the common findings on imaging – mucosal thickening, edema, fat stranding, and “thumbprinting” (haustra of the large bowel becoming thickened and projecting into the intestinal lumen at regular intervals). The patient then underwent colonoscopy which showed patchy erythematous, edematous, and friable mucosa consistent with ischemic colitis. We were very lucky to have Dr. Cynthia Hsu, an alumnus of our residency and current GI fellow as a discussant to walk us through the findings.

We then talked about the causes of ischemic colitis, which can broadly be divided into occlusive and non-occlusive etiologies. We also discussed one common reason to have ischemia in “watershed” areas of the colon – episodic hypoperfusion. The exact cause of ischemic colitis in any given patient is often difficult to find, and in this case, there was reason to suspect that the patient’s TNF-alpha inhibitor (adalimumab) for RA was the culprit. This adverse event has been described in the literature for biologic agents. Additionally, the patient had been transitioned from etanercept to adalimumab two years prior due to colitis that at the time was not further specified. 

Our surgical colleagues were consulted, but the patient did not require intervention and improved over several days of conservative management. She was treated for 5-day course of antibiotics – the routine use of antibiotics is not necessary, but this patient’s clinical status was concerning (rising leukocytosis and extensive colonic involvement on endoscopy) that the team needed to treat potential bacterial gut translocation.

A special thank you to Dr Hsu for all her high-yield clinical pearls!

Morning Teaching Conference – Mon 10/26

On Tuesday morning we discussed a case of a 77-year old man who presented with epigastric abdominal pain and was found to have gallstone pancreatitis. The patient went on to develop a prolonged ileus and an extended hospital stay. Two weeks later, the patient developed a new leukocytosis and tachycardia and was found to have pancreatic necrosis. We brainstormed the early and late complications of pancreatitis. We additionally discussed the standard recovery timeline from pancreatitis. The development of walled-off necrosis is a key distinction in the evaluation of post-pancreatitis complications.  Our teams also came up with the antibiotic choices they would consider when treating the patient. Finally, we discussed the procedural considerations to treatment of necrotic collections. The initial approach often involves placement of percutaneous or transluminal drain (or stent). Serious cases may also need to be treated with necrosectomy  – either surgical using video-assisted retroperitoneal debridement (VARD) or endoscopic. A special thank you to our discussant, Dr. Phil Fejleh, the advanced endoscopy GI fellow, for sharing all of his expertise!

MTC 6/15/20 Eosinophilic esophagitis

Today Dr. Joe Ryan presented a case of a 30-year old man who presented to the ED with food impaction in his esophagus. We discussed the general approach to dysphagia, as well as the differential for esophageal impaction in our patient. We discussed how glucagon is often used as first-line medical therapy for food impaction but that the evidence is not robust for its efficacy. Our patient received two doses without improvement before he underwent an endoscopy that advanced the food bolus into his stomach and found linear furrows in his esophagus. His biopsy ultimately showed eosinophilia, and he was diagnosed with eosinophilic esophagitis (EoE). He was discharged home with an 8 week trial of PPI therapy. PPI therapy has an anti-inflammatory effect that is independent of its acid suppression. Maintenance therapy is achieved by viscous/swallowed inhaled corticosteroids. Our expert discussant, Dr. Rena Yadlapati, a gastroenterology expert in esophageal disorders, helped us make the diagnosis and discussed the treatment of

read more MTC 6/15/20 Eosinophilic esophagitis

Art of Innovation: 3rd Annual Interventional Endoscopy Course 6/6

FREE WEBINAR Saturday June 6th

This educational program is hosted by the West Coast Chapter
of Women in Interventional Endoscopy and supported by the UCSD
Divisions of Gastroenterology.

This Course aims to promote the knowledge of recent and cutting- edge approaches in interventional Gastroenterology, in both current and emerging practice; addressing not only technological and procedural
advances but also factors affecting endoscopists’ wellbeing

Registration LINK

Grand Rounds 2/19: Pathophysiology of diarrheal diseases: Still a scourge

Today Kim E. Barrett, Ph.D., Distinguished Professor of Medicine in the Division of Gastroenterology, gave us a fascinating talk on diarrheal diseases. Dr. Barrett started out by describing how foodbourne illnesses are a constant threat to public health, as they have a significant overall disease burden, and impedes socioeconomic development in the developing world.

The vast majority of foodbourne illnesss are caused by microorganisms via pore-forming toxins, enterotoxins, adherent pathogens and invasive pathogens, or by direct toxin forms or by contaminants. There are sequels of food-borne illnesses including post-infectous IBS, reactive arthritis, GBS, reactivation/activation of IBD, developmental/cognitive impacts, and growth stunting.  In particular enteric dysfunction may lead to systemic inflammatory effects and increased nutrient need in nutrient deficient conditions for those in developing countries, leading to ultimately stunted growth.

Dr. Barrett then reviewed the role of the intestinal epithelium in regards to water and electrolyte transport and nutrient absorption during digestion, as well as a barrier for toxins and pathogens. She noted the balance between absorption and secretion across the villi vs crypts, which is important for maintaining the appropriate amount of gut flora. Dr. Barrett then demonstrated how infection with bacteria or viral pathogens can change these mechanisms and lead to excess chloride secretion and decreased nutrient absorption.

Next Dr. Barrett went on to focus on non-typhoidal Salmonella, which is the leading cause of death from diarrheal illness in vulnerable population. It is a disease that has increasing antibiotic resistance but it’s mechanism of disease is still poorly understood. She and other researchers at UCSD, particularly Drs. Josh Fierer and Don Guiney, set about trying to better understand this pathophysiology though various mouse models. They have concluded that there is a decreased capacity for electrogenic transport, decreased capacity for electroneutral NaCl absorption, epithelial proliferation and diarrhea symptoms independent of neutrophil activation.

Dr. Barrett then spoke about a current project her lab is currently working on addressing the effects of tyrosine kinase inhibitor-EGFr therapy on the intestinal tract. Physiologically, there is inhibition of chloride secretion by EGF receptor via an apical membrane effect. Therefore, these immunotherapy agents have a propensity to cause diarrhea by reversing this inhibitory effect on chloride secretion. So it appears that drugs targeting receptors and transporter on the membrane may be the key to treating these diarrheal illness, and it is an area of active investigation.

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Thank you for a very thoughtful talk, Dr. Barrett!


Today one of our amazing Resident as Clinician Educator (RACE) track residents Dr. Maggie Kozman led us through a fascinating case of a young woman with HIV and priorly diagnosed disseminated MAC affecting the liver who presents with diffuse abdominal pain and fevers after restarting ARVs for 6 weeks. We learned that she had markedly elevated alkaline phosphatase and GGT levels and diffuse abdominal and pelvic lymphadenopathy.
Dr. Kozman lead us through a diagnostic schema for an HIV patient coming in with fever and abdominal pain, with the help of our expert Owen discussant, Dr. Jill Blumenthal and taught us about HIV cholangiopathy. Ultimately, we learned that the patient had likely IRIS from MAC infection in the setting of her recently restarted ARVs, as her CD4 count had a marked recovery with a corresponding significant drop in the viral load.
Thank Dr. Kozman for that interesting case and excellent teaching, and Dr. Blumenthal for your additional clinical pearls!

Teaching points:

1) When thinking of the differential for fever and focal infectious symptoms consider the categories of 1) common infections 2) opportunistic infectious and 3) IRIS.

2) HIV/AIDs cholangiopathy is a cause of secondary biliary sclerosis in HIV patients.  Patients who have had infections with cryptosporium or CMV may be more at risk. They can present with fever, RUQ pain and diarrhea and can have a markedly elevated AP and ggt, as well as biliary strictures visualized on MRCP.

3) IRIS or immune reconstitution syndrome is a diagnosis of exclusion in HIV patients presenting with fever, particularly those with an initial low CD4 count and high VL who have a significant response and immune recovery after restarting ARVs. Infectious etiologies should be ruled out prior to patients being  diagnosed with IRIS and getting treated with steroids.

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HC MTC 2/3: Outpatient medicine – GERD

Image result for GERD

Today at Hillcrest, we discussed a case of a clinic patient initially presenting with heartburn, suggestive of GERD. We then followed his course over a few years to the point where he started to have nocturnal symptoms despite adequate therapy, which prompted a referral to GI for an EGD. His EGD resulted in the discovery of an esophageal adenocarcinoma, for which he ultimately underwent an esophagogastrectomy with adjuvant chemotherapy. We used this case to build a discussion about many important aspects of GERD and the potential sequelae , highlighted below!

Take Home Points:

  1. GERD is a clinical diagnosis and it is appropriate to treat empirically with an 8 week trial of PPI in the absence of alarm symptoms. Always address lifestyle modification as well!
  2. Once symptoms are controlled, efforts should be made at least annually to deescalate PPI therapy as tolerable.
  3. Alarm features (constitutional symptoms, dysphagia, hematemesis/melena/unexplained anemia, or recalcitrant symptoms) can develop later in the disease course, so be thoughtful in follow-up as an EGD may be warranted when initially it was not indicated.

VA MTC 1/27: Acute Acalculous Cholecystitis

Today at the VA, Dr. Hairan Zhu presented a fascinating case of a middle-aged patient who was admitted for uncomplicated alcohol withdrawal syndrome, but after 4 days of therapy and a plan for discharge, he spiked a fever, became tachycardic, and started to complain of abdominal pain. We walked through a basic differential for (LEID) new onset fevers in the hospital and discussed how people wanted to work-up the case. Ultimately the patient was diagnosed with acute acalculous cholecystitis complicated by gall bladder perforation, but he ultimately did well with surgical management. We finally discussed the illness script for this uncommon, but very morbid disease process (see below)!

VA MTC 1/6: Outpatient Medicine – Chronic Diarrhea

Today at the VA, we started off a series of outpatient focused cases by discussing a patient in his 50’s who presented with 1 year history of diarrhea and 70 lbs of weight loss. The teams collectively discussed their approach to diarrhea and an overall schema for the outpatient setting. We discussed the alarm features for diarrhea and, for our patient, the need for urgent colonoscopy. With a history of alcohol use disorder, CT findings of chronic pancreatitis, and an abnormal fecal elastase, the teams astutely diagnosed our patient’s diarrhea as malabsorption secondary to exocrine pancreatic insufficiency (EPI).