Craig A. Munroe

A tandem colonoscopy study of adenoma miss rates during endoscopic training: a venture into uncharted territory

BACKGROUND Tandem colonoscopy is regarded as the reference standard for the evaluation of the adenoma detection rate (ADR) and adenoma miss rate (AMR) during colonoscopy. Pooled results from previous tandem studies yield AMRs of 22%. The AMR of trainees is important to estimate the number of colonoscopies required to develop competence in screening for colorectal neoplasms. OBJECTIVE To measure the ADR and AMR of trainees as a function of experience. METHODS Prospective tandem colonoscopy study at an academic VA medical center. A trainee initially attempted colonoscopy. If the trainee was able to intubate the cecum, the trainee performed the withdrawal, and the colonoscopy was then repeated by the attending physician to assess the AMR. RESULTS Twelve trainee endoscopists were included in the study. Trainees had between 0 and 33 months of previous endoscopic experience and had done between 0 and 605 previous colonoscopies. A total of 230 patients were evaluated for the study, and 218 patients were enrolled. Complete tandem colonoscopy was performed in 147 patients. There was a 54% ADR. The mean (standard deviation) size of the adenomas in the cohort was 5.9 (5.3) mm. Significant variables in multivariate logistic regression analysis for missed adenomas were trainee experience (P = .011) and patient age (P < .001). The AMR decreased with increasing experience, and it is estimated that 450 colonoscopies are required to attain AMRs of less than 25% in a 60-year-old patient. LIMITATIONS Single-center study; the attending physician performing the second pass was not blinded to the first pass. The AMR was only analyzed for cases in which the trainee was able to reach the cecum with no or minimal assistance. CONCLUSIONS Our tandem colonoscopy study demonstrates that the AMR decreases as the experience of trainees increases and is a late competency attained during training. Future training may need to incorporate these findings to serve as a basis for determining appropriate training guidelines.

Current Perception of Nutrition Education in U.S. Medical Schools

Historically, physicians have perceived the quality of nutrition training during medical school as inadequate. A literature review suggests that this perception has not significantly changed since the 1950s. Many schools have worked to create clinical nutrition curricula for use during medical school. Interestingly, data suggest that medical students’ perception of the importance of clinical nutrition can decrease during medical school. Recent data support the importance of targeted nutritional therapy to reduce morbidity and mortality, yet the number of physicians interested in nutrition appears to be declining, and fewer hours of nutrition training are occurring in medical school. One possible solution to improve both training and awareness of the problem is to implement a certification program for both students and preceptors modeled after the Cardiac Life Support training offered by the American Heart Association.

Integrating urgent multidetector CT scanning in the diagnostic algorithm of active lower GI bleeding

Lower GI bleeding (LGIB) is defined as ongoing blood oss originating from a site distal to the ligament of Treitz. The everity of this common condition can range from trivial pisodes of bright red blood per rectum to a massive hemrrhage requiring hospitalization, intravenous resuscitation, nd urgent intervention. Although most cases of LGIB are elf-limited and may not present to medical care, approxiately 21 in 100,000 adults in the United States require ospitalization.1 Predictors of negative outcomes include adancing age, intestinal ischemia, and comorbid medical conitions.2 Thankfully, the overall mortality rate remains low 4% in 1 large series).2 The initial evaluation of patients resenting with active LGIB includes assessment of the seerity of bleeding and prompt hemodynamic resuscitation nd stabilization with fluids and blood followed by timely nd effective maneuvers to identify and treat the culprit esion. According to one of the most widely accepted algoithms for the management of active LGIB,3 patients with onbloody return on nasogastric lavage are given a bowel reparation and then undergo urgent colonoscopy. Howver, there are significant limitations with this approach. In any patients, bleeding ceases before the patient finishes the to 6-hour bowel preparation and the colonoscopy findings re negative, the bowel preparation is incomplete, or the xamination merely demonstrates diverticula that are preumed to be the bleeding source. In this situation, it can be ifficult to determine in retrospect whether the patient truly ad a diverticular bleed or bled from a small-bowel source uch as angiodysplasia, tumor, or even a Meckel’s diverticuum. In contrast, patients with more severe and ongoing leeding may be better served by alternative approaches, articularly in centers with less expertise in endoscopic mangement. In these select cases of rapid bleeding on presenation, because colonoscopy in the setting of active LGIB is hallenging, expedited embolization or even surgery may be referable to delaying treatment for a bowel purge that may e inadequate. Multidetector contrast-enhanced CT scanning (CT angiogaphy), which is readily available in most hospitals, can be

Suppurative (Phlegmonous) Gastritis Presenting as a Gastric Mass

A 58-year-old physician with untreated chronic hepatitis B virus infection initially presented with a 2-week history of severe epigastric abdominal pain, nausea, and anorexia. The first episode of pain awoke the patient from sleep, and subsequently occurred intermittently every 2–3 h throughout the day. There was no associated vomiting. The pain was described as squeezing, episodic, and intense, lasting 5–10 s, and located in the epigastrium and right upper quadrant. The pain did not radiate to the back, shoulders, or chest. The patient reported subjective fevers and shaking chills while at home, and documented a temperature of 100.8 F orally. The epigastric pain became associated with food intake 5 days prior to admission. At this point, the discomfort was constant and unrelenting, and the patient began to note extreme anorexia in addition to early satiety. In spite of these symptoms, the patient continued to work until 3 days prior to admission. Pain medications gave him only partial relief. Eventually, even ambulating exacerbated the pain. Based on his known history of chronic hepatitis B and concern for an acute exacerbation of his hepatitis, the patient serially monitored his liver function tests and referred himself to a gastroenterologist. A computed tomography (CT) of the abdomen and pelvis (Fig. 1) and an endoscopy were performed. On endoscopy, a 5-cm submucosal mass was identified and appeared to be causing a partial gastric outlet obstruction. The mass was confirmed by endoscopic ultrasound (EUS) (Fig. 2). The patient became febrile, and was started empirically on antibiotics and subsequently sent to Stanford University Medical Center for evaluation. On review of systems, the patient denied melena, hematochezia, sick contacts, night sweats, chronic cough, hemoptysis, prior blood transfusions, jaundice, or pruritus. His past medical history was significant only for chronic hepatitis B, and he had no previous operations or known drug allergies. His travel history was only significant for a recent recreational trip to Cancun, Mexico, on vacation. The patient worked as a primary care physician. He denied smoking or illicit drug use, and drank alcohol only socially. The patient was of Vietnamese heritage, and moved to the United States in 1975. He last visited Vietnam in 2005. His family history was significant only for a father who died from a perforated peptic ulcer at age 70. Upon admission, the patient was receiving oral levaquin 750 mg/day, metronidazole 1,500 mg/day, Vicodin 5/500 mg/day, ranitidine 150 mg/day, esomeprazole 40 mg/day and tramadol 50 mg/day. On physical examination, the patient was awake, alert, and fully oriented. His temperature was 36.6 C, pulse 76, blood pressure 117/77, respiratory rate 16, and oxygen saturation 97% on room air. He appeared well, albeit slightly pale, and he was in no acute distress. His neck was supple and there was no jugular venous distension, lymphadenopathy, or thyromegaly. His lungs were clear to auscultation bilaterally, and he had a regular heart rate and rhythm without murmurs, rubs, or gallops. Abdominal examination revealed voluntary guarding in the right upper quadrant, but there was no hepatomegaly, splenomegaly, or palpable masses. He had hypoactive bowel sounds. There were no stigmata of chronic liver disease. C. A. Munroe (&) A. Chen Division of Gastroenterology and Hepatology, Department of Medicine, Stanford University Medical Center, 300 Pasteur Drive, MC: 5187, Stanford 94305-5187, CA, USA e-mail: camunroe@stanford.edu

The Optimal Lipid Formulation in Enteral Feeding in Critical Illness: Clinical Update and Review of the Literature

Suitable and timely early enteral nutrition is paramount to providing optimal patient care for the critically ill. Lipids serve many essential roles throughout the human body, and are important components of most enteral formulations. This paper reviews lipid structure, function, and optimal utility for this macronutrient in enteral feeds. The use of omega–3 fatty acids has become common in critical care formulations, and their clinical efficacy is outlined separately. Available evidence is reviewed, and future directions are discussed.

Meckel's Diverticulum with Gastrointestinal Bleeding: Role of Computed Tomography in Diagnosis

A 26-year-old white male with a prior history of a benign cardiac arrhythmia and seasonal allergies presented with gastrointestinal bleeding and anemia. Two months prior to admission, he was seen in an urgent care clinic with intermittent, crampy left lower quadrant abdominal pain, worse 15–60 min after eating, and associated with alternating constipation and diarrhea. During that visit, a comprehensive metabolic panel, complete blood cell count and right upper quadrant ultrasound were normal. The patient was given the diagnosis of ‘‘vigorous gastrocolic reflex’’ and was successfully treated with Miralax . The patient remained in excellent health until 1 day prior to admission when he began to experience diffuse, infraumbilical, intense pain estimated to be six out of ten in severity, and an urge to defecate. While on the commode, he had an episode of transient pre-syncope. Two large, liquid maroon-colored stools and continuous bowel urgency prompted him to come to the emergency department. He denied any prior history of gastrointestinal bleeding, use of non-steroidal anti-inflammatory drugs, aspirin, alcohol or recreational drugs. He reported nausea but not vomiting and had no change in appetite or weight loss. His family history was negative for gastrointestinal malignancy. He was employed as a lawyer and had smoked one pack of cigarettes per day for 10 years. In the emergency department, his temperature was 36.2 C, pulse 67, blood pressure 97/60 mmHg, respiratory rate 20, and oxygen saturation 99% on room air. He was thin and well appearing, anicteric and slightly pale. There were no stigmata of chronic liver disease. Lungs were clear to auscultation bilaterally. Heart exhibited a regular rate and rhythm, without murmurs, rubs or gallops. His abdomen was soft, nontender and not distended; there was no organomegaly or palpable masses. Rectal examination revealed normal anal tone, no masses and liquid maroon stool. Two large bore intravenous catheters were placed, a 1-L saline bolus was given, and a nasogastric tube was placed without return of blood or bile. Laboratory tests showed white blood cell count 7,900/mm, hematocrit 36.8%, platelet count 123,000/mm, sodium 137 mmol/L, cloride 103 mmol/L, carbon dioxide 29 mmol/L, blood urea nitrogen 22 mg/dL, and creatinine 1.0 mg/dL. Liver function tests were normal. He was admitted to the general medical service, kept fasting with an active blood bank sample, and stool studies were sent to rule out infectious colitis. A pantoprazole drip was empirically initiated. A colonoscopy was performed the following day after bowel preparation, and blood was seen throughout the colon and terminal ileum. Twenty-four hours later, in the setting of continuous rectal bleeding, his hematocrit dropped to 24.2%. After a total of six units of packed red blood cells throughout the ensuing day, his hematocrit was 27%. In order to localize the source of bleeding, a computed tomography (CT) scan was performed using an angiography protocol. The CT revealed active contrast extravasation into loops of the distal ileum, with no associated mass or arteriovenous malformation (Fig. 1a, b). Because these findings were most consistent with bleeding from a Meckel’s diverticulum, an exploratory C. A. Munroe (&) A. Copland R. Pai S. Friedland G. Triadafilopoulos Division of Gastroenterology and Hepatology, Department of Medicine, Stanford University Medical Center, 300 Pasteur Drive, MC: 5187, Stanford, CA 94305-5187, USA e-mail: camunroe@stanford.edu

Endoscopic Management of a Spontaneous Gallbladder Perforation and Bile Leak

A 53-year-old man with a past medical history of alcoholic liver disease complicated by esophageal varices, ascites, hepatic hydrothorax, and hepatic encephalopathy presented to a local community hospital with 10-day history of abdominal pain. His pain was 10/10 in intensity, constant, worse in the supine position, increasing on the dependant side of the abdomen (when lying on the left side, the pain worse on left and vice versa), and improved in the upright position. The pain was not worsened by food and was not associated with fevers, chills, nausea or chest pain. He also reported shortness of breath and diarrhea, but denied rectal bleeding. When he was admitted to the local hospital, his white blood cell (WBC) count was 15,000/mm, predominantly bands and neutrophils. Because of concern for spontaneous bacterial peritonitis, empiric antibiotics were started and a nasogastric tube was placed. An abdominal ultrasound revealed a cirrhotic liver and a contracted gallbladder with mild gallbladder wall thickening. There was insufficient ascites to perform a diagnostic paracentesis. An abdominal radiograph series was negative for free air. Over the next 24 h, his pain continued to worsen and there was intermittent abdominal distention. A computed tomography (CT) of the abdomen and pelvis revealed a nodular liver capsule consistent with cirrhosis and large volume ascites (Fig. 1a). The gallbladder was contracted around dependent radio-opaque calculi (arrow, Fig. 1a). Two radio-opaque calcified structures in pelvis (arrow, Fig. 1b) consistent with gallstones with associated free fluid in pelvis were also seen. He was transferred to our institution. The patient’s past medical history was significant for alcoholic cirrhosis, and he had been on the liver transplant list. He also had a history of an incarcerated umbilical hernia that was repaired in 2008, as well as cholelithiasis. Upon transfer he was receiving piperacillin and tazobactam, vancomycin, ondansetron, pantoprazole, lactulose and hydromorphone as needed. He had no known drug allergies. He was single and did not smoke tobacco. The patient had discontinued alcohol use in 2008, and had no history of illicit drug use. Family history was negative. On physical examination, his vital signs were stable. The patient appeared to be in no acute distress with icteric conjunctiva and a nasogastric tube in place. There were decreased breath sounds bilaterally with a diffusely distended abdomen with tenderness to palpation in all quadrants. There was shifting dullness and a fluid wave consistent with ascites, but no guarding or rebound. The patient had scrotal and lower extremity edema but no asterixis. The patient had a WBC count of 10,300/mm, hematocrit 27.2%, mean corpuscular volume 84.7, platelet count 86,000/ mm, sodium 136 mmol/L, carbon dioxide 19 mmol/L, blood urea nitrogen 42 mg/dL, creatinine 1.5 mg/dL, albumin 3.1 g/dL, total bilirubin 8.3 mg/dL, alkaline phosphatase 130 U/L, aspartate aminotransferase 37 U/L, alanine aminotransferase 29 U/L, and international normalized ratio for C. Munroe (&) G. Triadafilopoulos J. Van Dam G. Lutchman Division of Gastroenterology and Hepatology, Department of Medicine, Stanford University School of Medicine, Stanford University Medical Center, 300 Pasteur Drive, Always Building, Rm M211, Stanford, CA 94305-5187, USA e-mail: camunroe@stanford.edu