Author Archives: gutsandgrowth

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About gutsandgrowth

I am a pediatric gastroenterologist at GI Care for Kids (previously called CCDHC) in Atlanta, Georgia. The goal of my blog is to share some of my reading in my field more broadly. In addition, I wanted to provide my voice to a wide range of topics that often have inaccurate or incomplete information. Before starting this blog in 2011, I would tear out articles from journals and/or keep notes in a palm pilot. This blog helps provide an updated source of information that is easy to access and search, along with links to useful multimedia sources. I was born and raised in Chattanooga. After graduating from the University of Virginia, I attended Baylor College of Medicine. I completed residency and fellowship training at the University of Cincinnati at the Children’s Hospital Medical Center. I received funding from the National Institutes of Health for molecular biology research of the gastrointestinal tract. During my fellowship, I had the opportunity to work with some of the most amazing pediatric gastroenterologists and mentors. Some of these individuals included Mitchell Cohen, William Balistreri, James Heubi, Jorge Bezerra, Colin Rudolph, John Bucuvalas, and Michael Farrell. I am grateful for their teaching and their friendship. During my training with their help, I received a nationwide award for the best research by a GI fellow. I have authored numerous publications/presentations including original research, case reports, review articles, and textbook chapters on various pediatric gastrointestinal problems. In addition, I have been recognized by Atlanta Magazine as a "Top Doctor" in my field multiple times. Currently, I am the vice chair of the section of nutrition for the Georgia Chapter of the American Academy of Pediatrics. In addition, I am an adjunct Associate Clinical Professor of Pediatrics at Emory University School of Medicine. Other society memberships have included the North American Society for Pediatric Gastroenterology Hepatology and Nutrition (NASPGHAN), American Academy of Pediatrics, the Food Allergy Network, the American Gastroenterology Association, the American Association for the Study of Liver Diseases, and the Crohn’s and Colitis Foundation. As part of a national pediatric GI organization called NASPGHAN (and its affiliated website GIKids), I have helped develop educational materials on a wide-range of gastrointestinal and liver diseases which are used across the country. Also, I have been an invited speaker for national campaigns to improve the evaluation and treatment of gastroesophageal reflux disease, celiac disease, eosinophilic esophagitis, hepatitis C, and inflammatory bowel disease (IBD). Some information on these topics has been posted at my work website, www.gicareforkids.com, which has links to multiple other useful resources. I am fortunate to work at GI Care For Kids. Our group has 17 terrific physicians with a wide range of subspecialization, including liver diseases, feeding disorders, eosinophilic diseases, inflammatory bowel disease, cystic fibrosis, DiGeorge/22q, celiac disease, and motility disorders. Many of our physicians are recognized nationally for their achievements. Our group of physicians have worked closely together for many years. None of the physicians in our group have ever left to join other groups. I have also worked with the same nurse (Bernadette) since I moved to Atlanta in 1997. For many families, more practical matters about our office include the following: – 14 office/satellite locations – physicians who speak Spanish – cutting edge research – on-site nutritionists – on-site psychology support for abdominal pain and feeding disorders – participation in ImproveCareNow to better the outcomes for children with inflammatory bowel disease – office endoscopy suite (lower costs and easier scheduling) – office infusion center (lower costs and easier for families) – easy access to nursing advice (each physician has at least one nurse) I am married and have two sons (both adults). I like to read, walk/hike, bike, swim, and play tennis with my free time. I do not have any financial relationships with pharmaceutical companies or other financial relationships to disclose. I have helped enroll patients in industry-sponsored research studies.

Think twice about checking thyroid

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Hypothyroidism is not a frequent cause of constipation in children (JPGN 2012; 54: 285-87).  According to this study, the yield on checking for hypothyroidism in pediatric patients with constipation is no greater than in the general population.

This retrospective study examined the records of 873 patients who underwent thyroid testing ordered by pediatric gastroenterology; 443 (51%) had isolated constipation.  In all, 56 had abnormal thyroid function testing though 40 were normal on repeat testing. Of these 16 remaining cases, 7 were known to have hypothyroidism.  Of the nine remaining “new” cases, 3 had slow growth (2 without constipation), 3 had trisomy 21, and 2 were taking medications which affect thyroid function.  This leaves only 1 patient who presented with constipation without a clear risk factor or other indication for testing.

The authors state that 1/443 (0.2%) is quite similar to background incidence of hypothyroidism (0.3%).  The costs of identifying this case would exceed $18,000 but could be considered much higher (~$200,000) when all of the costs of false-positives are considered (eg. endocrinology consultations, followup testing).  In patients with slow growth (with or without constipation), about 2.5% had hypothyroidism.

In short, think twice about checking thyroid status in patients with isolated constipation.

Additional references:

  • -JPGN 2011; 53: S2. 49, 55. ‘Rarely do children with constipation need w/u’–only if alarming features: Delayed meconium, bilious vomiting, bloody stools, fever, bladder disorders, poor growth, NO RESPONSE to conventional treatment, abnormal exam. 25% of functional constipation problems may persist into adulthood.
  • -JPGN 2010; 51: 155. Lack of utility of AXR -suggested only in uncooperative pts, concerns about abuse/concerns about psychologic impact of exam
  • -J Pediatr 2010; 156: 461-5. MRI in children with chronic constipation or not-retentive soiling (n=130, n=28) -MRI showed lumbar sacral abnormalities in 3% –none required neurosurgery (1 w spina bifida occulta, 3 w terminal filum lipomas). Prospective study.
  • JPGN 2006; 43: e1Ye13.  http://www.naspghan.org/user-assets/Documents/pdf/PositionPapers/constipation.guideline.2006.pdf  Guidelines suggest checking thyroid, calcium, celiac and lead if not responding to therapy.

Unexplained chest pain

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Not surprisingly -unexplained pediatric chest pain has a high association with anxiety/psychiatric disorders (J Pediatr 2012; 160: 320).  In this study, the authors compared patients (8-17 years) with chest pain (n=100) to a cohort referred with innocent heart murmur (n=80).  In addition to cardiology evaluation, patients had a structured interview and a child health questionnaire to assess for psychiatric disorders; also, the investigators interviewed the parent(s).

Based on DSM-IV criteria, 70% of chest pain patients had an anxiety disorder and 9% had depression.  In contrast, 33% of heart murmur patients had an anxiety disorder and none were depressed.  Among the chest pain subjects, 26% had abdominal pain and 26% had headaches -both higher than the control group, 9% and 10% respectively.  Also, 90% of patients with chest pain had psychiatric disorders which preceded the chest pain.

For pediatric gastroenterologists, a take home message from this article is that chest pain is quite similar to abdominal pain (see references below); it might be interesting to discuss with cardiologists.

  • Do cardiologists experience the same reluctance from families to seek help from mental health?
  • How much testing is required before a functional diagnosis is accepted?
  • Do they follow patients with functional chest pain or send back promptly to primary care physician?

This article does not examine parental mental health issues.  This would be interesting.  In functional abdominal pain, maternal anxiety has been ascribed as the most consistent predictor of outcome (Acta Paediatr 2007; 96: 697-701).  Another factor that would be of interest would be level of activity; exercise helps reduce symptoms of irritable bowel/abdominal pain.

At the same time, the issue of reflux is not addressed by this article and not infrequently the issue of whether reflux is causing chest pain needs to be considered.  An article (Gut 2011; 60: 1473-78) regarding chest pain in adults indicates that patients with pH-probe (or endoscopic) proven GERD often respond partially (>50% reduction in symptoms) to PPI use.  This study reviewed RCTs involving chest pain and PPIs -six met inclusion criteria.  The RR of therapeutic gain for PPI usage was 4.3 for those with proven reflux and 0.4 for those with pH-probe (or endoscopic) negative chest pain.  Interestingly, in this study, heartburn was not predictive of whether chest pain was due to GERD on pH study.

Additional references:

  • -Pediatr Emerg Care 2010; 26: 830-6.  Psychopathology among children presenting to ER with unexplained chest pain.
  • -Clin Gastro 2008; 6: 329-32.  Depressive symptoms common in RAP -45%
  • -Pediatrics 2004; 113: 817.  Anxiety & depression commonly associated with RAP.  anxiety in ~79%, depression ~43%; anxiety often precedes RAP.
  • -JPGN 2011; 53: 200. n=98. 79% of FAP responded to low dose tricyclics
  • -Gastroenterology 2009; 137: 1261, 1207– Editorial.  Amitriptyline helped in 66% vs 58% with placebo. n=90. dose 10mg <35kg, 20mg >35kg. 89% had failed Rx prior to study. ‘Inability to use placebo.. in practice may justify amitriptyline’ Rx. Consider hypnotherapy/CBT first.
  • -Gut 2011; 60: 1473-78. PPI use in unexplained chest pain.
  • -Pain 2006; 122: 43-52. (Walker LS et al), J Pain 2006; 7: 319-26.  Distraction/ignoring important.
  • -J Pediatr 2009; 154: 313 (editorial), 322. Prospective school study. n=237. Weekly prevalence of abd pain was 38%. 18% with persistence for >12 weeks.
  • -Clin Gastro Hepatol 2008; 6: 329-32.  FAP persists into adulthood in 1/3 to 1/2 of cases.
  • -Gastroenterol 2006; 130: 1459-1465.  Functional esophageal d/o.
  • -Clin Gastro & Hep 2006; 4: 558. Review.
  • -Ann Heart J 2000; 40: 367-372.  Sertraline decreased chest pain independent of mood alteration/psychological scores.

Can I go?

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How safe is it for IBD patients to travel?  A retrospective study from adult patients with IBD (n=222) compared with controls (n=224) indicates that the risk of travel for IBD patients is only a little more than the general population (Clin Gastroenterol Hepatol 2012; 10: 160-65).

IBD patients with an average age of 37 years had infections during 15% of trips compared with 11% for controls.  92% of infections were due to enteric disease. However, this increased risk was identified in travel to industrialized countries not to developing countries.  This likely indicates that much of the increase is due to IBD flares rather than increased susceptibility to infections.  Nearly half of patients in this study were receiving immunosuppression: immunomodulators 29%, biologics 5%, dual therapy 6%, or corticosteroids 4%.  Not surprisingly, patients with increased IBD flares (OR 1.9) and IBD-related hospitalizations (OR 3.5) represent a group with higher risk for illness.  Most illnesses were mild & self-resolving in a few days.  Only five IBD patients required hospitalization for the following: dehydration, perianal abscess, malaria, flare, & small bowel obstruction).

Additional references:

  • -Clin Gastro & Hep 2010; 8: 490. Review of traveler’s diarrhea. Recs pepto if emesis, rifaximin or cipro or azithromycin if watery diarrhea, azithromycin if bloody diarrhea
  • -Clin Gastro & Hep 2007; 5: 451. Use of rifaximin (200mg tid)-loperamide provided rapid improvement.
  • -NEJM 2006; 354; 119. Traveler’s diarrhea.
  • -NEJM 2002; 347: 505.  Illness after travel.
  • -www.cdc.gov/travel/index.htm

It’s worth the cost

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Recently the cost of Sitzmarks® increased to $175 (for 12)–it’s worth the cost.  According to one study, the use of a transit study helps determine which patients will benefit from colonic manometry (JPGN 2012; 54: 258-62).  A retrospective review of 24 children showed that all five children with normal oral-anal transit (OTT) studies had normal colonic manometry.  In contrast, 9/19 (47%) with abnormal (slow OTT) had abnormal colonic manometry.

The authors define their approach to OTT which is helpful.

  • In patients with a fecal impaction, this was cleared prior to starting study
  • If patients had difficulty with capsule ingestion, markers were administered by embedding in part of a banana or mixed with applesauce
  • Stimulant laxatives withheld for 72hrs prior to study
  • AXR obtained on days 3 and 5
  • Slow OTT (abnormal) defined as >6 markers proximal to rectum on day 5

Of those with abnormal colonic manometry, two-thirds (6) were referred for surgical intervention; one patient with normal OTT had surgery.  Surgeries:  3 cecostomy, 4 subtotal colectomy.

Additional references:

  • -JPGN 2004; 38: 75. Colostomy in 10 children with intractable constipation.
  • -Arch Dis Child. 2004 Jan;89(1):13-6. Benninga MA, Voskuijl WP, Akkerhuis GW, Taminiau JA, Buller HA. Related Articles,  Colonic transit times and behaviour profiles in children with defecation disorders.
  • -J Pediatr Surg. 2004 Jan;39(1):73-7. Youssef NN, Pensabene L, Barksdale E Jr, Di Lorenzo C.  Is there a role for surgery beyond colonic aganglionosis and anorectal malformations in children with intractable constipation?
  • -Am J Gastroenterol. 2003 May;98(5):1052-7.  Pensabene L, Youssef NN, Griffiths JM, Di Lorenzo C. Related Articles, Colonic manometry in children with defecatory disorders. role in diagnosis and management.
  • -JPGN 2002 Jul;35(1):31-8. Gutierrez C, Marco A, Nogales A, Tebar R. Total and segmental colonic transit time and anorectal manometry in children with chronic idiopathic constipation.
  • -JPGN 2001 Nov;33(5):588-91.  Villarreal J, Sood M, Zangen T, Flores A, Michel R, Reddy N, Di Lorenzo C, Hyman PE.  Colonic diversion for intractable constipation in children: colonic manometry helps guide clinical decisions.
  • -http://www.sitzmarks.com/buyonline.aspx

Help with hepcidin

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Over the past several years, the mechanisms involved in iron overload have been carefully examined and the genetic basis for most of these disorders is now understood.  Several review articles on these disorders have been published; the most recent with excellent diagrams is in last week’s NEJM (NEJM 2012; 366: 348-59 & NEJM 2012; 366: 376-77). Although the process is quite complicated, the most important aspect regarding iron homeostasis is a feedback loop involving hepcidin-ferroportin.  Hepcidin functions as a ‘hypoferremia hormone.’  It down regulates ferroportin release of iron into the circulation.  Hepcidin is also an acute-phase protein and inflammation affects its function.

Hepcidin levels fluctuate in response to the body’s iron needs: more hepcidin causes less iron absorption & less hepcidin causes more iron absorption.

  • Iron balance disorders can usually be attributed to altered hepcidin production.
  • Anemia of chronic disease, though multifactorial, is mostly due to increased hepcidin production in response to inflammation.
  • Hemochromatosis results from genetic mutations causing lack of normal hepcidin production.  The severity of these disorders correlates with hepcidin levels.
  • Hepcidin agonists could be used to treat hemochromatosis and other iron overload conditions (eg. thalassemia with transfusion therapy).  For hemochromatosis, phlebotomy will be less expensive.
  • Hepcidin antagonists could treat anemia of chronic disease

Additional references:

  • -Hepatology 2011; 54: 328.  Review.  Guidelines.
  • -Hepatology 2010; 52: 925.  HFE homozygotes, n=31,192 w low risk of clinical symptoms if ferritin <1000.
  • -Gastroenterology 2010; 139: 393. Review –pathogenesis/dx/Rx
  • -Hepatology 2009; 50: 94.  C282Y/H63D compound heterozygotes (n=180) are at low risk for hemochromatosis-related morbidity compared with control group.
  • -Hepatology 2008; 48: 991.  Review.
  • -Hepatology 2007; 46: 960, 1071.  Review of clinical phenotypes.  Of C282Y homozygotes, only 1-2% develop HCC, 6% cirrhosis, 25% liver fibrosis, 38% Fe overload, 61-75% develop raised serum iron indices.
  • -Hepatology 2007; 46: 1291. Review of hemochromatosis
  • -Hepatology 2007; 45: 253. Review of iron metabolism
  • -NEJM 2004; 350: 2383. Review.  Several genetic mutations associated with clinical phenotype.  type 1: Classic HFE, types 2A & 2B: (Juvenile type)  HJV & HAMP (gene products hemojuvelin & hepcidin), type 3:TFR2 (transferrin receptor 2), and type 4:SLC40A1
  • -NEJM 2005; 352: 1011. Algorithm.  If transferrin saturation <16%, check ferritin.  If ferritin less than 30, Fe-deficiency; if >100, anemia of chronic disease.  If 30-100, check soluble transferrin receptor (level of sTranReceptor/log ferritin less than 1 is c/w anemia of chronic disease whereas when this ratio is greater than 2, c/w combined Fe-def anemia and anemia of chronic disease).  Hepcidin is produced by hepatocytes and regulates iron homeostasis.  Hepcidin interacts with ferroportin, an iron export protein on enterocytes (& other cells), & facilitates internalization and degradation of ferroportin.  It may lead to decreased dietary iron absorption and to retention of iron body stores.  Hepcidin expression can be up-regulated by high iron levels or during acute phase inflammatory responses (thus can contribute to anemia of chronic disease).  Hereditary hemochromatosis associated with low hepcidin levels in the face of increased iron body stores.  Several genes can affect hepcidin loss of function, including HFE, hemojuvelin (HJV), and transferrin receptor 2 (TFR2).
  • -Gastroenterology 1996; 110: 1107.  Sentinel article discussing long-term survival in hemochromatosis and role of iron.

More on ethanol locks

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In a post earlier this week (Four advances for intestinal failure), ethanol locks were discussed.  More on information this subject (Pediatrics 2012: 129: 318-29) comes in a meta-analysis.  These authors identified 4 retrospective studies in pediatric IF populations.  Ethanol locks reduced infections by 81% and line replacements by 72%.  The studies in this meta-analysis overlapped with the six studies cited in the previous post.  Adverse events were rare and included thrombotic events.

Additional reference:

  • -JPEN 2012; 36: 36S-42S

What is calretinin?

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Calretinin is a ‘calcium-binding protein that is normally expressed in cholinergic nerves.’ (NEJM 2012:366: 361-72)  The absence of calretinin-positive mucosal neurites helps establish a diagnosis of Hirschsprung’s disease, even when suction-biopsy specimens may have previously been considered inadequate.  It is not known why calretinin neurites are absent in Hirschsprung’s disease nor why abnormal acetylcholinesterase-positive neurites are present.

More information on the technical aspects of diagnosing Hirschsprung’s disease and illustrations of these stains is available in this case record.

Additional references:

  • -Mod Pathol 2009; 22: 1379-84. Calretinin in Hirschsprung’s.
  • -Pediatr Dev Pathol 2009; 12: 6-15. Calretinin & acetylcholinesterase in Hirschsprung’s.
  • -JPGN 2011; 53: 75.  Problems post-op.
  • -JPGN 2008; 46:13.  Nice review.
  • -Pediatrics 2002; 109: 914-918.  Review of surgical treatments.
  • http://www.ccdhc.org/diseases/Hirschsprung.html

Blood is not enough

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…to resolve the problems of sickle cell anemia.  The effects of transfusions for sickle cell patients’ hepatobiliary function are poorly understood.  By lowering the level of hemoglobin S and reducing sickling, can this lead to improvement in organs damaged by sinusoidal congestion and infarction?  Well probably not (J Pediatr 2012; 160: 281-85).

Strokes are known to occur in 5-10% of sickle cell patients by 20 years of age and if untreated, >50% have recurrence.  This has led to transfusion programs.  The ‘Stroke with Transfusions Changing to Hydrdoxyurea’ (SWiTCH) study is a multi-center randomized trial trying to determine how current treatment (transfusions and chelation) compares with hydroxyurea/phlebotomy for preventing stroke and managing iron overload.  As part of this study, a baseline assessment with ultrasound showed widespread problems -despite an average of 7 years of transfusions.  In this cohort of 149 patients, the following findings were identified:

  • Spleen volumes were increased in more than 1/3rd of patients leading to hypersplenism (low platelet counts). 12 subjects had nonvisible spleens due to autoinfarction.
  • Nephromegaly was present.  This finding is known to occur with sickle cell disease and is a marker of glomerular hyperfiltration.
  • Hepatobiliary disease was nearly ubiquitous.  37 of 148 had previous cholecytectomy; of the remaining, 46 of 111 (41%) had gallstones and 14% had gallbladder sludge.  Liver lengths were significantly longer as well.

Conclusions: Transfusion therapy was insufficient to reverse or prevent organ damage in children with sickle cell anemia.  An important limitation– the severity of the underlying prevalence of organ dysfunction prior to initiation of transfusion therapy was not known.

Additional references:

  • -Blood 2011; 117: 772-9.  Silent cerebral infarcts occur despite regular blood transfusions.
  • -Clin Gastro & Hep 2007; 5: 1469.  Reviews types of sickle cell associated liver disease.
  • -Pediatric Hematology and Oncology.  2006 Mar;23(2): 95-102(8).  Sickle cell intrahepatic cholestasis (SCIC), which is related to intrahepatic sinusoidal RBC sickling (due to relative hypoxia) and can be associated with progressive hepatomegaly, mild transaminitis, extreme hyperbilirubinemia
  • -JPGN 2004; 39: 200.  Review of sickle cell hepatic crisis.  Cholestasis resolves over 3 months.  Acute crisis treated with hyperhydration & transfusion. Cohort of 350; 6 developed hepatic crisis.
  • -J Pediatr 2001; 139: 785-789 & 790-796.  Transfusions and hydroxyurea for SS dz.

Four advances for intestinal failure

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Several advances in the management of intestinal failure have the potential to improve the outlook for our intestinal failure (IF) (aka Short Bowel Syndrome) patients (JPEN 2012; 36: 36S-42S).

Although IF patients already have improving survival with rates of 80-95% over followup ranging from 1-5 years, many still do not survive, primarily due to bacterial infections or chronic liver disease.  Ongoing research has made some promising steps in the management of these pediatric patients.  This article focuses on four of these steps.

1. Citrulline monitoring

  • Major source of citrulline is enterocyte production.  Citrulline is an amino acid not encoded in human genetic code; it is present in some proteins as a product of posttranslational modification.
  • Watermelon is one of few dietary sources.
  • Useful biomarker for bowel length/absorption –independent of inflammatory markers
  • Levels >15-20 μmol/L indicate good likelihood of achieving enteral autonomy
  • Levels <12μmol/L indicate a very low likelihood of achieving enteral autonomy

2. Teduglutide therapy

  • Analog of glucagon-like peptide 2 (GLP-2) but harder to degrade (longer half-life)
  • Preliminary studies in adults indicate improvement in absorption and villous histology after subcutaneous administration for three weeks.  Improvements reverse when drug is discontinued.
  • Since GLP-2 is produced by colon & increased in IF (if colon present), unclear whether exogenous administration will be as beneficial in patients with residual colon

3. Lipid minimization &/or fish oil lipids

  • Cholestasis increases in patients receiving more than 1 g/kg/day of intralipids (soy based).
  • Fish oil (Omegaven) has shown benefit in lowering cholestasis in numerous case reports.  This may be due the high content of anti-inflammatory ω-3 fatty acids.
  • Another preparation SMOFLipid is a mixed formulation and may be safer than pure fish oil; randomized controlled studies of both of these lipid formulations are underway.
  • Fish oil has not been shown to improve histology
  • Parenteral nutrition associated liver disease (PNALD) may improve with lowering lipids & may not need omegaven

4. Ethanol locks

  • May be beneficial in treating and preventing central line infections.  In both situations, in small studies, ethanol locks lowered incidence of recurrent infections.
  • Six studies involving 75 patients (66 pediatric patients) lowered infection rates from approximately 10 per 1000 catheter days to 2 per 1000 catheter days.
  • Ethanol concentrations were mostly 70% in these studies, though 25% has been used.
  • Dwell times ranged from 2-14 hours.
  • Randomized studies are in progress.
  • Fewer infections should reduce the likelihood of death from sepsis and death due to loss of venous access.

Additional references:

  • -NEJM 2010; 362: 181.  Letter to editor describes use of fish oil in (n=125) Boston pediatric patients.
  • -JPGN 2009; 48: 209. n=12. SBS.9/12 improved with omegaven. 3 had transplant (L-ITx). No controls.
  • -NEJM 2009; 361: 998. Intestinal Rx.  Review claims ~90% 1yr survival. 47% 5yr, 61% 3yr (expecting to go higher)
  • -JPGN 2009; 48: 334. Isolated liver w SBS feasible IF 50cm small bowel remaining or 30cm w ICV, 50% enteral nutrition >4 weeks with good growth, no dysmotility.
  • -Pediatrics 2008; 121: e678. n=18. use of fish oil improved cholestasis compared to historical controls.
  • -Gastroenterology 2008; 135: 61, 303. Survival of ITx (vs. HAL).  In many conditions, better off from survival standpoint without Tx. Tx if failure of TPN (severe liver dz/thrombosis of >/= 2 central veins, multiple bouts of sepsis/frequent dehydration), high risk of death, severe short bowel (<10cm in infants and <20cm in adults), pseudoobstruction, unwillingness to accept long-term tpn. 93% of TPN patients who did not have TPN-complications had 93% survival rate.  Thus, TPN is first line Rx as survival and quality of life often better.
  • -Pediatrics 2006; 118: e197-e201.  Reversal of TPN-AC c IV omega-3 fatty acids (fish oil-derived) instead of intralipids
  • -Liver Transplantation 2006; 12: 1062, 1040. Liver transplant alone reasonable to consider in some SBS patients who tolerate >50% enteral therapy and are less than 2 years old.
  • -Gastroenterology 2006; 130. Supp 1. Summary of NIH workshop on intestinal failure. TX Indications: Liver disease, thrombosis of major veins, recurrent catheter-related sepsis, frequent severe dehydration/electrolyte imbalance.
  • -JPGN 2005; 41: 47A (pg507). Poor prognosis: <40cm, needing >40kcal/kg PN, increased bili (>150 μmol/L)
  • -J Pediatr 2005; 146: 542. Serum citrulline > 19 μ/L associated with bowel adaptation/weaning off HAL.
  • -J Pediatr 2004; 145: 157-163. Survival of SBS with as little as 15
  • -Arch Pediatr Adolesc Med 2006; 160: 104953.  Use of ethanol lock (70%, 08-1.4mL for 12-24hrs, then withdraw). n=51.  High success rate in salvaging line
  • -J Pediatr 2001; 139: 27-33. Review of 30 pts. 3 of 30 pts with bowel length 40cm or less able to wean PN.
  • -Gastroenterology 2001; 120: 806-815. Glucagon-like peptide 2 improves nutrient absorption marginally.

Speed matters

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Capsule endoscopy is cool.  Like any technology, it has certain advantages and some shortcomings.  Understanding that this technology has limited sensitivity and specificity is an important matter in clinical practice.

The suboptimal sensitivity is apparent in a recent study (Am J Gastroenterology, (10 January 2012) | doi:10.1038/ajg.2011.461).  In this study titled, “Detection of Lesions During Capsule Endoscopy: Physician Performance Is Disappointing,” the authors compare the performance of 17 capsule endoscopists in reading clips from 24 capsule procedures.  18 of these clips were abnormal but only abnormal in <0.1% of frames.  They compared different reading modes, speeds and the experience of the physicians.  By using clips, they were able to truncate the sessions to a similar length as an individual capsule procedure.

Their findings showed detection rates of 69% for angioectasias, 38% for ulcers/erosions, 46% for masses/polyps, and 17% for blood.  For all categories the detection rate was ~45% for SingleView15, QuadView20, and QuadView30; however, SingleView25 had a 25% detection rate.  One surprising finding was how little experience mattered; there was no significant advantage in having more experience.  In fact, the best performer who correctly identified 78% of the abnormalities had read only 45 capsule studies previously; the worst performer with a 17% score had read more than 11,000 previously.

In a typical capsule study, 40,000-60,000 images are generated.  If there is not a diffuse disease, then the lesion may go undetected.  The findings of these studies, though limited by the small number of interpreting physicians, confirm problems with sensitivity from other studies.  One aspect of this study that deserves emphasis is that speed matters.  As with colonoscopy, additional time reviewing the study does increase the likelihood of identifying abnormalities.  Ultimately, technological innovation may improve the results with capsule endoscopy.  With newer versions of the software,  “suspected blood indicator” (SBI) quickly identified six of the 18 lesions and “QuickView” identified 11 of the 18 lesions.  As with any test, though, if the clinical suspicion is high, having another physician review the study or using an alternative imaging tool may be necessary.

Another problem to keep in mind with capsule endoscopy (or wireless capsule endoscopy -WCE) is that especially in adults there is a significant background abnormality rate that may be clinically unrelated (Clin Gastro & Hepatol 2005; 3: 133-141. n=413. 13.8% with baseline mucosal injury).

Additional references:

  • -IBD 2008; 14: 1219. Correlation of capsule & MRI enteroclysis. Capsule detected more mucosal lesions.
  • -JPGN 2008; 47: 31. Capsule endoscopy may reclassify pediatric IBD.
  • -Dig Liver Dis 2008; 40: 216-223. Study comparing capsule vs EGD in detecting varices.
  • -JPGN 2008; 46:4. Review.
  • -Gastroenterology 2007; 132: 855. Capsule outperforms push enteroscopy.
  • -IBD 2007; 13: 331. Role of WCE in IBD.
  • -Pediatrics 2006; 118: e904. Use of capsule endoscopy for HSP
  • -Clin Gastro & Hep 2005; 3: 959. WCE should be 2nd step in obscure bleed, p egd/col.
  • -Clin Gastro & Hep 2005; 3: 772. WCE outperforms enteroclysis in identifying Crohn’s sm bwl dz.
  • -Gastroenterology 2005; 128: 1172. NSAID injury witnessed in 68% of healthy volunteers p 2 week course; 75% c increased fecal calprotectin.
  • -Clin Gastro & Hepatol 2005; 3: 411. Practical applications & review.
  • -Clin Gastro & Hepatol 2005; 3: 264-70. Study of 30 children; helpful in diagnosing obscure bleeding.
  • -Endoscopy 2005; 37: 960-65. Results of capsule endoscopy trials
  • -Clin Gastro & Hepatol 2005; 3: 133-141. WCE to assess NSAID injury, n=413. 13.8% with baseline mucosal injury. Celebrex with fewer lesions than Naproxen plus omeprazole.
  • -Gortzak Y, Lantsberg L, Odes HS. Video capsule entrapped in a Meckel’s diverticulum. J Clin Gastro 2003; 37: 270-271.
  • -Clin Gastro & Hep 2005; 3: 55. visible lesions c NSAIDs
  • -IBD 2004;10: 278-285. WCE for Crohn’s (review) Capsule can help differentiate UC from Crohn’s.
  • -Clin Gastro & Hepatology 2004; 2:xx. Dx of Peutz-Jeghers w WCE.
  • -Gastro 2004; 126: 643-653. WCE performs well for occult bleeding, especially active bleeding (87% detection rate)
  • -Clinical Gastro & Hepatology 2004; 2: 14-15, 31-40.
  • -Gastroenterology 2003; 124 (suppl 1) A37. abnl small bowel findings common in healthy subjects.
  • -JPGN 2003; 37: 332 (18A), n=58. Crohn’s, polyposis, occult bleeding
  • -Gastroenterology  2003; 124: suppl 1, A-37 (284) 22% of normal pts c abnl wireless findings
  • -Gastroenterology  2002; 123: 999-1005, 1385-88. capsule is superior to radiographs for suspected small bowel dz.
  • -Gastro Endosc 2002; 56: 452-456. Algorithm suggests using this modality if negative upper & lower endoscopy & no acute overt bleeding. If capsule endoscopy is negative & patient is stable, observation appropriate.
  • -Gastro Endosc 2002; 56: 621-24. ASGE guidelines.