Category Archives: Uncategorized

How much radiation from your CT scanner?

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Our children’s hospital, along with many others, has made a concerted effort to reduce radiation exposure by adjusting CT scan settings.  Even a single abdominal CT scan may confer a small but real risk of developing cancer.  The trade-off with low-dose CT techniques has been a concern about poor image quality.  New research indicates that low-dose CT scan is not inferior to standard-dose CT with respect to detecting appendicitis (NEJM 2012; 366: 1596-605).

This single-center study examined 441 patients assigned in a single-blind fashion to low-dose CT (median dose: 116 mGy-cm) in comparison to 447 patients receiving a standard-dose CT (median dose: 521 mGy-cm).  All patients had CT for suspected appendicitis.  The negative appendectomy rate was 3.5% in the low-dose group and 3.2% in the standard-dose group.  There was no significant difference in appendiceal perforation rate or proportion of patients needing more imaging.

How much radiation do your patients receive with a CT scan?

Related newspaper article:

FDA issues guidelines to lower radiation exposure in children:

http://www.ajc.com/health/child-sizing-radiation-doses-1434081.html

Related posts:

Magnetic resonance enterography for Crohn’s disease

More imaging needed?

Additional references:

  • -NEJM 2010; 363: 1, 4. Safety of CT.  Can have overdose of radiation and even standard doses could cause complications.  Also, a big issue is downstream unnecessary testing due to incidental findings.
  • -JPGN 2011; 52: 280. Documents high exposure to radiation in large IBD pediatric cohort.
  • -J Clin Gastroenterol 2011; 45: 34-39. High levels of ionizing radiation thru CT scan in pts with IBD.
  • -Pediatr Radiology 2002; 32: 217-313. Minimizing radiation exposure, risk/benefit of CT. Proceedings from conference.
  • -Pediatr Radiology 2002; 32: 700-706. Risk of CT for young child: ~ 1 in 1000 risk of fatal cancer later in life.

Proton pump inhibitors–infection risk with cirrhosis

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In a previous post (The Medical Pendulum and Gastroesophageal Reflux), I note that enthusiasm for proton pump inhibitors has started to wane.  In addition, a significant number of reported of potential side effects were referenced.  Another potential adverse effect is increasing the rate of spontaneous bacterial peritonitis (SBP) in patients with cirrhosis (Clin Gastroenterol Hepatol 2012; 10: 422-27).

This retrospective study examined 65 hospitalized cirrhotic patients with paracentesis-proven SBP between 2006-2009 and compared them to 65 contemporaneous hospitalized cirrhotic patients without SBP.   Patients with SBP had a higher incidence of use of PPI within previous 7 days: 71% versus 42%.  Of patients with SBP receiving PPI, the authors state that 68% did not have a documented indication for PPI use.

Additional references/previous posts:

  • –Treating reflux does not help asthma
  • -Risk of Hypomagnesemmia -2011. http://www.fda.gov/drugs/drugsafety/ucm245011.htm
  • –Gastroenterology 2010; 139: 1115.  Review of safety of PPIs.
  • –Gastroenterology 2010; 139: 93. n=167,000. PPIs associated with hip fracture risk, OR 1.3, in patients with other risk factors.
  • –Gastroenterology 2010; 138: 896-904. 5 yrs of PPI -no increase risk in hip/spine fx.
  • –Arch Intern Med 2010; 170: 765-71, 747 (ed). PPI not related to hip fx (n=161,806) women 50-79. INCREASE risk of spine fx, hazard risk 1.47
  • –Arch Intern Med 2010; 170: 772-8. PPIs increase risk of Clostridium difficile infection (hazard ratio 1.42 –42% increase in risk), n=1166.
  • –Arch Intern Med 2010; 170: 784-90. n=101,796. OR 1.74 for daily PPI, OR 2.36 if BID Rx; thus ~70% increase risk of nosocomial infection.
  • –Clin Gastro & Hep 2010; 8: 504. Increased bacterial overgrowth with PPI use.
  • -JAMA 2009; 301: 2120-2128. Use of PPIs associated with INCREASED hospital acquired pneumonia by ~30%. Could result in 180,000 HAP cases/yr with ~33,000 deaths. n+ 63,878 admissions, 52% on PPIs or H2RAs (83% PPIs, 17% H2RAs). H2RAs NOT associated with HAP cases.

Does it make sense to look for parasites in RAP?

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Probably not, in the absence of other symptoms.  A small study from Switzerland shows that treatment of Blastocystis hominis does not help recurrent abdominal pain (RAP) more than placebo (JPGN 2012; 54: 677-79).

This study result is not surprising.  A previous study of 157 RAP pediatric patients (JPGN 2007; 44: 524-26) showed that testing for ova and parasites was unnecessary as the incidence of parasitic infections in this population was not increased in RAP patients compared with controls. In this 2007 study, stool samples were positive for parasitic infection in 15 children, with no difference in prevalence between children with chronic abdominal pain (6/87; 7%) and healthy control children (9/70; 13%).

The current study had 37 patients complete the study.  The pain index (PI) for all patients improved in the study; however, there was no difference between patients who received antibiotics (trimethoprim-sulfa was used as first-line agent) compared to those who received placebo.

Regarding the methodology, the PI was either a visual analog scale with numbers from 0 to 10 or a standardized face scale; the specific scale was determined by the patient age.  Also, among the 20 patients who received antibiotics, 13 continued with B hominis in their stool tests after an initial round of therapy.  Yet the change in pain was virtually identical.  In antibiotic-treated patients, initial PI was 7.1.  After treatment, those with persistent B hominis detected in the stool had a PI of 4.2 whereas those with negative stool specimens had a PI of 4.1.  The placebo patients started with a PI of 7.4; after placebo treatment, a similar proportion cleared the B hominis from their stool –in this group, at the conclusion of the placebo treatment the PI was 2.4; the placebo group with persistent detection of B hominis had a PI of 3.2 at the conclusion of the study.

Although the potential pathogenicity of B hominis in humans remains unclear, it is not unusual in clinical practice for patients with this finding to receive treatment.   Besides trimethoprim-sulfa, metronidazole is frequently administered. Based on this study, placebo would be as helpful as an antibiotic in improving clinical symptoms.

Related blog entries:

What to make of FODMAPs

Pain changes brain

Disease modifying treatment in IBD

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As noted in this blog (Only one chance to make first impression) and other sites as well, many have argued for early “top down” treatment to try to modify the natural history of Crohn’s disease (CD).  Early in the course of CD when an inflammatory process predominates, theoretically, treatment at this time point can prevent the development of intestinal fibrosis/strictured IBD phenotype.

Support for this approach can now be extrapolated from a mouse model as well (Inflamm Bowel Dis 2012; 18: 460-71).  In this study, the authors eliminated an inflammatory stimulus, Salmonella typhimurium, with levofloxacin treatment.  Treatment was initiated at sequential time points during infection.  Subsequently, the effects of the inflammation on the development of fibrosis was determined by examining histopathology; in addition, the effects on mRNA expression and protein expression were determined.  The time course of a number of cytokines is followed including TNFα, TGFβ, IL12p40, IL-17, IL-1β, and IL-6. While intestinal fibrosis developed even in those with early treatment, early treatment lessened, but did not eliminate, the development of fibrosis.

Since no effective antifibrotics exist and fibrosis may autopropagate even in the absence of inflammation, the authors postulate that early effective treatment has the best opportunity to alter the natural history.

Indomethacin to prevent post-ERCP pancreatitis

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“Take two and call me in the morning” may now apply to the use of indomethacin in preventing post-ERCP pancreatitis.  A multicenter, randomized, placebo-controlled, double-blind clinical trial has shown that rectal indomethacin (two 50 mg suppositories) can reduce the rate of post-ERCP pancreatitis (NEJM 2012; 366: 1414-22).

A total of 602 adult patients were enrolled.  Patient selection favored those at increased risk for post-ERCP pancreatitis (eg. suspicion of sphincter of Oddi dysfunction) and excluded those at low risk for this complication (eg. routine biliary stent exchange, chronic calcific pancreatitis, or a pancreatic head mass).  Other exclusion criteria included active pancreatitis, elevated creatinine (>1.4 mg/dL), active peptic ulcer disease, and those already receiving a NSAID.

The suppositories (or placebo) were administered immediately after ERCP while the patient remained in the procedure room.

Post-ERCP pancreatitis developed in 27 of 295 patients (9.2%) in indomethacin group and in 52 of 307 patients (16.9%) in placebo group.  In addition, moderate-to-severe pancreatitis was reduced as well 4.4% compared with 8.8% respectively.  In addition, there were no increased adverse events in the treatment arm; there was no increased risk of bleeding in particular.

While the mechanism of improvement is unclear, NSAIDs are potent inhibitors of phospholipase A2, cyclooxygenase, and neutrophil-endothelial interactions, all of which are known to play a role in the pathogenesis of acute pancreatitis.

Additional references:

  • -Am J Gastroenterol 2007; 102: 978-83.  Use of indomethacin to reduce pancreatitis after ERCP
  • -Gut 2008; 57: 1262-7.  Meta-analysis of rectal NSAIDs to prevent post-ERCP pancreatitis

“Watch for change in the stools”

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Many years ago I noticed the tremendous burden that coin ingestions cause in terms of ER visits and need for endoscopy/anesthesia.  As a result, I contacted the US treasury.  I think if any other product resulted in this many hospitalizations and endoscopic procedures it would be removed from the market.  Well, the treasury stated that the coins are mandated by Congress and any change would need to be initiated in Congress. So, I contacted our Georgia senator and informed the office about the problem.  Apparently, it could be a while before this becomes a priority for him.

Some good news, though, based on a recent article, watchful waiting may be appropriate for many esophageal coins (Emerg Med J 2012; doi: 10.1136/emermed-2011-200958).  (The blog title quote comes from Bill Balistreri who use to say that it was not worth it to take out anything less than a quarter —just watch for change in the stools.)

Acheson J et al performed a retrospective review of esophageal coin ingestions between 2004-2010 (age <16 years).  Among asymptomatic patients who were told to wait 18 hours for a repeat xray, 33 of 37 passed spontaneously.

Exclusion criteria:

  • Previous esophageal disease
  • Previous tracheal disease
  • Coins present >24 hours

All mid-to-lower coins (that were given 18 hours) passed in this study.  The authors note that previous studies had spontaneous passage rates of 30-60%.  Some of the difference may be related to differences in the UK coins compared to coins in US.  In the UK, the authors suggest that patients who are asymptomatic and with no other risk factors should be sent home and reevaluated the next day.

**Before sending them home, make sure the “coin” is not really a button battery by examining the radiograph carefully.

Additional references:

  • -Pediatrics 2005; 116: 752 (editorial), 614-19 (article). 25-30% of coins (esp distal -56%) will pass spontaneously if given time (8-16hrs)–in this randomized study.
  • -Arch Pediatr Adol Med 1999; 153: 1073. 28% of uncomplicated esophageal coins pass c/in 24hrs
  • Emerg Med J doi:10.1136/emermed-2011-200958
    [Link to free full-text EMJ article]

Inadequate treatment of anemia in IBD

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In some patients with inflammatory bowel disease (IBD), treatment of anemia associated with IBD sometimes results in more symptomatic benefit than treatment of the IBD.  Yet, anemia remains common in IBD, both in children and adults (Inflamm Bowel Dis 2012; 18: 513-19).

Using a cross-sectional observational study design, a tertiary adult and pediatric IBD center reviewed consecutive clinic patients in April 2009.  The prevalence of anemia was 70% (41/59) children, 42% (24/54) adolescents, and 40% (49/124) adult.  In addition, iron deficiency anemia was more common in the pediatric population: 36/41 children and 20/23 adolescents.  In the adults with anemia, only 55% (27/49) were iron deficient.  One of the key determinants of anemia was disease activity.

Interestingly, among patients with iron deficiency, younger age was inversely associated with treatment with iron therapy: 13% of children, 30% of adolescents, and 48% of adults.

Other important aspects of anemia in IBD:

  • Anemic patients can have quality of life scores as poor as those seen in malignancy
  • Almost all IBD patients will respond to either oral or parenteral iron.  Erythropoetin reserved for patients who do not respond to parenteral iron.

Additional references:

  • -NEJM 2005; 352: 1011. Anemia algorithm.  If transferrin saturation <16%, check ferritin.  If ferritin less than 30, then patient with Fe-deficiency; if >100, anemia of chronic disease.  If 30-100, could check soluble transferrin receptor (level of sTranReceptor/log ferritin < 1 is c/w anemia of chronic disease whereas when > 2, c/w combined Fe-def anemia and anemia of chronic disease)
  • -JPGN 2010; 51: 708. 25-50% still anemic 1yr post IBD diagnosis.
  • -IBD 2007; 13: 1545-53. Guidelines for anemia mgt w IBD. Max oral absorption is 10-20mg/day; thus IV iron often needed. Goal for iron Rx is transferrin saturation of 15-50% and ferritin > 30 mcg/L (>100 if active inflammation). Anemia of chronic disease likely if TS <16% and ferritin > 100. Rec IV iron Rx prior to use of Epo. IV iron effective alone in 70-80%. Epo if no response to IV iron & Hgb <10. Consider folic acid & B12 deficiency if high MCV. AZA/6MP usually associated with pancytopenia not isolated anemia.
  • -Gastroenterology 2011; 141: 846. Ferric carboxymaltose better than iron sucrose (Ferrlecit/Venofer) b/c can use higher dose & give more rapidly.

More on magnet ingestions

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Magnet ingestion has been a popular topic this past week on the pediatric GI listserv and follows a recent post on this blog as well (Magnet ingestion –urgent removal needed).  Two useful links are listed below:

Infliximab for children with Ulcerative Colitis

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A large multicenter study of patients 6-17 years of age has shown that infliximab (IFX) can be effective for ulcerative colitis (UC) (Clin Gastroenterol Hepatol 2012; 10: 391-99). Our pediatric GI group was part of this multicenter study which enrolled 60 patients. Stanley Cohen was lead CCDHC investigator and is one of the authors.

At week 8, 44 patients (73.3%) had a clinical response to IFX.  This group of ‘responders’ were eligible for the maintenance phase of the study and were divided into a q8 week treatment group (Q8) and a q12 week treatment group (Q12).  During the maintenance phase, patients who had lost response were eligible to have a dose escalation from 5 mg/kg/dose to 10 mg/kg/dose. At week 54,  patients receiving every Q8 had a remission rate of 38% (8 of 21) whereas among the Q12 responder group only 18% (4 of 22) were in remission.  Overall, the authors projected that if the entire cohort had been placed on every 8 week treatment, the response would have been 28% at week 54; in addition, analysis with ‘real-world’ dose adjustments could achieve a 42.8% remission rate.

The main serious adverse events reported during the study was worsening of UC.  Two patients were receiving immunomodulators during the study. Five of 60 patients required a colectomy within the 54-week study period.

The risk/benefit ratio of TNF antagonists for UC has been discussed in related posts (see below).

Previous related posts:

TNF antagonists and UC

Only one chance to make first impression

Additional references:

  • -Am J Gastroenterol (Oussalah A et al) 2010; 105: 2617-25. Multicenter study of IFX for UC.
  • -Gastroenterology 2010; 138: 2282. Severe pediatric UC. 25/33 responded to IFX. colectomy rate 19% at 1 year.

CLMP–why some children are born with a short gut

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CLMP stands for Coxsackie- and adenovirus receptor-like membrane protein. It is required for intestinal development (Gastroenterology 2012; 142: 453-62).

In this study of seven patients from five families with congenital short-bowel syndrome (SBS), the authors identified a loss-of-function of CLMP in five of the patients.  CLMP is a tight-junction-associated protein that is expressed in the intestine of human embryos throughout development.

To study the effect of CLMP expression, the authors created a zebrafish model with compromised CLMP activity.  This lead to offspring with a foreshortened body and intestine, strengthening the evidence that CLMP dysfunction is responsible for congenital short-bowel syndrome.

Additional references/previous related posts: