Do we need an esophagram to evaluate a spontaneous pneumomediastinum in kids?

The paper was published in JPS a few days after the subject was brought up amongst our group.  Basically, what do we do with a kiddo who presents with a pneumomediastinum with no antecedent history of trauma or retching, and who is otherwise doing well with no fever or signs of mediastinitis.

In this paper, the authors retrospectively reviewed 27 patient with a spontaneous pneumomediastinum(SPM) who underwent an esophagram as part of their evaluation. The authors noted that none of the patient had a demonstrable injury to the esophagus. They concluded that an esophagram is not necessary for the evaluation of SPM. They felt the source of the air in this group of patients was alveolar disruption and not an esophageal injury.

Needles to say, a series of 27 patients is not sufficient to make a final conclusion on the subject. That being said, the series helps us support any decision we make regarding clinical follow up on a patient with a SPM, who is otherwise well with no other signs of esophageal injury such as dysphagia or pleural effusion on a CXR. 

Do we really need screening UGI's before G tube placement?

The logic behind performing screening UGI studies before g tube placement has always escaped me.  I understand the rationale behind screening for malro before a Nissen +/- g tube, since reflux could be due to some level of partial obstruction from malro; but why UGI's for g tubes without reflux?  It certainly is not a useful test to screen for reflux.  We definitely do not need to know where the stomach is before place a g tube, so why the radiation exposure?

A study by Abbas et al noted that the incidence of unexpected malro identified by screening UGI's performed for patients undergoing a routine gastrostomy tube placement is 1.7% (5/229).

Even if one accepts that avoiding a potential catastrophic event in 2 patients is worth the risk of radiation (300 cGy/UGI study) to the other 98, this logic should be applicable to all preop patients (since the need for a g tube does not necessarily select out a population at higher risk of malrotation).

So why do we not screen all preop patients with UGI's?(not suggesting that we should, for the trolls out there!).

Some more data to help support what we do (or don't do). 

Hepatico-Jejunostomy or Hepatico-duodenostomy after resection of a choledochal cyst?

Cholangitis!!!... is that not the main concern when food is passing right next to the hepatic ducts after a hepatico-duodenostomy (HD), with no interposed common bile  duct or sphincter of Oddi?  That was what I thought until I was told otherwise, and confirmed with the limited available evidence.

When a Kocherized (salute to the verb-nouns) duodenum can reach the hepatic ducts for reestablishing continuity after choledochal cyst resection, the laparoscopic operation becomes simpler, more physiologic, and avoids potential complications related to the roux-en-y reconstructions.  Additionally, it allows for future endoscopic access to the anastomosis in case an anastomotic stricture or intrahepatic stones develop. No much controversy there.

But what about cholangitis, how can it be OK for food to pass right by the hepatic ducts and not cause an infection.

In a paper by Santore et al out of CHOP, the authors retrospectively reviewed charts of 59 patients who underwent open resection by the same surgeon with reconstruction using either HD (66%) or HJ (34%). After a mean of 2.3 years follow up for HD and 3.5 years follow up for HJ, only one patient in the HJ developed cholangitis.  Additionally, there was no significant difference in the rate of postoperative leaks or strictures.

Another argument against reconstruction with a HD relates to the risk of bile gastritis.  A meta-analysis of several papers with a total of 679 patients (60% of whom underwent reconstruction with a HD) suggested that patients who are reconstructed using a HD are at increased risk of bile gastritis (5.9% for HD vs. 0% for HJ).  It is clear how reconstruction with a HJ completely diverts bile away from the stomach and thus prevents any bile gastritis.  It is unclear to me, however, how placing the anastomosis in the duodenum, and downstream of a perfectly healthy pylorus, is any different from the normal physiologic drainage of bile, and why that would cause gastritis.

At this point, it seems reasonable to me to chose a HD over a HJ if technically feasible.

1.7 cm carcinoid in the appendectomy specimen, now what?

I have yet to walk away from a conversation about the management of incidentally found carcinoid tumors of the appendix satisfied.  Today, I was determined to find some kind of an answer.

My basic understanding is that an incidentally found lesion which is < 2 cm and with negative margins is essentially treated with the appendectomy.  Otherwise, a hemicolectomy is needed.

If we were to extrapolate form the adult literature, the simplest recommendation is that of the NCCN version 2.2014 (National Comprehensive Cancer Network). Simply stated, a tumor < or = 2cm completely removed with the specimen is essentially cured with no further operative management needed.  Surveillance is performed "as clinically indicated". The document does acknowledge the fact that the management of tumors between 1 and 2 cm with poor prognostic factors such as mesoappendiceal invasion, lymphovascular invasion, or atypical histologic features, is controversial.

The NANETS (North American Neuro Endocrine Tumor Society) guidelines officially take into account local invasion.  They recommend right hemicolectomy for patients with evidence of tumor invasion to the base of the appendix, if the tumor is >  2 cm, if tumor size cannot be determined, if tumor is incompletely resected, if there is lymphovascular invasion or invasion of the mesoappendix, in patients with intermediate or high grade tumors, and in patients with mixed histology tumors.

A recent paper, Kim et al reported their experience with the management of incidentally found carcinoid tumors. The authors noted that out of their 13 cases, only one tumor was larger than 2 cm (2.1 cm) and that was the only patient, out of three who had a right hemicolectomy, who was found to have regional metastatic disease.

As is the overall case with carcinoid of the appendix, the numbers are just too small to make solid recommendations, especially for tumors in the 1 to 2 cm range. A good conversation with the patient and family about the numbers and management options is central to decision making.

So much for finding an answer today.

Neutropenic colitis gems

From memory:

1. Neutropenic colitis occurs in neutropenic patients
2. Mimics appendicitis (trap!)
3. Don't call it typhlitis, as it falsely suggest that it can only occur in the cecum
4. A concomitant C diff infection worsens prognosis 
5. Broad spectrum antibiotics including flagyl
6. Best solution, normalize WBC

From reading "neutropenic colitis in children":

Neutropenic colitis was found in 1.4% of children treated for a malignant condition. Although the majority of patients were profoundly neutropenic (Mean ANC = 164), 12% had a normal neutrophil count. The episode of colitis, which presents with vague signs and symptoms, is usually preceded by a precipitous drop in ANC.

Although most cases involve the cecum, the colitis may involve the ascending colon, and even the terminal ileum.

Treatment involves bowel rest, decompression, broad spectrum antibiotics (including anti-fungals), and occasionally G-CSF. Operative management is reserved for patients with bowel perforation, bleeding, or clinical deterioration.

So learned a couple of things today.

How do Senna laxatives work?

My frustration with my inability to find a good reference that explains how Senna based laxatives work (before I prescribed it to one of my patients with HD and encopresis) was relieved by one of our fine Pedi GI folks.  She promptly sent me this paper from the deep archives of an appropriately name journal.

Here's the answer.

Senna, an anthraquinone laxative, is a glycoside that is metabolized in the GI tract into oxy-methyl anthraquinone.  OMA's (just made that up; not the official name) soften the stool by decreasing water absorption from the colon and promote colonic contraction by stimulating the Auerbach plexus of nerves.

There you go.

Outcome of endorectal pull through with ileal-pouch vs straight ileo-anal anastomosis

The satisfaction gained from taking a child from a state of misery and malnutrition to "he is doing so wonderfully after his colon came out" is only tempered by the conversation that must follow. Asking a child and their parents to choose between too evils (multiple bowel movements/incontinence vs the risk of pouch complications/pouchitis) when discussing the next step can only be made more palatable when we have some outcome data to share.

A paper by Seetharamaiah et al in published in JPS in 2009 provided that data.

The authors retrospectively looked at 203 children (average age 15 years) who underwent either a straight ileo anal pull through vs a pouch anastomosis for UC or familial polyposis.  The authors compared several outcome variables, including the rate of complications (pouchitis/enteritis) and long term bowel functions as reflected by the modified Hoschneider scoring system (incorporates number/consistency of stool, risk of daytime/nighttime incontinence, severity of urgency, and need for therapy for stool control).

The authors noted that, as one would expect, the patients who underwent a straight pull through had more BM's per day than those who underwent a pouch anastomosis.  Interestingly, after 24 months, the number of bowel movements approached that of patients who underwent a pouch anastomosis (mean number of bowel movements for straight pull through vs. pouch anastomosis were 8 vs 6 per day, respectively).

As to the general quality of bowel function, both groups eventually scored similarly on the modified Holschneider coring system, and ultimately ~90% became totally continent after 24 months, regardless of type of operation.

As to pouchitis, the nagging complication of pouch creation, the authors noted that patients had a 49% risk of documented pouchitis, vs 24% risk of ileitis, the counterpart in a patient with a straight pull through.

Based on this data, it appears that both options area reasonable, with the benefit of a better outcome in terms of bowel function for the first two years, when a pouch is created, balanced against the increased risk of pouchitis and what is entails in terms of pain/discomfort, need for antibiotics, and potentially hospital admissions. 

What is the chance that asymptomatic GB stones in kids will cause problems in the future?

As I prepared to see a kiddo in the office for asymptomatic gall stones, I decided to do a quick review of the literature to see what's new.

Not surprisingly, couldn't find any good studies that looked at the outcome of this patient population.  The best paper I found was by Bogue et al, who retrospectively reviewed charts of 382 patients with GB stones and identified a group of patients who were incidentally found to have cholelithiasis (asymptomatic).  Of the 382 patients, 50% were asymptomatic.  Their mean age was 8 YO, and they had their u/s for unrelated causes, manly other abdominal pathology.

The authors reported that follow up for these asymptomatic kids was "an annual clinical and ultrasound assessment for 1 to 2 years" unless they had other pathology that necessitated longer follow up.  With this strategy, their mean follow up for this patient group was 3+/- 1.7 years.  During this follow up period, only 4.6% of the patients developed complications related to their stones (pancreatitis, choledocholithiasis, cholecystitis). Interestingly, they noted that 19% of GB stones eventually resolved, as demonstrated by follow up ultrasounds (when they were done).

So what does this mean?  Not much when it comes to counseling parents.  At best I can suggest to them that there is very little chance the stones will cause problems in the near future, but that we can not predict their behavior (or even their persistent existence) over the long run.

Reference:
Bogue C O et al.  Risk factors, complications, and outcomes of gallstones in children: a single-center review. Journal of Pediatric Gastroenterology and Nutrition (2010) 50:p303

What is the fate of abnormal looking bowel seen on prenatal ultrasound?

While reviewing the literature on prenatal imaging and their prognostic implications, I came across this relevant article by Ruiz et al from Morgan Stanley Children's Hospital.

The authors looked to study the relationship between abnormal prenatal ultrasound findings in the bowel and the presence of an actual bowel abnormality at birth.  They divided patients into two groups, those with hyperechogenic bowel and those with dilated bowel.

Of the fetuses with a finding of hyperechogenic bowel, the authors noted a 20% rate of prenatal demise.  Otherwise, only 10% of those patients were born with abnormal bowel (usually from meconium disease).  During follow up prenatal ultrasound studies, 65% of the findings resolved in that group of patients.

The group with the dilated bowel on u/s had a higher chance of having a true bowel abnormality when born.  Although the rate of prenatal demise in that group was lower (10%), fetuses with dilated loops of bowel on prenatal u/s had a 53% chance of being born with abnormal bowel (usually from intestinal atresia).  On follow up prenatal ultrasound studies, only 20% of the findings resolved in that group of patients.

This data sheds some light on the significance of bowel abnormalities found on prenatal ultrasounds, and thus helps better counsel parents on what to expect.

Reference:

Ruiz JR et al.  Neonatal outcomes associated with intestinal abnormalities diagnosed by fetal ultrasound.  Journal of Pediatric Surgery (2009) 44,71

Do we need to administer antibiotics before enema reduction of intussusception?

When reading the chapter on intussusception in Grosfeld's Pediatric Surgery, I noticed that the authors recommended that antibiotics be administered to patients before attempts at air enema reduction. No good explanation was given for this practice, which we do not follow where I train. Patients go for their enema reduction, and if that fails, get preoperative antibiotics at the time of surgery, just like everyone else.

 

An article the May issue of JPS attempted to answer the question of the benefit of pre-contrast enema reduction antibiotics. The authors performed a retrospective, cohort study comparing outcome of patients form two different institutions; one that routinely gives pre-reduction antibiotics and one that does not.

 

The main end-points of this study were the incidence of post-reduction fever (as a marker of bacteremia) as well as adverse reactions to antibiotic administration. The authors noted no significant difference in either, suggesting (despite the usual shortcomings of a retrospective study) that antibiotics are not necessary.

 

Although it would take a prospective randomized study to better answer this question, it does not seem to make sense to give antibiotics before enema reduction.

 

Reference: Al-Tokhais et al. Antibiotics administration before enema reduction of intussusception: is it necessary? JPS (2012);47:928

Why should kids with short gut syndrome be on proton pump inhibitors?

During rounds today, I noticed that someone had changed an order for a proton pump inhibitor to an H2 blocker on one of our patients with short gut syndrome. The reason was some form of shortage, so they decided it was OK to switch.

So it was time for that discussion again.

Patients with intestinal failure secondary to substantial small bowel loss need proton pump inhibitors because they are in a state of hypergastrinemia, as gastrin is primarily metabolized in the small bowel.

Elevated gastrin levels cause an increase in the volume and acidity of gastric secretions, which results in an acidic environment in the small bowel. The increase in volume worsens the fluid and electrolyte balance which is already tenuous in patients with short gut. Additionally, the acidic environment in the small bowel exacerbates malabsorption by causing bile acids to precipitate (sabotage micelle formation) and by inactivating pancreatic enzymes.

He's back on his proton pump inhibitors.

Reference:
Kocoshis SA. Medical management of pediatric intestinal failure. Seminars in Pediatric Surgery (2010);19:20

Is a bowel prep necessary before colostomy reversal?

Another paper that supports omitting bowel preps before pediatric bowel operations came out in this month’s issue of JPS. In this study, the authors conducted a retrospective, multi-institution study and compared the outcome of 272 children who underwent colostomy reversal with and without (187 vs. 85) a polyethylene glycol bowel prep.

The authors noted a significantly higher rate of wound infection (14.4% vs. 5.8%), as well as a longer hospital stay (5.6% vs. 4.4%) in the group who underwent a bowel prep. Additionally, they noted that the risk for other complications such as abdominal abscess formation (~1%) and ansastomotic leak (~1%) was the same whether a bowel prep was used or not.

Reasons given for the potential deleterious effects of the bowel prep included the characteristics of liquid stool (bowel prep) that make it more difficult to contain, the fact that the bacterial load in prep’d stool is not necessarily lower than unprepped stool (papers sited), and the potential harmful effect of the bowel prep on the integrity of the bowel mucosa.

As with all retrospective studies, the authors acknowledged the limitations of their results, but stressed that, except for intra-pelvic rectal surgery, a bowel prep is likely unnecessary for colonic surgery in children.

Reference:
Serrurier K et al. A multicenter evaluation of the role of mechanical bowel preparation in pediatric colostomy takedown. JPS (2012);47:190-193

What is the normal length of small bowel in a preemie?

After informing a dad that his preemie baby has only 45 cm of small bowel left after surgery for NEC, he asked me a question that caught me off guard.
“So how much should he have at 27 weeks gestation?”
Knowing that the small bowel almost doubles in length at the last trimester, I estimated 100 cm’s but then headed back to the books/PDF files to figure out a more exact answer.

Fortunately, there had been some back and forth emails between two of my attendings about papers that looked into expected bowel lengths for preemies.
Went home, pulled the emails out of my ‘Educational’ folder in ‘Mail’, transferred the PDF’s to my ‘Papers’ software, synced my MBP with my iPad (go paperless!), then read the articles during my 45 post-call spin session.

In the first article (via Dr Philip Glick), by Touloukian et al, the authors measured the length of small bowel obtained from autopsy specimens of 30 babies of various gestational ages. The authors documented the bowel length over three age ranges and noted that the small bowel more than doubled its length during the third trimester. As attractive as this article is in its simplicity, several confounding factors, including the fact that post mortem changes may affect the measured length of bowel, limit the accuracy of these bowel measurements.

In the second article, published more than 30 years later (via Dr Doruk Ozgediz), by Strujis et al, the authors obtained intraoperative measurements of small bowel in 108 patients whose post conceptual age ranged from 24 weeks to 5 years. The authors linked the bowel length to gestational age, weight, and patient length at time of surgery. They noted that all three variables predicted the length of bowel with similar accuracy, and suggested that patient height be used since it is more consistent and easier to measure.

Why is this important? Knowing the expected normal length of bowel in a preemie baby makes estimations of the potential risk of short gut syndrome and other outcomes, after intestinal resection, easier; this helps better council parents. It also helps answer the question: "Well, how much bowel should my baby normally have?”

References:
1. Touloukian RJ, et al. Normal intestinal length in preterm infants. Journal of Pediatric Surgery (1983) 18(6):720
2. Strujis M, et al. Establishing norms for intestinal length in children. Journal of Pediatric Surgery (2009) 44:933

What is the 'leading edge' of a transition zone in Hirschsprung's disease, and why is it important?

Time to dip into the old stash for an interesting paper. This one was out of St Louis, MO and looked at the properties of the transition zone of ganglion cells in HD by taking sequential cross sections of surgical specimens and quantifying the ganglion cells in the submucosal and myenteric plexus.

The authors noted that the transition zone was not uniform, but instead had a leading edge (analogous to dripping paint). This leading edge of the transition zone was measured to be up to 2.1 cm (average 1.1 cm) and 2.4 cm (average 1.4 cm) long in the submucosal and myenteric plexuses, respectively. Additionally, the number of ganglion cells at the tip of the leading edge was normal.

The significance of this finding is that a frozen section biopsy performed at the transition zone may result in a pull-through that includes abnormal bowel and potentially poor functional results. The authors thus recommended that a pull-through be performed using bowel that is at least 2 cm proximal to the area of 'normal' ganglionated bowel identified intraoperatively by frozen section

Reference:
White et al. Circumferential distribution of ganglion cells in the transition zone of children with Hirschsprung's disease. Pediatric and Developemental Pathology (2000) 3, 216

How often are common bile duct stones found in children suspected of having them?

This read stemmed from a literature search looking for articles addressing missed CBD stones in children not suspected of having them (no hx of jaundice, pancreatitis, normal CBD on U/S etc..). Instead I ran into this interesting article, out of Sick Kids in Toronto, looking at kids with findings consistent with CBD stones who were either managed by pre-operative ERCP, or had undergone an intra-operative cholangiogram, followed by ERCP when the IOC was positive.

202 patients with gallbladder stones, 48 of whom (23.7%) had suspected CBD stones. Preoperative ERCP, which was performed on a third of patients with suspected CBD stones, was positive in 21.4% of cases. Most of the rest of patients with suspected CBD stones underwent an IOC, which was positive in 6.5% of cases. Based on their results, the authors recommended an IOC as the initial investigative study since it involves less risk to the patient than does an ERCP, which was negative in around 80% of cases.

An IOC seems to be an excellent way to avoid unnecessary ERCP's, as long as a skilled gastroenterologist with a high ERCP success rate is available (to avoid a situation where a CBD stones are identified intraop, and an attempt at ERCP fails post op!). What is interesting about this study is the discrepancy between the finding of stones in the preoperative ERCP group and the IOC group. This could be because the ERCP may be more sensitive than the IOC, but potentially there might have been a selection bias, where patients who were more likely to have CBD stones (elevated bilirubin (8 vs 2), markedly dilated CBD (14 vs. 7) etc...) might have been selected to undergo and ERCP vs IOC.

Reference
Mah et al. Management of suspected CBD stones in children: role of selective IOC and ERCP. Journal of pediatric surgery (2004)39 :808-812

How can laparoscopy help evaluate patients with suspected rotational anomalies?

Again, the subject of rotational anomalies and equivocal UGI findings came up. The next day, this paper by Hsiao et al out of Sick Kids in Tornoto was in JPS. Here the authors discuss the utility of diagnostic laparoscopy as a tool to help corroborate UGI findings, or as a tie breaker for equivocal UGI studies.

The article was based on two premises. The first is what defines malrotation vs. non-rotation. Malrotation, here, was defines as the DJJ and the cecum near the midline, and the base of the mesentery less than 50% of the diameter of the abdomen. Non-rotation was defined as DJJ to the right of midline, ceceum in the lower left or central abdomen, small bowel on the left side, colon on the right, and base of mesentery is longer than 50% of the diameter of the abdomen. The other premise is that the small bowel is not at risk of midgut volvulus when the base of the mesentery is longer than 50% of the diameter of the abdomen (as in normal and non-rotation), and a Ladd's procedure is not necessary.

Very few people would argue that an infant with bilious emesis who is found to have an abnormal UGI needs exploration. The issue becomes more controversial when abnormal UGI studies are found in children with no symptoms or chronic and/or non-specific symptoms. This is the group of patients this paper addressed.

The UGI results studies included findings consistent with malrotation, malrotation with volvulus, non-rotation, or equivocal findings. Of the patients with UGI findings consistent with malrotation, ~60% had malrotation confirmed by laparoscopy (with or without volvulus), and the rest had either non-rotation (30%) or were normal (10%) (both conditions the authors believe do not need surgical correction). When UGI's showed non-rotation, laparoscopic evaluation was consistent with the diagnosis in all patients. Finally, of the patients with an equivocal UGI, a third had malrotation with/without volvulus, and the rest were found to be either non-rotated (48%) or normal (21%) on laparoscopic evaluation.

So if we accept that a mesenteric base longer than 50% of the diameter of the abdomen constitutes a stable mesenteric base not prone to volvulus (a finding confirmed by laparoscopy), laparoscopy can be an important tool that can help us manage this perplexing population of patients with no/vague symptoms and inconclusive UGI studies.


Reference:
Hsiaoo M, Langer JC. Value of laparoscopy in children with a suspected rotation abnormality on imaging. Journal of Pediatric Surgery (2011) 46, 1347-1352

4 mechanisms of esophageal injury by button batteries

Coins, the most commonly encountered ingested foreign body in children, cause complications related to chronic impaction and erosion. Button batteries are more dangerous. Methods by which they can cause damage (mostly when stuck in the esophagus) include

1. Toxic effect of mercuric oxide: some batteries contain lethal levels of mercuric oxide (5g). Batteries containing other heavy metals, lithium, or manganese are not toxic.
2. Electrical discharge from the battery
3. Pressure necrosis (as with coins)
4. Caustic injury from leakage of the battery's contents

Interestingly, batteries smaller than 1.6cm in diameter do not get lodged in the esophagus. Restricting the size of batteries produced to less than 1.6cm may help prevent serious injuries that can occur in as little as 5 hours after ingestion.

Reference:
Yardeni et al. Severe esophageal damage due to button battery ingestion: can it be prevented?
Pediat Surg Int (2004) 20:496

A bowel prep is not necessary before colosotmy reversal in kids (APSA 2011)

In this retrospective study looking at data from three institutions, the authors compared LOS and complication rates after colostomy takedown between pediatric patients who underwent a mechanical bowel prep and those who did not.

When they reviewed the data from 272 children (187 underwent a prep) they noted a longer hospital LOS for the prep group (5.6 vs 4.4 days); 122 of them had been pre-admitted for the prep. They also noted a higher rate of wound infections for the prep group (14.4 vs 5.8%). No significant difference was noted in the rate of abdominal abscess formation, anastomotic leaks, or C-diff infections.

Despite the limitations of this retrospective study, which may be comparing individual surgeon outcomes rather than the effect of bowel preps, this is another nail in the coffin of the pre-op bowel prep dogma that will hopefully be sealed by a PRS by the same group.

Reference:
A multi-center evaluation of the role of mechanical bowel preparation in pediatric colostomy takedown.
Serrurier K, Liu j, Breckler F, et al.

What's the Pediatric Appendicitis Score (PAS) and is it actually helpful?

So who hasn't received the call for a kiddo with 'classic' appendicitis only to see the kid and send him home because he's constipated.

What if there was a consistent and reliable way of communicating the "classic'ness" of someone's abdominal pain between healthcare workers; NP from an outside hospital calling for a transfer or ED physician calling for a surgical consult.

Enter PAS.

The PAS was introduced by Maden Samuel in 2002 as a way to stratify children's risk of having appendicitis when they present with abdominal pain. The scoring system consists of 8 findings (6 worth 1 point, and 2 worth 2 points for a total score of 10 points). Since Samuel's inception, several studies have addressed the sensitivity and specificity of this scoring system and attempted to develop strategies for it's use, mostly in deciding whom to take to the OR without imaging, whom to image, and whom to send home.

Goldman et al from Sick Kids in Toronto prospectively tested the PAS on unselected children with abdominal pain. Based on the scoring system, they noted that if they had sent kids with a score less than or equal to 2 home, there would have been a 2.5% missed appendicitis rate. on the other hand, if they took anyone with a score greater or equal to 7 to the OR, the rate of negative appendectomies would have been 4%.

Another study by Bhatt et al looked at the use of PAS on children suspected of having appendicitis and noted that sending home children with a PAS of 4 or less would have resulted in a missed appendicitis rate of 2.4%, while operating on those with a PAS greater or equal to 8 would have resulted in a negative appendectomy rate of 8.8%.

Reading through the papers, it is clear that the PAS is not perfect. What about the female who is mid cycle and has severe, sudden onset abdominal pain, nausea, and right lower quadrant tenderness. I wouldn't take her to the OR without imaging even if her score was 10/10. Clearly there's an important role of the "intangible ingredient" in patient evaluation, and no scoring system could take the place of a thorough history, exam, and experience. What the PAS does do is help standardize the way we communicate the level of suspicion for appendicitis, and may have a role in developing pathways to help physicians decide on whom to image, and whom not to, before a surgical consult is called.

So instead of 'classic' appendicitis (which clearly means different things to different people), a phone call about a patient with PAS of 8 would probably be much more meaningful to all parties involved.

References:

Maden S. Pediatric appendicitis score. Journal of Pediatric Surgery 2002;37:877

Goldman et al. Prospective validation of the pediatric appendicitis score. Journal of Pediatrics 2008;153:278

Bhatt et al. Prospective validation of the pediatric appendicitis score in a Canadian pediatric emergency department. Academic Emergency Medicine 2009;16:591

IBD markers are not screening tools

Again, I am fascinated by how some physicians order an "IBD panel" in a kid with abdominal pain to r/o Crohn's disease (CD) or Ulcerative colitis (UC). Unless I am confused, an IBD panel's role is to help differentiate the two types of IBD, and not make the diagnosis (substantial false positives and false negatives).

Here is some information I found useful:

Main laboratory markers:

ANCA: anti-neutrophil cytoplasm antibody
ASCA: anti-Saccharomyces cervisiae antibody
Anti-OmpC: anti E coli-related outer membrane porin C
Anti I2
Anti-Cbir1: antibody against flagellin

pANCA present in two thirds of UC patients and one third of CD
pANCA-positive CD patients have a clinical picture similar to UC
ASCA (IgG or IgA) present in half of patients with CD
High titers of ASCA in the absence of pANCA highly predictive of CD
Antibodies to OmpC and I2 are associated with more strictures and internal perforations
Anti-Cibr1 associated with CD, particularly penetrating disease, fibrosing disease, and SB involvement.
pANCA positive CD patients less likely to respond to inflixamab than ASCA positive or totally seronegative

Reference:
Wyllie R, Hyams JS, Kay M (2011). Crohn's Disease. In Wyllie R, Hyams JS, Kay M (Edx.), Pediatric Gastrointestinal and Liver Disease 4th ed (pp 462-489). Elsevier.
T

This publication from the Mayo clinic is concise and useful too.