A gene for autosomal dominant sacral agenesis maps to the holoprosencephaly region at 7q36.

Sacral agenesis is a rare disorder of uncertain incidence that has been reported in diverse populations. Although usually sporadic and most commonly associated with maternal diabetes, there is a hereditary form which may occur in isolation or with a presacral mass (anterior meningocele and/or presacral teratoma) and anorectal abnormalities, which constitute the Currarino triad (MIM 176450). The radiological hallmark of hereditary sacral agenesis is a hemi-sacrum (sickle-shaped sacrum) with intact first sacral vertebra. Bowel obstruction is the usual neonatal presentation, but, unlike other neural tube defects, adult presentation is not uncommon. The major pathology is confined to the pelvic cavity and may present as a space-occupying lesion or meningitis due to ascending infection. All recurrences in families have been compatible with autosomal dominant inheritance except for those associated with the isomerism gene at Xq24-q27.1 (ref. 3). Several associated cytogenetic defects have been reported, including 7q deletions. Previous studies failed to detect linkage to HLA markers, but we now present evidence for a location on 7q36. The same region also contains a gene for holoprosencephaly, an early malformation of the extreme rostral end of the neural tube.

Analysis of differential gene expression in colorectal cancer and stroma using fluorescence-activated cell sorting purification.

Tumour stroma gene expression in biopsy specimens may obscure the expression of tumour parenchyma, hampering the predictive power of microarrays. We aimed to assess the utility of fluorescence-activated cell sorting (FACS) for generating cell populations for gene expression analysis and to compare the gene expression of FACS-purified tumour parenchyma to that of whole tumour biopsies. Single cell suspensions were generated from colorectal tumour biopsies and tumour parenchyma was separated using FACS. Fluorescence-activated cell sorting allowed reliable estimation and purification of cell populations, generating parenchymal purity above 90%. RNA from FACS-purified and corresponding whole tumour biopsies was hybridised to Affymetrix oligonucleotide microarrays. Whole tumour and parenchymal samples demonstrated differential gene expression, with 289 genes significantly overexpressed in the whole tumour, many of which were consistent with stromal gene expression (e.g., COL6A3, COL1A2, POSTN, TIMP2). Genes characteristic of colorectal carcinoma were overexpressed in the FACS-purified cells (e.g., HOX2D and RHOB). We found FACS to be a robust method for generating samples for gene expression analysis, allowing simultaneous assessment of parenchymal and stromal compartments. Gross stromal contamination may affect the interpretation of cancer gene expression microarray experiments, with implications for hypotheses generation and the stability of expression signatures used for predicting clinical outcomes.

Influence of delays on perforation risk in adults with acute appendicitis.

PURPOSE: This study analyzed whether prehospital or in-hospital delay was the more significant influence on perforation rates for acute appendicitis and whether any clinical feature designated patients requiring higher surgical priority. METHODS: A retrospective analysis was conducted over one year at a tertiary referral hospital without a dedicated emergency surgical theater. Admission notes, theater logbook, and the Hospital Inpatient Enquiry system were reviewed to identify the characteristics and clinical course of patients aged greater than 16 years who were operated upon for histologically confirmed acute appendicitis. RESULTS: One hundred and fifteen patients were studied. The overall perforation rate was 17 percent. The mean duration of symptoms prior to hospital presentation was 38.1 hours with the mean in-hospital waiting time prior to operation being 23.4 hours. Although body temperature on presentation was significantly greater in patients found to have perforated appendicitis (P < 0.05), only patient heart rate at presentation and overall duration of symptoms, but not in-hospital waiting time, independently predicted perforation by stepwise linear regression modeling. CONCLUSION: In-hospital delay was not an independent predictor of perforation in adults with acute appendicitis although delays may contribute if patients are left to wait unduly. Tachycardia at presentation may be a quantifiable feature of those more likely to have perforation and who should be given higher surgical priority.

What a signature adds to the consent process.

BACKGROUND: "Consent is a process by which a patient is informed and becomes a participant in decisions regarding their medical management." It is argued, however, that providing a signature to a form adds little to the quality of this process. METHODS: Views regarding the consent ritual of nonselected patients undergoing endoscopy (cystoscopy or sigmoidoscopy) were prospectively studied together with those of the attending staff. Patient volunteers were randomly assigned to one of two groups and given verbal explanation before the procedure, either alone (group A) or with a request to sign a form in addition (group B). A standardized questionnaire regarding preferences then was applied. RESULTS: A total of 37 patients (22 men) were studied along with seven staff members. Most surveyed felt that signing a consent form helped to empower the patient (group A, 84%; group B, 83%; staff, 100%). Although the patients mainly believed that it functioned primarily to protect the hospital and doctor (group A, 89%; group B, 67%), only one patient (3% of total) felt that such a formality undermined the patient-doctor relationship. Most staff members favored signing a form (86%). The majority of patients either favored it (group A, 47%; group B, 78%) or expressed no strong preference (group A, 32%; group B, 11%). Interestingly, more women than men preferred signing (73 vs. 55%; p = 0.25), perhaps because more women believed that it functioned to preserve autonomy (93 vs. 77% of men). Age was no particular determinant of perspective. CONCLUSION: Although it may be viewed as primarily serving to protect the doctor and hospital, the formal process of signing written consent forms appeals to patients and staff.

Laparoscopic surgery protects against the oncologic adverse effects of open surgery by attenuating endothelial progenitor cell mobilization.

BACKGROUND: Endothelial progenitor cells (EPCs) derived from bone marrow incorporate into foci of neovascularization to propagate tumor growth. These cells are mobilized in response to surgical injury. Laparoscopic surgery may protect against the oncologic adverse effects of open surgical tumor excision, and this may be related to attenuated mobilization of EPCs. METHODS: For this study, 132 C57BL/6 mice were randomized to standardized laparotomy, laparoscopy, or control groups. The animals were killed at 6, 24, 48, and 72 h. Femur bone marrow and peripheral blood were harvested. Bone marrow EPCs were detected by flow cytometric dual staining for the stem cell antigen-1/cKit phenotype. Circulating EPCs were characterized in blood by vascular endothelial growth factor receptor 2 positive/macrophage activating complement-1 negative staining. Separately, 12 C57/bl6 mice bearing 3LL Lewis lung tumors 12 days after laparotomy or laparoscopy had their tumors excised and examined for endothelial cell expression (marker P1H12). RESULTS: Laparoscopy decreased circulating EPCs and bone-marrow EPC levels, as compared with laparotomy, at all time points. Bone marrow EPC levels were 2.95% +/- 0.32% after laparotomy, as compared with 0.65 +/- 0.21 in the laparoscopy group (p < 0.05). The circulating EPC level in the laparotomy group was 35.2% +/- 6% of cells, as compared with 3.1% +/- 0.2% in the laparoscopy group (p < 0.05). In homogenized tumors, the percentage of P1H12 expression among laparoscopy-treated animals was 22.1% +/- 4.2%, as compared with 39% +/- 8% in the laparotomy group (p < 0.05). CONCLUSION: Laparoscopy decreased EPC levels in both bone marrow and circulation, resulting in decreased tumor endothelial cell burden. This may represent a novel mechanism by which laparoscopy protects against the oncologic adverse effects of open surgical tumor excision.

The incidence of postoperative venous thrombosis among patients with ulcerative colitis.

BACKGROUND: Patients with Ulcerative Colitis (UC) have inherent prothrombotic tendencies. It is unknown whether this necessitates the use of additional perioperative anti-thrombotic prophylaxis when such patients require major surgery. METHODS: The postoperative courses of 79 patients with UC undergoing 180 major abdominal and pelvic operations were examined for clinical and radiological evidence of venous thrombosis. Eighteen patients with Familial Adenomatous Polyposis (FAP) having surgery (35 operations) of similar magnitude were also studied. Standard anti-thrombosis prophylaxis was utilised in all patients. RESULTS: Nine patients with UC were clinically suspected of developing postoperative venous thrombosis, but only three (3.8%) had their diagnosis confirmed radiologically (all had a pulmonary embolus). Therefore, the overall postoperative thrombosis rate, on an intention to treat basis, was 1.7% (3/180). No patient with FAP developed significant venous thrombosis. CONCLUSION: Standard perioperative antithrombotic modalities are sufficient to maintain any potential increase in postoperative thrombotic risk at an acceptable level in patients with UC undergoing operative intervention.

Circulating granulocyte macrophage colony-stimulating factor in plasma of patients with the systemic inflammatory response syndrome delays neutrophil apoptosis through inhibition of spontaneous reactive oxygen species generation.

In the normal resolution of an acute inflammatory response apoptosis of neutrophils is essential to maintain immune homeostasis and limit inappropriate host tissue damage by decreasing neutrophil tissue load, function, and release of phlogistic reactive oxygen species and proteases. The systemic inflammatory response syndrome (SIRS), a massive pro-inflammatory immune state, is associated with delayed neutrophil apoptosis, however, the systemic circulating factors and intracellular signal transduction pathways important in regulating neutrophil apoptosis in SIRS are poorly described. Neutrophils isolated from patients with SIRS on admission to the intensive care unit showed significantly (p<.01) delayed spontaneous neutrophil apoptosis compared with healthy neutrophils as quantified using annexin V-FITC and terminal deoxyuridine triphosphate (dUTD) nick end labeling (TUNEL) flow cytometry methods. Plasma from SIRS patients markedly (41.5+/-7.2%, p<.01) inhibited apoptosis of healthy neutrophils compared with controls (69.7+/-4.8%) indicating the presence of soluble circulating factors that can modify the expression of neutrophil apoptosis. Various pro-inflammatory (IL-6, granulocyte macrophage colony-simulating factor, interleukin (IL)-1beta, tumor necrosis factor-alpha) mediators, known to modulate neutrophil apoptosis in vitro, were elevated in the plasma of our cohort of SIRS patients compared with controls. However, the anti-apoptotic effect of SIRS plasma was specifically attenuated (75.5%, p<.01) by neutralizing SIRS plasma of granulocyte macrophage-colony-stimulating factor, but not IL-6, IL-1beta, tumor necrosis factor-alpha. Although the anti-inflammatory cytokine IL-10 was elevated in SIRS plasma (median level 7.2 pg/mL), further boosting SIRS plasma with recombinant human IL-10 (10 ng/mL, levels found in septic shock patients) significantly countered (63.8%, p<.01) the inhibitory effect of SIRS plasma on neutrophil apoptosis. Suppression of neutrophil apoptosis was concomitant with delayed spontaneous elevation of reactive oxygen species, quantified as peroxide production, and reversed by addition of neutralizing antibodies to GM-CSF, and recombinant human IL-10 to SIRS plasma. These results identify circulating GM-CSF as a significant inhibitor of neutrophil apoptosis in patients with SIRS, and that this effect can be countered by boosting SIRS plasma with IL-10. GM-CSF and IL-10 appear to modulate neutrophil apoptosis by altering reactive oxygen species generation in neutrophils.

Nasogastric intubation causes gastroesophageal reflux in patients undergoing elective laparotomy.

BACKGROUND: The routine use of nasogastric tubes in patients undergoing elective abdominal operation is associated with an increased incidence of postoperative fever, atelectasis, and pneumonia. Previous studies have shown that nasogastric tubes have no significant effect on the incidence of gastroesophageal reflux or on lower esophageal sphincter pressure in healthy volunteers. We hypothesized that nasogastric intubation in patients undergoing laparotomy reduces lower esophageal sphincter pressure and promotes gastroesophageal reflux in the perioperative period. METHODS: A prospective randomized case-control study was undertaken in which 15 consenting patients, admitted electively for bowel surgery, were randomized into 2 groups. Group 1 underwent nasogastric intubation after induction of anesthesia, and Group 2 did not. All patients had manometry and pH probes placed with the aid of endoscopic vision at the lower esophageal sphincter and distal esophagus, respectively. Nasogastric tubes, where present, were left on free drainage, and sphincter pressures and pH were recorded continuously during a 24-hour period. Data were analyzed with 1-way analysis of variance. RESULTS: The mean number of reflux episodes (defined as pH < 4) in the nasogastric tube group was 137 compared with a median of 8 episodes in the group managed without nasogastric tubes (P =.006). The median duration of the longest episode of reflux was 132 minutes in Group 1 and 1 minute in Group 2 (P =.001). A mean of 13.3 episodes of reflux lasted longer than 5 minutes in Group 1, with pH less than 4 for 37.4% of the 24 hours. This was in contrast to Group 2 where a mean of 0.13 episodes lasted longer than 5 minutes (P =.001) and pH less than 4 for 0.2% of total time (P =.001). The mean lower esophageal sphincter pressures were lower in Group 1. CONCLUSIONS. These findings demonstrate that patients undergoing elective laparotomy with routine nasogastric tube placement have significant gastroesophageal reflux in the perioperative period and a reduced ability to clear refluxed acid from the distal esophagus. Due to the associated risk of postoperative pulmonary complications, we recommend that nasogastric intubation be performed on a selective rather than routine basis.

Inhibition of neutrophil apoptosis after elective surgery.

BACKGROUND: Neutrophils play a crucial role in host defense against infections, but their inappropriate infiltration and activation within tissues can cause host tissue damage through release of reactive oxygen metabolites, metalloproteinases, and proinflammatory cytokines. The termination of a neutrophil-mediated inflammatory response is effected through programmed cell death or apoptosis. Delayed neutrophil apoptosis is associated with proinflammatory diseases, such as the systemic inflammatory response syndrome. Surgery induces a profound inflammatory response; therefore, neutrophil apoptosis of patients undergoing elective surgery was investigated. METHODS: Nonseptic patients undergoing elective orthopedic surgery while under epidural anesthesia had neutrophils and platelet-poor isolated from whole venous blood harvested at 4 time points: pre-epidural, 45 minutes postepidural but before surgical intervention, 1 hour postsurgical incision, and 24 hours postsurgery. Neutrophil apoptosis was quantified at 1, 12, and 24 hours in culture by immunofluorescence flow cytometry of annexin V and propidium iodide staining and confirmed by TUNEL (terminal deoxynucleotidyl transferase nick end labeling) assay for DNA strand breaks. Serum cytokines were quantified by specific enzyme-linked immunosorbent assay. RESULTS: Spontaneous neutrophil apoptosis after elective surgery was significantly (P < .001) inhibited with an effect evident within an hour of surgical incision and persisting at 24 hours postsurgery. The addition of patients' 24 hour postoperative plasma to healthy neutrophils markedly (P < .01) reduced neutrophil apoptosis, whereas plasma taken an hour after surgical incision was ineffective. Interleukin (IL)-6 was notably increased (1395 +/- 196 pg/mL, P < .01) 24 hours postsurgery and at this postoperative concentration inhibited (P < .01) apoptosis of normal neutrophils. Levels of other inflammatory mediators (IL-1 beta, tumor necrosis factor alpha, granulocyte-macrophage colony-stimulating factor, soluble Fas, soluble Fas ligand) were unaltered. The anti-inflammatory cytokine IL-10 was only slightly increased 24 hours postsurgery (8.32 +/- 2.99 pg/mL); however, the addition of recombinant human IL-10 (10 ng/mL) counteracted (P < .05) inhibition of neutrophil apoptosis induced by IL-6 and post-surgery plasma. CONCLUSIONS: These results identify marked inhibition of neutrophil apoptosis after elective surgery and suggest that the inhibition of neutrophil apoptosis in the postoperative period is, at least in part, a result of soluble circulating factors. The marked imbalance favoring proinflammatory over anti-inflammatory cytokine release in the immediate postoperative period mediates the overwhelmingly antiapoptotic net capacity of postsurgery plasma.

Desmoid tumours.

Desmoid tumours exhibit fibroblastic proliferation and arise from fascial or musculoaponeurotic structures. Despite their benign microscopic appearance, and their negligible metastatic potential, the propensity of desmoid tumours for local infiltration is potentially significant in terms of deformity, morbidity and mortality due to pressure effects and obstruction of vital structures and organs. The rarity of desmoid tumours, coupled with the variability in their clinical course, renders these lesions a vexing entity, and makes demonstration of the efficacy of any specific intervention difficult. Failure to recognize the potential for malignant behaviour in this tumour renders desmoids susceptible to inadequate treatment. This distinct pathological entity is reviewed with a specific focus on aetiology and treatment.

Motor nerve transplantation.

The motor nerve transplantation (MNT) technique is used to transfer an intact nerve into a denervated muscle by harvesting a neurovascular pedicle of muscle containing motor endplates from the motor endplate zone of a donor muscle and implanting it into a denervated muscle. Thirty-six adult New Zealand White rabbits underwent reinnervation of the left long peroneal (LP) muscle (fast twitch) with a motor nerve graft from the soleus muscle (slow twitch). The right LP muscle served as a control. Reinnervation was assessed using microstimulatory single-fiber electromyography (SFEMG), alterations in muscle fiber typing and grouping, and isometric response curves. Neurofilament antibody was used for axon staining. The neurofilament studies provided direct evidence of nerve growth from the motor nerve graft into the adjacent denervated muscle. Median motor endplate jitter was 13 microsec preoperatively, and 26 microsec at 2 months, 29.5 microsec at 4 months, and 14 microsec at 6 months postoperatively (p < 0.001). Isometric tetanic tension studies showed a progressive functional recovery in the reinnervated muscle over 6 months. There was no histological evidence of aberrant reinnervation from any source outside the nerve pedicle. Isometric twitch responses and adenosine triphosphatase studies confirmed the conversion of the reinnervated LP muscle to a slow-type muscle. Acetylcholinesterase studies confirmed the presence of functioning motor endplates beneath the insertion of the motor nerve graft. It is concluded that the MNT technique achieves motor reinnervation by growth of new nerve fibers across the pedicle graft into the recipient muscle.

Cyclooxygenase-2 expression in primary human colorectal cancers and bone marrow micrometastases.

BACKGROUND: Both the expressions of the inducible form of cyclooxygenase-2 and the presence of bone marrow micrometastases are poor prognostic markers in patients with colorectal carcinoma. AIMS: As cyclooxygenase-2 expression in these tumours is associated with increased metastatic potential in vitro, our objectives were to determine the relationship between cyclooxygenase-2 and haematogenous spread to bone marrow. PATIENTS AND METHODS: Thirty-two patients with resection of colorectal carcinoma were evaluated (median age: 69.5 years). Bone marrow was obtained from all patients from both iliac crests before manipulation of the primary tumour. The tumours were of varying stages at diagnosis (5 Dukes' A, 14 Dukes' B, 11 Dukes' C and 2 Dukes' D). Tumour sections were stained for cyclooxygenase-2 using the avidin-biotin immunohistochemical technique. Extent of staining was graded depending on the percentage of epithelial cells staining positive for cyclooxygenase-2. Micrometastases were detected by staining contaminant cytokeratin-18 positive cells in the bone marrow aspirates by either immunohistochemical (ARAAP) or immunological (flow cytometry) methods. Fisher's exact probability test was used to calculate statistical significance. RESULTS: Cyclooxygenase-2 expression in the primary tumour was detected in 72% of the patients. Twelve (38%) patients had bone marrow micrometastases detected by either immunohistochemistry or flow cytometry. Of the 12 patients who had bone marrow micrometastases, 8 tumours demonstrated increased expression of cyclooxygenase-2 protein (66.6%). In contrast, 9 out of the 20 (45%) patients in whom micrometastases were not detected expressed increased levels of cyclooxygenase-2 (P = 0.29). When dividing the patients into subgroups of localised (Dukes' A and B) versus disseminated (Dukes' C and D) disease, there was no further association between cyclooxygenase-2 expression and bone marrow micrometastases (P = 0.179 and 1.0). CONCLUSION: In this pilot study, there was no association between cyclooxygenase-2 expression and bone marrow micrometastases in patients with otherwise localised or disseminated disease.

Attenuation of pancreatitis-induced pulmonary injury by aerosolized hypertonic saline.

BACKGROUND: The immunomodulatory effects of hypertonic saline (HTS) provide potential strategies to attenuate inappropriate inflammatory reactions. This study tested the hypothesis that administration of intratracheal aerosolized HTS modulates the development of lung injury in pancreatitis. METHODS: Pancreatitis was induced in 24 male Sprague-Dawley rats by intraperitoneal injection of 20% L-arginine (500 mg/100 g body weight). At 24 and 48 h, intratracheal aerosolized HTS (7.5% NaCl, 0.5 mL) was administered to 8 rats, while a further 8 received 0.5 mL of aerosolized normal saline (NS). At 72 hours, pulmonary neutrophil infiltration (myeloperoxidase activity) and endothelial permeability (bronchoalveolar lavage and wet:dry weight ratios) were assessed. In addition, histological assessment of representative lung tissue was performed by a blinded assessor. In a separate experiment, polymorphonucleocytes (PMN) were isolated from human donors, and exposed to increments of HTS. Neutrophil transmigration across an endothelial cell layer, VEGF release, and apoptosis at 1, 6, 12, 18, and 24 h were assessed. RESULTS: Histopathological lung injury scores were significantly reduced in the HTS group (4.78 +/- 1.43 vs. 8.64 +/- 0.86); p < 0.001). Pulmonary neutrophil sequestration (1.40 +/- 0.2) and increased endothelial permeability (6.77 +/- 1.14) were evident in the animals resuscitated with normal saline when compared with HTS (0.70 +/- 0.1 and 3.57 +/- 1.32), respectively; p < 0.04). HTS significantly reduced PMN transmigration (by 97.1, p = 0.002, and induced PMN apoptosis (p < 0.03). HTS did not impact significantly upon neutrophil VEGF release (p > 0.05). CONCLUSIONS: Intratracheal aerosolized HTS attenuates the neutrophil-mediated pulmonary insult subsequent to pancreatitis. This may represent a novel therapeutic strategy.

Coexistent Hirschsprung's disease and esophageal achalasia in male siblings.

Achalasia of the esophagus developed in two male siblings soon after birth, and they were successfully treated by surgery. Persistent signs resulted in the later diagnosis of Hirschsprung's disease. One required subtotal colectomy and ileoanal anastomosis, and the other is managing well on conservative treatment. Genetic analysis of the genes encoding the RET protooncogene, endothelin-3, and the endothelin-3 receptor did not show any defect. Familial achalasia of the esophagus in combination with Hirschsprung's disease has never been reported.

Starting laparoscopic cholecystectomy--the pig as a training model.

Laparoscopic cholecystectomy is a reality and units must convert from open to endoscopic technique. To this end we have used the pig, whose biliary anatomy resembles the human, as a laboratory in vivo training model. Laparoscopic cholecystectomy has been performed in 35 animals. Techniques of pneumoperitoneum, vision, manipulation, clipping, ligation, cutting, diathermy and gall bladder removal were quickly mastered. All surviving animals underwent postmortem examination after 4 weeks. Following this laboratory programme, laparoscopic cholecystectomy in the human was introduced and has been completed successfully in 70 cases.

Laparoscopic cholecystectomy in adult cystic fibrosis.

Two female patients with Cystic Fibrosis, attending the Adult Regional Cystic Fibrosis centre at the Cork University Hospital, were investigated for upper abdominal pain and found to have gallstones at ultrasonography. Laparoscopic cholecystectomy was performed successfully and, without complication, in both patients.

Biliary surgery for benign disease a study of 500 consecutive operations.

An analysis of 500 consecutive operations on the biliary tract for benign disease, performed over a 5 year period is presented. Twenty-two per cent of patients had common duct exploration, and the incidence of choledochotomy increased with advancing age. The overall incidence of choledocholithiasis was 15.2% and calculi in the common duct were found more frequently in the elderly. The use of operative cholangiography increased over the 5 year study period, but was not associated with any change in the incidence of common bile duct exploration or choledocholithiasis. Four patients had re-exploration for retained calculus (0.8%). The overall operative mortality was 0.6%.

Open common bile duct exploration--end of an epoch?

With the advent of laparoscopic cholecystectomy and the impending replacement of open common bile duct exploration, we have reviewed our ten year experience of conventional common bile duct exploration. Open cholecystectomy was performed in 1681 patients and the common bile duct was explored in 325 (19%). Following initial duct exploration, rigid choledo identified residual choledocholithiasis in 58 and periampullary neoplasia in 2 patients. Unexpected retained stones were identified in 3 patients (0.9%). In a further 4 patients, stones which could not be dislodged from the hepatic ducts were confirmed on 10 day T-tube cholangiogram--transduodenal sphincteroplasty had been performed at the time of original surgery in all four. The mortality was 1.9% overall and 1% during the last 5 years. Endoscopic exploration must compare favourably with these data for safe transition to less invasive techniques.

Ingested foreign bodies in the paediatric patient.

BACKGROUND: Paediatric foreign body (FB) ingestion is a common problem and while most can be managed conservatively, a sub-population require intervention. AIMS: To establish clear guidelines for management of paediatric FB ingestion. METHODS: A retrospective chart review analysing all paediatric admissions with FB ingestion over a 10-year period from 1990 to 1999. RESULTS: Of 339 patients presenting to the accident and emergency department with FB ingestion, 59 required admission. Ingestion was accidental in 93.0% of patients. The reasons for admission were as follows: large FBs; dangerous FBs; and living far from the hospital. Nineteen patients (32.2%) were discharged without intervention. Thirty-seven (62.7%) required endoscopic retrieval. In two, the FB was not identified at endoscopy. Only three (5%) required surgery. CONCLUSION: Conservative management of FB ingestion in the paediatric population is possible in the majority of cases. However, a minority require intervention. While guidelines for intervention are ill-defined, definitive indications include symptomatic patients, or dangerous objects.

Predicting outcome after appendicectomy.

AIM: To validate an intraoperative appendicitis severity score (IASS) and examine outcome following emergency appendectomy. METHODS: A prospective study was undertaken, enrolling consecutive patients undergoing emergency appendicectomy. Data were obtained independently on preoperative Alvarado scores, IASS (0-3: 0 no inflammation, 1 engorged appendix/no peritonitis, 2 peritoneal reaction/exudate or 3 evidence of perforation/abscess) and postoperative outcome parameters. RESULTS: There were 149 patients identified with a mean age of 20.7 years. There was no association between Alvarado score and length of hospital stay, septic complication, patient sex or duration of symptoms (p>0.05). IASS was found to be an independent risk factor for septic complication, wound infection (p<0.05) and length of hospital stay (p<0.001). There was no correlation between preoperative duration of symptoms or time until surgery and intraoperative score. CONCLUSIONS: This simple scoring system can identify patients more likely to suffer morbidity following emergency appendicectomy. Specifically, this system identifies patients who have a high risk of sepsis and therefore could be of use when comparing healthcare performance.