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עמוד בית
Mon, 09.12.24

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March 2021
Monica Goldberg-Murow MD, Zvi Steiner MD, Yaniv Lakovsky MD, Elena Dlugy MD, Arthur Baazov MD, Enrique Freud MD, and Inbal Samuk MD

Background: Pancreatic trauma is uncommon in pediatric patients and presents diagnostic and therapeutic challenges. While non-operative management (NOM) of minor pancreatic injuries is well accepted, the management of major pancreatic injuries remains controversial.

Objectives: To evaluate management strategies for major blunt pancreatic injury in children.

Methods: Data were retrospectively collected for all children treated for grade III or higher pancreatic injury due to blunt abdominal trauma from 1992 to 2015 at two medical centers. Data included demographics, mechanism of injury, laboratory and imaging studies, management strategy, clinical course, operative findings, and outcome.

Results: The cohort included seven boys and four girls aged 4–15 years old (median 9). Six patients had associated abdominal (mainly liver, n=3) injuries. The main mechanism of injury was bicycle (handlebar) trauma (n=6). Five patients had grade III injury and six had grade IV. The highest mean amylase level was recorded at 48 hours after injury (1418 U/L). Management strategies included conservative (n=5) and operative treatment (n=6): distal (n=3) and central (n=1) pancreatectomy, drainage only (n=2) based on the computed tomography findings and patient hemodynamic stability. Pseudocyst developed in all NOM patients (n=5) and two OM cases, and one patient developed a pancreatic fistula. There were no differences in average length of hospital stay.

Conclusions: NOM of high-grade blunt pancreatic injury in children may pose a higher risk of pseudocyst formation than OM, with a similar hospitalization time. However, pseudocyst is a relatively benign complication with a high rate of spontaneous resolution with no need for surgical intervention.

February 2006
M. Iuchtman, T. Steiner, T. Faierman, A. Breitgand and G. Bartal

Background: Intramural duodenal hematoma generates partial or complete obstruction that develops slowly and progressively with a consequent delay in diagnosis. Many diagnostic and therapeutic measures remain debatable and justify a review of current management policy.

Objectives: To highlight the diagnostic and therapeutic steps in pediatric IDH[1].

Methods: The records of 12 children with post-traumatic IDH who were treated in the Hillel Yaffe Medical Center between 1986 and 2000 were retrospectively reviewed. Three of them had clotting disorders and were excluded. The interval between their admission and diagnosis as well as the therapeutic decisions were evaluated and analyzed.

Results: Nine children were treated for IDH. The interval between admission and diagnosis ranged from 24 hours to 6 days. Five children had associated traumatic pancreatitis. Initially, all the children were conservatively treated. In seven the hematoma resolved after 9–20 days. Two children were operated upon because the obstruction failed to resolve. All nine children recovered without permanent complications.

Conclusions: Intramural duodenal hematoma has many clinical and therapeutic puzzling aspects. Bicycle handlebar, road accidents and sports trauma are the main etiologic factors in children, but child abuse should be kept in mind. Associated traumatic pancreatitis is common. Gastroduodenal endoscopy may be useful to clarify doubtful cases. Pediatric surgeons should increase awareness regarding IDH in order to reduce delay in diagnosis and the need for surgical decompression.






[1] IDH = intramural duodenal hematoma


March 2004
R. Shaoul, B. Enav, Z. Steiner, J. Mogilner and M. Jaffe

Background: Hypertrophic pyloric stenosis classically presents as projectile vomiting during the third to fourth week of life associated with good appetite. Additional classical presenting findings include palpation of the pyloric tumor, described as olive-shaped, a visible gastric peristaltic wave after feeding, and hypochloremic, hypokalemic metabolic alkalosis. It was recently claimed that this presentation has changed due to the easier access to gastrointestinal imaging.

Objective: To validate this contention and discuss possible reasons.

Methods: We conducted a retrospective chart review of all patients who underwent pyloromyotomy for HPS[1] between 1990 and 2000. Only patients with confirmed HPS at the time of surgery were included. We also performed a comprehensive review of older studies for comparison.

Results: Seventy patients underwent pyloromyotomy over the 10 year period. Overall, 81% of patients were male infants and the mean age at diagnosis was 40 days. The mean duration of symptoms was 8 days. A firstborn child was noted in 43% of the cases. The classical symptom of projectile vomiting was absent in one-third of the patients, a pyloric tumor was not palpated in one-half of the cases, bicarbonate was higher than 28 mEq/L in 20% and a pH of above 7.45 was present in 25% of patients. Hypochloremia was noted in about one-third. We found a good correlation between ultrasonographic width and length of the pylorus and the intraoperative findings. Pylorus length ≥ 24 mm correlated with significantly longer duration of symptoms. When compared with previous studies, the main findings were not significantly different; namely, mean age at diagnosis, percentage of male gender and duration to diagnosis. The decrease in the number of pyloric tumors palpated paralleled the increase in the use of upper gastrointestinal series and ultrasonography in particular.

Conclusions: The clinical presentation of HPS has not actually changed despite the easier accessibility of GI imaging studies. However, the one significant change is the low percentage of pyloric tumors palpated, probably due to declining clinical skills, accompanied by earlier utilization of imaging studies. The use of imaging and laboratory studies did not change the age at diagnosis but may have shortened the time for diagnosis and reduced the postoperative stay. Imaging and laboratory studies may be helpful for the subgroup with a non-classical clinical presentation.






[1] HPS = hypertrophic pyloric stenosis


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