Biomedical subjects

S A Engum

Publications and source records attributed to S A Engum.

25 records · Page 2Linked to original sources

PubMed1996

Improved survival in children with esophageal perforation.

OBJECTIVE: To analyze the cause, location, signs and symptoms, presence of underlying disease, time interval to diagnosis, treatment, and morbidity and mortality in 24 children (19 boys and 5 girls) with esophageal perforation who were treated from 1975 to 1995. DESIGN: Data were collected retrospectively from hospital and office records. SETTING: A tertiary care children's hospital. RESULTS: The average age at diagnosis was 58 months (range, 1 day to 19 years). Fourteen children had underlying esophageal disease (atresia, n = 7 and gastroesophageal reflux, n = 7). Iatrogenic perforations occurred in 17 children: 8 during dilatation, 5 during an antireflux procedure, 2 during endoscopy, and 2 after passage of a feeding tube. Trauma was the cause of perforation in 6 children. In 2 cases the cause was unknown. Perforation occurred in the thoracic esophagus in 12 cases, abdominal esophagus in 7, cervical esophagus in 5, and involved both the thoracic and abdominal esophagus in 1. Signs and symptoms included dysphagia (15 patients), dyspnea (14), fever (12), cyanosis (8), abdominal pain (6), chest pain (5), and subcutaneous emphysema (3). Management of esophageal perforation included nonoperative management (7 patients), drainage alone (1), primary closure (16), and resection and diversion (1). Two perforations occurred in 1 child. Complications occurred in 11 (44%) of the 25 cases and were more common after delayed diagnosis (73%). The average hospital stay was 20 days. There was 1 death (4%) attributed to esophageal perforation. CONCLUSIONS: Morbidity and mortality are directly related to delays in diagnosis and therapy. Most cases of esophageal perforation in children can be closed primarily and the esophagus salvaged despite delayed presentation. The mortality rate in children with esophageal perforation (4%) is significantly less than that for adults (25%-50%).

Adolescent↗

PubMed1996

Gastrointestinal perforation and peritonitis in infants and children: experience with 179 cases over ten years.

BACKGROUND: Premature infants continue to have a high mortality after gastrointestinal perforation. This report describes 179 patients with gastrointestinal perforation and peritonitis and compares etiologic factors, mortality, and causes of death in premature infants and older children in an attempt to predict outcome. METHODS: The 113 boys (63.1%) and 66 girls (36.9%) had an age range of newborn (n = 139, 77.6%) to 17 years. Site of perforation was gastric in 16, duodenal in 9, small bowel in 105, colon in 37, and undesignated in 12. Eighteen had multiple perforations. Etiologic factors in newborns (younger than 2 months) included necrotizing enterocolitis (NEC) (75, 41.9%), isolated ileal perforations (30, 21.5%), malrotation/volvulus (8), iatrogenic causes (5), and others (6). Gestational age was 29.6 +/- 4.3 weeks for NEC versus 31.4 +/- 5.4 weeks for non-NEC. Birth weight for patients with NEC was 1.45 +/- 0.8 gm and 1.81 +/- 1.0 gm for non-NEC babies. Etiologic factors in 33 older children (older than 2 months to 17 years) were trauma (10), Meckel's diverticulum (4), intussusception (2), pseudomembranous colitis (2), adhesions (2), stomal leak (2), others (4), and nondesignated (7). Gastric perforations (n = 16) were iatrogenic in 7, idiopathic in 5, and caused by an ulcer in 4. RESULTS: Mortality for NEC was 36 of 75 (48%), 15 of 55 (27.2%) for non-NEC infants (p < 0.05 versus NEC), 15.1% (5 of 33) for older children (p < 0.05 versus NEC), and 4 of 16 (25%) for gastric perforation. Infant deaths were related to overwhelming sepsis, immaturity of systems, and multiorgan failure. Deaths for older children were a result of sepsis, multiorgan failure, and immunodeficiency. CONCLUSIONS: Gastrointestinal perforation is more common in premature infants with the highest mortality (48%) noted in NEC. Despite surgical intervention and advances in neonatal intensive care unit care, premature low birth weight infants (especially NEC) continue to have a high mortality.

Adolescent↗

PubMed1996

Increased risk of necrotizing enterocolitis in premature infants with patent ductus arteriosus treated with indomethacin.

OBJECTIVE: The authors evaluated the risk of necrotizing enterocolitis (NEC) in very low birth weight infants receiving indomethacin (INDO) to close patent ductus arteriosus (PDA). BACKGROUND DATA: Controversy exists regarding the best method of managing very low birth weight infants with PDA and whether to employ medical management using INDO or surgical ligation of the ductus. METHODS: Two hundred fifty-two premature infants with symptomatic PDA were given intravenously INDO 0.2 mg/kg every 12 hours x 3 in an attempt to close the ductus. Patients were evaluated for sex, birth weight, gestational age, ductus closure, occurrence of NEC, bowel perforation, and mortality. RESULTS: There were 135 boys and 117 girls. The PDA closed or became asymptomatic in 224 cases (89%), whereas 28 (11%) required surgical ligation. Ninety infants (35%) developed evidence of NEC after INDO therapy. Fifty-six were managed medically; surgical intervention was required in 34 of 90 cases (37.8%) or 13% of the entire PDA/INDO study group. Bowel perforation was noted in 27 cases (30%). Factors associated with the onset of NEC included gestational age < 28 weeks, birth weight < 1 kg, and prolonged ventilator support. The overall mortality rate was 25.5%, but was higher in infants with NEC versus those without. The highest mortality was noted in perforated NEC cases. The PDA/INDO patients were compared with a control group of 764 infants with similar sex distribution, birth weights, and gestational ages without PDA who did not receive INDO. Necrotizing enterocolitis occurred in 105 of 764 control patients (13.7%), including 13 (12.3%) with perforation. The overall mortality rate of controls was 25%, which was similar to the overall 25.5% mortality rate in the PDA/INDO study group. CONCLUSION: These data indicate that there is increased risk of NEC and bowel perforation in premature infants with PDA receiving INDO. Mortality was higher in the PDA/INDO group with NEC than those PDA/INDO infants without NEC.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed1995

Analysis of morbidity and mortality in 227 cases of esophageal atresia and/or tracheoesophageal fistula over two decades.

OBJECTIVE: This report analyzes the morbidity and mortality in 227 infants (127 boys and 100 girls) with variants of esophageal atresia and/or tracheoesophageal fistula who were treated from 1971 to 1993. DESIGN: Data were collected retrospectively from hospital and office records. Mean follow-up was 76 months, ranging from 1 month to 22 years. SETTING: Patients were treated at a tertiary care children's hospital. RESULTS: The mean birth weight was 2557 g (range, 1100 to 4460 g), and the mean gestational age was 38 weeks (range, 28 to 42 weeks). Classification included 29 cases of type A esophageal atresia (13%); two cases of type B (1%), 178 cases of type C (78%), five cases of type D (2%), and 13 cases of type E (6%). Associated anomalies occurred in 146 infants (64%), including cardiac defects in 86 (38%), skeletal defects in 44 (19%), neurological defects in 34 (15%), renal defects in 35 (15%), anorectal defects in 18 (8%), and other abnormalities in 30 (13%). A single-layer anastomosis was performed in 81%, and a two-layer repair, in 17%. Esophagomyotomy was necessary in 9% of the patients. Anastomotic complications included leakage (16%), symptomatic stricture (35%), and recurrent tracheoesophageal fistula (3%). Gastroesophageal reflux was present in 127 cases (58%), with 56 (44%) requiring an antireflux procedure. Tracheomalacia occurred in 32 cases (15%), and 13 required operative treatment. Postoperative esophageal dysmotility was documented in 56 children (30%). The overall survival rate was 95%. The cause of death in 12 patients included severe cardiac anomalies (n = 3), fatal sleep apnea (n = 1), renal failure (n = 1), trisomy 18 (n = 2), accidental decannulation of tracheostomy (n = 1), pulmonary failure (n = 1), and unknown causes (n = 3). CONCLUSIONS: Early diagnosis, improved surgical technique, neonatal anesthesia, sophisticated ventilatory support, advanced intensive care management, early treatment of associated anomalies, responsiveness of anastomotic strictures to dilatation, and aggressive treatment of gastroesophageal reflux have influenced survival positively. Improved survival rates were noted irrespective of the traditional Waterston criteria, which now seem outdated. With few exceptions, most infants with esophageal atresia and/or tracheoesophageal fistula should survive in the current era.

Abnormalities, Multiple↗

PubMed1994

Does preoperative chemotherapy for hepatic tumors have an adverse effect on hepatic proliferation after delayed liver resection?

The authors evaluate the effect of preoperative cisplatin and Adriamycin on hepatic proliferation after delayed partial hepatectomy. Sprague-Dawley rats were placed into five experimental groups. Group I received 0.9% saline intraperitoneally (IP). Group II received 2 mg/kg of cisplatin IP. Group III received 4 mg/kg of cisplatin IP. Group IV received 6 mg/kg of Adriamycin intravenously. Group V received 0.9% saline IP. Groups I through IV underwent 70% partial hepatectomy 2 and 10 days after chemotherapy. They were killed 24 hours later, and analyses were performed. Group V animals underwent celiotomy and were killed. Hepatic proliferation was evaluated by tritiated thymidine (3H-TdR) incorporation into DNA, quantitative image analysis (QIA), and proliferating cell nuclear antigen immunostained hepatic nuclei (PCNA). 3H-TdR incorporation values in animals treated 2 days before partial hepatectomy in treatment groups II through IV were similar to those of the hepatectomized controls. Although among the animals treated 10 days before partial hepatectomy there was inhibition of 3H-TdR DNA incorporation in the Adriamycin group, no significant differences were noted between all treatment groups. QIA of the S-phase nuclei (an indicator of proliferation) indicated that the animals treated with 2 mg/kg of cisplatin had significantly more nuclei than those treated with Adriamycin. PCNA labeling showed a decrease in proliferating nuclei in all treatment groups compared with the control hepatectomized animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Early use of cisplatin is safe after partial hepatectomy.

Although cisplatin is widely used in the treatment of liver tumors, little information is available concerning its effect on liver regeneration. This report evaluates the effect of cisplatin on liver regeneration after hepatectomy (HPx). One hundred sixty male Sprague-Dawley rats were placed into five experimental groups following 70% hepatectomy. Group I (untreated controls, n = 32) received 0.9% saline intraperitoneally (IP); group II (n = 31), cisplatin 4 mg/kg IP; group III (n = 36), cisplatin 10 mg/kg IP; group IV (n = 34), cisplatin 20 mg/kg IP; and group V (n = 27), doxorubicin 6 mg/kg intravenously (IV). Five additional sham groups underwent celiotomy without hepatectomy (n = 106) followed by the above treatment protocols. Liver regeneration was evaluated by liver weight, DNA incorporation measured by tritiated thymidine (3H-TdR), and quantitative image analysis (QIA) of hepatic nuclei at 18, 24, 36, 48, and 72 hours, and 5 days postoperatively. 3H-TdR incorporation peaked at 36 hours and was similar in hepatectomized controls group I (404 +/- 110 counts per minute [CPM]/mg liver weight) and cisplatin-treated rats (groups II to IV) (P > .05, ANOVA). All sham groups were similar to controls. QIA of feulgen-stained touch preps identified polyploid, stem line, and proliferating nuclei in both controls and treated groups. At 36 hours, QIA showed differences in mitotic status of sham, control, and adriamycin-treated HPx rats, consistent with 3H-TdR incorporation. In contrast, although cisplatin-treated rats receiving 4 mg/kg showed proliferating nuclei, QIA demonstrated decreasing hepatocyte proliferation with higher doses of cisplatin (10 mg/kg, and 20 mg/kg).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Familial Hirschsprung's disease: 20 cases in 12 kindreds.

This report describes 20 infants and children with a family history of Hirschsprung's disease in 12 kindreds. A total of 260 patients were treated for Hirschsprung's disease (1972 to 1991), yielding a familial incidence of 8%. There were no families with consanguineous marriage. Sixteen patients were male and four were female. The mean age at diagnosis was 18 days. Clinical presentation included delayed passage of meconium in 15, abdominal distention in 11, vomiting in 9, feeding abnormalities in 3, and complete bowel obstruction in 1. Associated congenital anomalies occurred in 25% of the patients. The extent of aganglionosis was rectal in 4, sigmoid in 4, left colon in 2, transverse or right colon in 2, and total colonic in 8. Enterocolitis occurred in 7 patients (35%); 2 at diagnosis, 2 after an ostomy, and 3 after a pull-through procedure. There were no deaths associated with enterocolitis. All patients had a proximal diverting colostomy or ileostomy, and 19 of 20 underwent a definitive pull-through procedure. Three patients were lost to follow-up and one patient died of complications of multiple congenital anomalies unassociated with Hirschsprung's disease. Of the remaining 16 patients, all of whom have undergone a pull-through procedure, 11 are fully continent, 2 have nighttime soiling, 2 are too young to evaluate bowel function, and 1 still has an ostomy.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Distribution↗