Neonatal gastric perforation

Neonatal gastric perforation

ABSTRACTS diagnosed preoperatively or discovered intraoperatively. Case histories of each infant demonstrate that this diagnosis can be missed becaus...

122KB Sizes 1 Downloads 118 Views

ABSTRACTS

diagnosed preoperatively or discovered intraoperatively. Case histories of each infant demonstrate that this diagnosis can be missed because of (1) failure to obtain a barium "pouchgram" preoperatively, (2) error in interpretation of the contrast study as showing tracheobronchial aspiration at the laryngeal level, or (3) belief that the proximal fistula is a "'recurrent" fistula after primary repair. The authors advocate studies of the proximal pouch to facilitate correct diagnosis and to prevent increased morbidity and mortality associated with a missed proximal fistula.--Marleta Reynolds Gastroesophagaal Reflux Causing Strider. S.R. Orenstein, D.M.

Orenstein, and P.F. Whitington. Chest 84:301-302, (September), 1983. A newborn female presented with several episodes of vomiting and chocking and intermittent episodes of stridor. Barium swallow revealed GER, and pH probe monitoring revealed a temporal relationship between reflux and stridor. Medical treatment with bethanecol resulted in cessation of the episodic stridor. The stridor did not recur when the bethanecol was stopped after 5 months of treatment. The authors discuss other reports associating GER with stridor but comment that their case is the only reported one where the association was objectively demonstrated.--Randall 14/.Powell N e o n a t a l Gastric Perforation. P.G. Helardot, P. Elkoubi, C. Grapin, et al. Chir P6diatr 25:169-175, (May, June), 1984.

The authors reported 8 cases of neonatal gastric perforation over a 4-year period. Each case is analyzed. Seven were premature with birth weight below 2,500 gm. According to clinical history, gross findings, and histology, 2 etiologic theories are presented: vascular compromise with anoxia (3 cases), and mechanical distention (5 cases). In the latter cases perforation was linear. Prognosis remains grave with 3 postoperative deaths. A diagnosis before the 10th hour and before the appearance of the classic "saddle bag" sign can improve the prognosis.--J.M. Guys Hyperalimentation for Superior Mesenteric Artery (cast) Syndrome Following Correction of Spinal Deformity. S.W. Monns,

R.T. Morrissy, E.S. Golladay, et al. J Bone Joint Surg 66A:1175, (October), 1984. Three patients who developed superior mesenteric artery syndrome failed to respond to conventional nonoperative treatment. Institution of hyperalimentation effected a complete recovery in each case.--Anthony H. Alter Arteriomesenteric Occlusion of the Duodenum in Infants and Adolescents--A Rare Form of Inestinal Obstruction. R.G. Appell

and 1t4. Bolkenius. Z Kinderchir 39:310-314 (October), 1984. Arteriomesenteric occlusion is caused by compression of the inferior duodenum due to a flattened angle of the upper aortomesenteric junction. Predisposing factors are disorders of the spine, weight loss, and cachexia. The patients present with recurrent abdominal pain, spasms, feeling of pressure, singultus, and vomiting. Important radiologic criteria are a dilated proximal duodenum and delayed passage. Angiography may be useful in some cases. The authors report on 11 patients with arteriomesenteric occlusion. There were 8 boys and 3 girls. Except for acute obstruction the treatment was conservative in 9 patients. Feeding habits had to be changed, and frequent meals were recommended in order to gain weight. Occasionally, adjuvant psychotherapy was indicated. Surgical treatment consisted of gastroenterostomy in one case and mobilization of the duodenum in the other. Postoperative courses were uneventful in both instances.--Thomas A. Angerpointner

287

Neonatal Necrotizing Enterocolitis: An Update. D.L. Dudgeon, P.A. Schneider, P. Colombani, et al. South Med J 77:1389-1392, (November), 1984.

The authors reviewed 91 cases of neonatal necrotizing enterocolitis. A morbidity of 22% strictures (8%), and recurrence (8%) are reported. Early diagnosis of necrotizing bowel before perforation is difficult and contributes to the still high, but improved, overall mortality (36%). The use of surgery in the series (46%) is admittedly higher than that reported from other institutions, but it is thought that this might be biased in view of the large number of infants transported to this institution from other hospitals.George Holcomb, Jr. Surgical Therapy for Necrotizing Enterocolitis. R.R. Rieketts. Ann

Surg 190:653-657, (November), 1984. Fifty-one infants with necrotizing enterocolitis treated surgically by one surgeon under a uniform protocol are reported. Twenty-two (43%) of the patients were operated on for pneumoperitoneum and 24 (47%) for a positive paracentesis indicative of bowel infarction. The 5 other patients were operated on for abscess (2), clinical deterioration (2), and early bowel obstruction (1). The overall survival was 72.5%. Segmental intestinal resection and exteriorization of the bowel ends through the upper abdominal transerse incision was the usual procedure. The survival rate was not adversely affected by the patient's weight or age at the time of operation nor by the presence of bowel perforation. Fourteen patients died; 9 as a direct result of NEC. The 37 survivors suffered 32 major complications. The most common complication was developed of a patent ductus arteriosus, the majority of which required surgical ligation. The two major long-term complications were stricture formation, which occurred in 42% of evaluable patients, and short-gut syndrome, occurring in 11% of long-term survivors. Two thirds of the strictures occurred in the defunctionalized colon and were identified by contrast enema prior to planned enterostomy closure.--Richard J. Andrassy Total Parentaral Nutrition Inhibits Intastinal Adaptive Hyparplasia in Young Rats: Reversal by Feeding. W.D.A. Ford, R.U. Boe/houert,

W.W.K. King, et al. Surgery 96:527-533, (September), 1984. Seventy percent resection of the small bowel was accomplished in 7-week-old male Wistar rats weighing from 90 to 95 gin. Proximal jejunum and distal ileum were left, each equivalent to 15% of the original intestinal length. An end-to-end anastomosis was performed. Resected rats were divided into three groups: I (N = 50) received standard TPN via central line; I1 (N = 40) were given the same TPN solution orally; III (N = 40) had free access to standard rat chow. Nonoperated rats (N = 33) had access to the same standard chow. After I0 days of intravenous or oral TPN all rats were returned to 4 weeks of standard chow feeding. Extensive evaluation of the rats included somatic growth, intestinal elongation, mucosal growth, mucosal cell size, and mucosal sucrase activity. Results revealed that after intravenous or oral TPN administration villous height, crypt, depth, DNA and R N A content, RNA:DNA ratio, and sucrase activity were decreased. After returning to standard chow, the TPN rats achieved similar body weight and 15% greater intestinal length as compared to the rats that ate standard chow from the start, although their villous height, crypt, depth, and R N A : D N A ratio were decreased. The authors feel that the inhibition by TPN of intestinal adaptation after major intestinal resection in growing rats is reversible. Also, feeding a high calorie, high protein liquid diet before feeding a normal diet appears to promote adaptation after intestinal resection in growing rats.--Eugene S. Wiener