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Fifty-two premature, low birth weight infants presented mainly in the first week of life with sudden manifestations of intestinal ileus and an x-ray picture of pneumatosis intestinalis. Twenty-two of 32 patients treated with gastric decompression, antibiotics, intensive supportive therapy and intravenous hyperalimentation survived. Twenty other patients had progression of their disease and required operation. Twelve of these patients survived. Review of this material indicated that some medically treated patients might have survived if they had been operated upon. Indications for operation included free perforation and clinical signs of deterioration. Abdominal physical findings and x-rays were not reliable except as signs of far advanced pathology. Confirmation of ascites by paracentesis and gram stain of fluid was helpful when present. If patients were adequately treated and then developed sudden hyponatremia or progressive acidosis, they invariably had gangrenous bowel and required operation. The most striking finding was that a sudden, profound drop in the platelet count to levels below 100,000 reliably predicted the presence of gangrenous bowel and the need for operation. Other clotting studies indicated that disseminated intravascular coagulation is an important accompaniment of NNE with the complication of bowel gangrene prior to perforation. Gastrostomy and resection of involved bowel with staged anastomosis proved to be the most successful form of surgical management. Overall suvival was 66 per cent.

BECAUSE of its probable increased incidence there is need to be aware of the fatal-if untreated-condition called necrotizing enterocolitis. With this in mind the clinical and pathological features of ten infants with the condition are presented. The unreliability of radiological signs in diagnosis is stressed; the primary role of shock is supported and the necessity for prompt intervention is emphasised. It is concluded that the condition is not confined to neonates and it is suggested that it is identical to ischaemic colitis in adults. Treatment is discussed.

Significant bowel necrosis does not occur in the benign form of necrotizing enterocolitis.Seven cases are presented which can be placed in this category.The radiographic findings in this group include bowel dilatation, pneumatosis intestinalis, and portal venous gas.A benign prognosis may be suggested when pneumatosis intestinalis is present without bowel dilatation.

The practicality, effectiveness, and safety of feeding very low birthweight infants (less than 1,300 gm) by continuous nasoduodenal infusion was assessed by comparison with continuous nasogastric feeding. The nasoduodenal group appeared to have a clear advantage over the nasogastric group for the overall period in terms of caloric intake (131 cal/kg/day vs. 106 cal/kg/day), average weight gain (16 gm/day vs. 10 gm/day), and safety. This advantage was even more striking in the first two weeks of life. A caloric intake of 120 cal/kg/day could be reached within 48 to 72 hours after tube placement in the nasoduodenal group but only after a week in the nasogastric group. Nasoduodenal feeding resulted in faster weight gain than comparable published data on conventional feeding, peripheral intravenous alimentation, and parenteral alimentation. There were no cases of aspiration associated with tubes placed in the duodenum whereas two cases of aspiration pneumonia were associated with tubes placed in the stomach. With the tip of the catheter in the duodenum, none of the complications reported with nasojejunal tubes (intussusception, perforation, or necrotizing enterocolitis) were seen, either in the initial pilot study reported here or in 50 additional infants.

Sixty-four cases of necrotizing enterocolitis are reviewed. The diagnosis was based on tissue examination in 57 and on the clinical syndrome, including pneumatosis, in 7. Three factors are important in the development of the disease: injury to the intestinal mucosa, bacteria, and feedings. The indications for surgical intervention are pneumoperitoneum, signs of peritonitis, and intestinal obstruction. The importance of stress in the etiology of the disease is confirmed by the high incidence of perinatal complications, particularly hypoxia. The mortality was high, but results are improving with the institution of early aggressive treatment.

DOI: 10.3329/jcmcta.v21i1.7667 Journal of Chittagong Medical College Teachers' Association 2010: 21(1):30-33

Because of its abilities to reduce thrombus formation, low molecular-weight dextran was administered to eight newborns with necrotizing enterocolitis and two infants with midgut volvulus. The enterocolitis group which received dextran when compared with an otherwise similarly treated group which did not receive dextran, revealed the following differences: half of the dextran-treated group did not require operation while all of the patients not receiving dextran did. Although repeated perforation and late intestinal strictures occurred commonly in the group which did not receive dextran, no dextran-treated infant demonstrated either of these complications. The patients with midgut volvulus receiving dextran demonstrated remarkable recovery of bowel at reexploration, despite the widespread ischemic appearance of bowel at initial operation. No complications from the use of dextran were encountered.

Summary Early awareness of the diagnosis of necrotizing enterocolitis in infants led to immediate nasogastric drainage, placement of a central venous catheter, and initiation of antibiotics. Blood pressure and urine output were vigorously supported by colloid administration. The same physician followed the clinical course of these infants at hourly intervals, and abdominal roentgenograms were obtained every four hours to rule out perforation. These measures led to steadily improving nonoperative survival. The indications for surgery included: (1) perforation, (2) sudden clinical deterioration, and (3) failure to improve within forty-eight hours. Clinical observations are made in forty-five infants with necrotizing enterocolitis, the last thirty of whom came under the specific regimen just outlined. Of these, twenty-four (80 per cent) survived. Etiologic factors are considered.

Summary A case is reported of neonatal Hirschsprung's disease complicated by necrotizing enterocolitis and gas in the portal venous system. Several factors which could lead to the accumulation of portal venous gas in such a patient are discussed.

The recognized late complications of necrotizing enterocolitis are intestinal stenosis and internal fistulae. Malabsorption is a possible complication but has not yet been reported. The case of necrotizing enterocolitis reported in this paper survived severe septicemia and later developed extensive proximal and distal colonic strictures and an intervening enterocyst. Intestinal stenosis in the newborn or the infant may follow such causes as necrotizing enterocolitis or exchange transfusion, but it is suggested that, whatever the immediate precipitating factor, a common pathogenesis exists, namely, intestinal ischemia resulting in necrosis of the bowel wall, followed by healing with fibrosis and consequent stenosis.

Prompt medical and particularly surgical therapy has caused a marked improvement in the survival of infants with necrotizing enterocolitis. In this series, the second largest reported to date, the survival is 67 per cent.

Necrotizing enterocolitis of infancy is a fulminating disease, not entirely restricted to the neonatal period, but with a predilection for the premature infant.Our review of the world literature and our own experience with 20 proven cases indicate that the roentgenographic findings have generally permitted accurate diagnosis. One or more of the following major roentgenographic findings were present in virtually all of the reported cases: pneumoperitoneum; pneumatosis intestinalis; portal venous gas; and small bowel distention. The colon was not usually distended unless it was extensively involved with roentgenographically apparent pneumatosis.The presence of pneumatosis on preliminary plain roentgenograms is an absolute contraindication to contrast enema examinations which are generally not needed to establish the diagnosis.The differential diagnosis from other pathologic processes is discussed.

Primary pneumatosis intestinalis occurs most frequently in the colon of adults and is usually cystic. This condition is relatively benign, and frequently resolves spontaneously. Pneumatosis intestinalis of the small intestine of infants is nearly always secondary to a serious underlying disease of the gastrointestinal tract. In the premature infant, it is usually associated with an underlying necrotizing enterocolitis. Small intestinal involvement, in the adult, is associated with a variety of conditions, many of them serious. The distribution of the gas is usually linear. Air in the portal system is a grave prognostic sign and generally indicates intestinal necrosis. An example of survival of a patient with gas in the portal system is reported.

The authors’ experience with 14 cases of the meconium plug syndrome and 13 cases of Hirschsprung’s disease is presented and the roentgenographic findings reviewed. Criteria for differentiation of meconium plug syndrome from Hirschsprung’s disease as well as from other pathologic processes, such as necrotizing enterocolitis of infancy and meconium ileus, are formulated and illustrated.The following roentgen findings were almost always present in the meconium plug syndrome: small and large bowel distention, mottled or bulky intraluminal colonic masses reflecting excessive meconium retention and producing ribbon-like or sausage shaped defects on contrast enema roentgenograms. Air-fluid levels in the bowel were uncommon. Long contracted colonic segments simulating the transition segments of Hirschsprung’s disease, and due to collapse of the colon distal to the plug, may be seen involving the descending colon down to the sigmoid and/or rectum.In distinction, excessive meconium was infrequently seen on plain fi...

Introduction: Birth asphyxia is defined by the World Health Organization "the failure to initiate and sustain breathing at birth." The WHO has estimated that 4 million babies die during the neonatal period every year and 99% of these deaths occur in low-income and middle income countries. Three major causes account for over three quarters of these deaths, serious infection (28%) complication of preterm birth (26%) and birth asphyxia (23%). This estimation implies that birth asphyxia is the cause of around one million neonatal deaths each year. One of the present challenges is the lack of a gold standard for accurately defining birth asphyxia. Because of same reason the incidence of birth asphyxia is difficult to quantify. Objective: The aim of this study was to assess the prevalence of birth asphyxia, identify the common obstetric and neonatal risk factors, and study the cause of death. Methodology: All babies born in Dhulikhel Hospital (DH) from Jan 2007 to Oct 2009 with a diagnosis of birth asphyxia (5 min Apgar < 7 and those with no spontaneous respirations after birth) were included in the study (n=102). Clinical information was collected retrospectively from maternal records (maternal age, gravida, type of delivery, presence of meconium, induced or spontaneous labour, and pregnancy complications). The NICU records provided additional information about new born infant (birth asphyxia, stages of birth asphyxia, birth weight, sex and subsequent mortality). Results: Among the 3784 live births there were 102 babies with birth asphyxia prevalence of 26.9/1000 live births. Babies with Hypoxic ischemic encephalopathy (HIE) Stage 1 had a very good outcome but HIE III was associated with a poor outcome. Males, primipara and pregnancies with complications were associated with a higher rate of birth asphyxia. Septicaemia, necrotizing enterocolitis, preterm delivery, convulsion and, pneumothorax were associated with higher mortality and morbidity. Conclusion: Birth asphyxia was one of the commonest causes of admission and mortality in NICU. Babies with HIE Stage III had a very poor prognosis. Birth asphyxia combined with other morbidities was associated with a higher mortality. Sepsis is the commonest morbidity in cases of birth asphyxia. Maternal gravida, pregnancy complication with PROM, meconium, APH, emergency caesarean section, preterm and male sex were the risk factors for birth asphyxia. Key words: Birth asphyxia; HIE; Neonatal sepsis DOI: 10.3126/jnps.v30i3.3916 J Nep Paedtr Soc 2010;30(3):141-146

A prospective study of the effect and mortality of exchange transfusion was carried out in the Kandang Kerbau Hospital, Singapore. Altogether 140 exchange transfusions were performed on 122 infants. The exchanges were done for hyperbilirubinaemia due to "idiopathic" jaundice, ABO haemolytic disease, and glucose-6-phosphate dehydrogenase deficiency. Eight infants deteriorated during the exchange, in three of whom the procedure had to be terminated prematurely. Two deaths occurred two days after the exchange--the procedure being partly responsible in one case; necrotizing enterocolitis was present in addition to the kernicterus. Exchange transfusion is not without hazards, and should be performed carefully with close monitoring of the clinical status of the infant during and immediately after the procedure.

Background: Perinatal asphyxia is the most important preventable cause of cerebral injury in the neonatal period leading to very high neonatal mortality and morbidity in developing countries. Little can be done for a baby affected by severe perinatal asphyxia. So, prevention is unquestionably desired. Objective: To identify the maternal and fetal risk factors for the development of birth asphyxiated babies and to see the short term outcome of the affected babies. Methods: An analytical type of or observational study was done in the Special Care Baby Unit (SCBU) of Dhaka Medical College Hospital from October 2003 to March 2004. Identification of the risk factors was done by retrospective comparison of the cases and controls. Outcome was analyzed by cross sectional comparative study. One hundred consecutive cases of birth asphyxia, admitted in SCBU, were enrolled in the study. Another 30 neonates admitted during this period for other reasons (i.e., jaundice, septicemia, low birth weight) were taken as control. Necessary information were collected by detailed history taking, clinical examination and close follow up of the hospital course, using pre-designed questionnaire and recording form. Results: Male: female ratio 3:2 both in the cases and controls. Mean age on admission was 13.8 hours and 2.6 days for case and control respectively. Identified important maternal risk factors were primiparity (57% in cases vs. 33.3% in control), hypertension (16.6% vs. 3.3%), pre-eclamptic toxemia of pregnancy (24% vs. 13.3%), prolonged rupture of membrane (33.3% vs. 6.7%), prolonged labour (34% vs. 3.3%) and use of oxytocin during labour (16% vs. none). All these were statistically significant (p

Three cases of stenosis of the colon following neonatal enterocolitis and one stricture of the ileum presumed to be due to neonatal enterocolitis are presented. If evidence of intestinal obstruction occurs in a patient who has recovered from necrotizing enterocolitis, intestinal stenosis may have developed.

A neonate with stenosis of the descending and sigmoid colon was successfully treated by a transverse colostomy on the second day of life, and a resection of the stenotic bowel with anastomosis 15 months later. It is postulated that this defect, as well as atresias and stenoses in other areas of the jejunum, ileum, and colon may, in some cases at least, arise as a result of an arterial embolus originating in an area of thrombophlebitis in the placenta and passing by way of the umbilical vein, the ductus venosus, the ductus arteriosus, and the aorta to a mesenteric artery supplying a segment of the small or large bowel. Depending on the degree of local tissue ischemia, stenosis or atresia results. To support this theory as to the etiology of this defect, indirect clinical evidence is drawn from the newborn where stenoses or bowel necrosis with perforation may occur, particularly in the neonate receiving an exchange transfusion. A case of a newborn who developed a stenosis of the colon after two exchange transfusions is presented in detail, and other examples of stenosis or bowel necrosis and perforation reported are discussed based on the hypothesis that in these cases also, the primary course is again an arterial embolus arising in the neonate from a propagating thrombus in the umbilical vein which breaks off, or is broken off, and passes through the ductus venosus, the right heart, the ductus arteriosus and the aorta to occlude a mesenteric artery. If bowel ischemia without full thickness necrosis results, stenosis will ultimately develop; if full thickness necrosis results, perforation will occur. Such arterial emboli may be the primary problem behind at least some of the cases of necrotizing enterocolitis in the newborn.

During a 24-mo period, 23 infants were treated for neonatal necrotizing enterocolitis. Diagnosis was established either at operation or by the triad of abdominal distention, gastrointestinal bleeding, and radiographic findings of pneumatosis intestinals. Fourteen of the 23 infants were admitted to the hospital before intestinal perforation had developed. They were treated with a therapeutic regimen which included nasogastric suction, intravenous fluids and blood, and both parenteral and topical antibiotics by gavage. None of the 14 babies developed free intestinal perforation. Our experience suggests that this method of treatment may improve the survival rate of infants with necrotizing enterocolitis, and merits further clinical trial.

Summary Acute appendicitis in 32 infants was characterized by delay in diagnosis, perforation (94%), and a significant morbidity (50%) and mortality rate (9.3%). Vomiting and fever were the most frequent symptoms and tenderness and abdominal distension were the common physical findings. Abdominal radiographs were helpful, particularly when a calcified appendicolith was observed (28%). In neonates with appendicitis, an underlying problem such as Hirschsprung's disease, necrotizing enterocolitis, or the meconium plug syndrome should be suspected. It is suggested that an “admit and observe” policy with frequent reevaluation of suspicious cases and a more meaningful physical examination with the aid of sedation may improve diagnostic effectiveness. A program of vigorous preoperative preparation, expeditious surgery, and careful postoperative care is vital to improved survival in infants with perforated appendicitis.

Between January 25 and March 30, 1971, septicemia with kanamycin-resistant Klebsiella pneumoniae type 33 occurred in 10 of 94 infants in an intensive care unit. All 10 infants also had evidence of localized infection (pneumonia in 5, infected aortic thrombi in 2, meningitis in 1, necrotizing enterocolitis in 1, and abdominal abscess in 1). There was widespread environmental contamination in the unit, but no common source of Klebsiella type 33 other than infected infants could be identified. Spread appeared to occur primarily via the hands of personnel. Control measures resulted in a decrease in cross contamination and dramatic slowing of the outbreak. The strains of Klebsiella type 33 isolated during this epidemic were more virulent than three other Klebsiella serotypes tested in virulence studies in mice.

Summario in interlingua Enterocolitis necrotisante es un morbo de neonatos que es altemente mortal. Illo se vide principalmente in prematuros e es characterisate per un tableau clinic de retention gastric, vomito biliari, distention abdominal, e feces a striation sanguinee o—a vices—diarrheic. Iste tableau resimila a vices, super toto initialmente, illo de obstruction intestinal. Perforation es un occurrentia commun. A base de un studio de 25 casos, le conclusion es formulate que perforation intestinal-manifeste in pneumoperitoneo roentgenographic—es le sol clar indication pro un intervention chirurgic.

Summary Five consecutive cases of neonatal necrotizing enterocolitis treated nonoperatively had colonic strictures. Four of five patients survived.

• Hyperviscosity, or decreased fluidity secondary to increased numbers of red blood cells, leads to tissue hypoperfusion. We report the case of an infant with hyperviscosity who died from necrotizing enterocolitis (NEC), and describe the presumptive association between NEC and hyperviscosity. (Am J Dis Child129:1192-1194, 1975)

Extensive colonization with a multiple antibiotic-resistant strain of type 26 Klebsiella pneumoniae in a neonatal ICU was followed in 12 patients by significant infections including sepsis, meningitis, peritonitis, and pyelonephritis. In addition, six of the 12 patients developed necrotizing enterocolitis. An average of 50% of the infants in the ICU harbored the organism during the period of the epidemic, and 25% of newly admitted infants acquired the strain. K. pneumoniae continues to be a significant pathogen in debilitated neonates where nosocomial colonization of the respiratory and/or enteric tract may be associated with an increased risk of systemic infection.

Livaditis, A., Wallgren, G. and Faxelius, G. (Departments of Pediatrics and Pediatric Surgery, Karolinska Sjukhuset, Stockholm, Sweden). Necrotizing enterocolitis after catheterization of the umbilical vessels. Acta Paediat Scand, 63:277, 1974. –Necrotizing enterocolitis is reported in 7 infants who had undergone umbilical vessel catheterization. Five of them were treated surgically with two fatalities, while the remaining two recovered following conservative management. Necrotizing enterocolitis is a potential complication of umbilical vessel catheterization in particularly predisposed infants. The disorder may occur regardless of the type of vessel used or the indications for the procedure. Unless the ductus venoms is easily passed, umbilical venous catheterization for cardiovascular studies should preferably be avoided.

As a result of an increasing awareness, the incidence of necrotizing enterocolitis and survival of infants affected have increased. Chances of survival are decreased by intestinal perforation. Our review suggests that persistent or increasing abdominal distention and tenderness are premonitory signs of perforation. Only the segments of intestine and colon that contain numerous and advanced necrotic lesions require resection, because the more proximal and distal ischemic lesions are superficial and reversible.

Because of concern about tissue uptake of pasticizers used in medical equipment, di-(2-ethylhexyl) phthalate was measured by gas chromatography-mass spectrometry in neonatal heart and gastro-intestinal tissue. Seventeen infants who had umbilical catheterization alone or with administration of blood products, and 13 stillborn or older controls were studied. The mean levels of the plasticizer for heart residue and pressed extract in the study group --1.27 plus or minus 0.42 and 0.66 plus or minus 0.22 mug per gram respectively--were significantly (pgreater than 0.005) higher than the corresponding control levels (less than 0.07 plus or minus 0.03 and less than 0.07 plus or minus 0.04 mug per gram). Higher levels were associated with larger amounts of blood products, more extensive use of catheters, and early death. Levels in gastrointestinal tissue from three infants who had died of necrotizing enterocolitis were significantly (less than 0.05) higher than those in gastrointestinal tissue from infants without this disease. Thus, plasticizer from medical use of plastics does accumlate in tissues of critically ill infants.

Hypoxia and hypovolemia result in similar ultrastructural changes. These changes are characterized by aggregation of platelets and leukocytes in the vascular space, focal endothelial cell disruption, and appearance of increased amounts of perivascular edema, and loss of ultrastructural organization of the mucosal cell. These changes appear to relate to variations in blood flow to the mucosa of different areas of the bowel and to follow the distribution observed for necrotizing enterocolitis in the human infant.

Eighteen cases of necrotizing ileocolitis are reported. Successes have been recorded with intensive medical therapy, but our experience suggests that surgical intervention is the safest path to follow.

Pneumatosis intestinalis (intramural bowel air) can be seen in several disease processes during the neonatal period, notably mechanical obstruction, vascular compromise, and necrotizing enterocolitis.Pneumatosis intestinalis seen with mechanical obstruction is often uneventful and self-limiting when the obstruction is relieved.Necrotizing enterocolitis will usually have a characteristic presentation of early onset in premature infants with distention, bile-stained emesis, and blood in the stool.Vascular thromboses with subsequent bowel ischemia can mimic necrotizing enterocolitis, but will occur later in the newborn period, may be localized to small bowel, and may be associated with indwelling umbilical artery catheters. Recovery is often complicated by indeterminate periods of malabsorption.The diagnosis of the underlying disease leading to pneumatosis intestinalis is necessary for proper management.

Colonic findings are presented in 2 infants who survived necrotizing enterocolitis. In one infant, nodular submucosal infiltrates were observed throughout the colon which roentgenographically and pathologically resemble benign lymphoid polyposis. The latter may represent a nonspecific reparative or immunologic response. The second infant demonstrated a stricture in the descending colon which is believed to represent the end-stage of an underlying ischemic process.

Eleven premature babies developed necrotizing enterocolitis in an epidemic of gastroenteritis and salmonella infection. This occurred in one of two premature baby wards over a period of 10 weeks. All affected babies had severe gastroenteritis and six had salmonella infection. No cases of necrotizing enterocolitis occurred in the unaffected ward during the same period. All other possible factors which might have predisposed to necrotizing enterocolitis occurred with equal frequency in both wards.There seems little doubt that infection was the significant factor in the pathogenesis.

Necrotizing enterocolitis is a relatively rare disease occur ring in premature infants. "Greater awareness with earlier diagnosis and treatment may improve the survival rate."

Necrotizing enterocolitis (N.E.C.) occurring in the neonatal period was first described in the late 1800's. 1 Increasing attention has recently been directed to this disease because of the poor survival rate and an apparently increased incidence. 2–4 The poor survival rate has been attributed to intestinal necrosis and perforation which could be corrected by appropriate surgical intervention; however, the timing and indications for surgery have not been clearly defined. We have reviewed the records of 65 patients with acute necrotizing enterocolitis seen in the neonatal unit of the Los Angeles County-University of Southern California Medical Center from July, 1970 through December, 1972. Particular attention has been directed to those patients who underwent a surgical procedure.

A syndrome consisting of vomiting, abdominal distention, gastrointestinal bleeding,and shock has been observed in premature infants. The disorder is usually fatal, and on postmortem examination, ulcerations are seen in the gastrointestinal tract, particularly the terminal ileum. History of maternal infection during delivery is significant. Anteand postmortem cultures in infants with enterocolitis reveal predominance of gramnegative organisms. Criteria for diagnosis are presented.

Necrotizing enterocolitis as a usually fatal disease of premature infants has been reported with increasing frequency in recent years, primarily in Europe (2, 11, 12, 14, 15, 23). Though the published cases have appeared under diverse titles including neonatal appendicitis (4, 18, 22), peritonitis (12), colitis (21), ileitis (1), pneumatosis intestinalis (20), or portal vein gas in infants (10, 24), we feel all reflect a basically similar disease process. The current report is based on a study of 21 cases of enterocolitis in newborn premature infants seen between 1954 and 1964; 7 were found in a six-month period in 1963. A more detailed study of the clinical and pathologic findings will be reported separately (9). Clinical Features More than 2,000 infants were admitted to the premature nursery of The Babies Hospital from 1954 to 1964. Seventeen died of enterocolitis (0.9 per cent), and 4 survived. Usually weighing under 1,500 grams at birth, the babies showed a similar clinical pattern. They seemed well d...

Necrotizing enterocolitis and intestinal perforation, occurring without distal obstruction of the gastrointestinal tract, are serious lesions of the neonatal period. The onset of gastrointestinal findings is often preceded by severe postnatal stress, usually of cardiorespiratory origin, producing hypoxemia, hypercarbia, and systemic acidosis. Resuscitated infants, usually premature, remain clinically well during a latent period until they develop characteristic signs of enterocolitis, including gastric retention, bile vomitus, abdominal distension and blood streaked, diarrheal stools. Hemorrhagic and necrotic lesions, with or without perforation, are most commonly found in the stomach, ileum, or colon at operation and/or autopsy. The pattern of asphyxia, resuscitation, and a latent period followed by gastrointestinal findings has been the subject of much speculation about the causal relationship of cardiorespiratory distress in infants with necrotizing enterocolitis. The temporal relationship of perinatal asphyxia to the acute onset of gastroenterocolitis is summarized on Fig. 1. An experimental model was designed that simulates conditions of postnatal respiratory distress and allows measurement of intramural and mucosal perfusion to the gut of asphyxiated and resuscitated neonatal piglets, as well as histologic studies of the gut. We suggest that the term “ischemic gastroenterocolitis of the neonate” be adopted to best describe this condition.

Gas in the portal veins of the liver has been heralded as an ominous sign (3) since Wolfe and Evans' (7) first report in 1955. They and other workers (5, 6) described the characteristic appearance which differentiates this condition from gas in the biliary system. The usual causes include intestinal necrosis (1, 4), septicemia with gas-forming organisms (6), and necrotizing enterocolitis (2). Because of the increased use of the umbilical vein in administering intravenous fluid, it is felt the introduction of air into the portal system is possible. Such a case is reported to illustrate this finding. Case Report During the process of radiographic examination for tracheoesophageal fistula in a 2-day-old term infant, gas was observed in the portal venous system of the liver (Figs. 1 and 2). Because of this finding the infant was re-examined but found essentially unchanged, only the abdominal gaseous distention being demonstrated. Noted at this same time were wetness and leaking around the umbilical catheter. ...

Of 720 newboms admitted to our NICU in a recent 38-month period, 54 (7.5%) developed NEC. In an attempt to better define the etiology of NEC, the acute course of these patients was compared to 98 control patients matched for birth weight. Survival was 37% in NEC as compared to 65% in control patients. The frequency of RDS (74%) and of perinatal asphyxia (32%), hypotension (20%) and hypothermia (20%) was comparable in the two groups. Stool cultures showed no predominance of a single organism in either group. Although DIG (48%) and sepsis (38%) both occurred three times as often in NEC patients as in controls, their onset usually coincided with, rather than preceded, the onset of NEC. On the day of life that NEC occurred, all 54 NEC patients and 63% of controls were receiving formula feedings, both at 80 cal/kg/day. 96% of NEC patients had umbilical arterial (UA) catheters and 78% were still in place within 24 hours of onset of NEC; 73% of controls had UA catheters. Average duration of UA catheters was 7.7 days in NEC as compared to 5.4 days in controls (P=.05). 69% of NEC and 43% of control patients (P=.05) had UV catheters. NEC patients were indistinguishable from controls prior to the onset of NEC. Although our data does not define one single etiology of NEC, the high incidence of formula feedings in NEC patients does suggest that formula feedings may be related to the etiology of NEC as well as to the extent of intramural gas.

An experimental model of necrotizing enterocolitis in newborn Sprague-Dawley rats has previously been described (Barlow et al., APSA 1974). It was found that newborn rats exposed to daily hypoxia all succumbed to this disease within two to five days if fed artificial formula (F) but not if fed breast milk (BM). These studies were undertaken to determine the protective factors in BM. In vitro, BM killed 99% of 107/cc Klebsiella in two hours, while frozen breast milk (FBM) killed none and F supported bacterial growth. The Klebsiella used was one which produced peritonitis and sepsis in the experimental model. FBM and F lack the 106/cc macrophages (mO) present in BM. FBM plus 106cc rat peritoneal mO or rat peripheral white cells or rat BM mO also killed these organisms in vitro. In the experimental model, all rats died if fed F, 90% died if fed FBM and 20% died if fed F plus peripheral white cells. These studies suggest the importance of the mO in milk as cells capable of killing potential bacterial pathogens and of preventing necrotizing enterocolitis in the appropriate stressed animal.

The records of all newborns with necrotizing enterocolitis (N-E) were reviewed for the years 1968-73. Of the 24 cases, 19 died & N-E was confirmed in all 18 autopsies. The previously reported associations with low birth weight, PROM or amnionitis, asphyxia, & RDS were found. Also, a relationship with feeding was seen—the infants forming 3 groups: Group I-18 infants begun on formula feedings between 4 hrs. to 8 days of life. They developed G.I. signs an average of 31 hrs. later (S.E.=5.6). Formula intake by the 2nd day of feeding averaged 72 cc/kg/day, 133% of the usual daily formula intake in this nursery for infants without overt illness. All 5 who lived (of which none perforated or had surgery) were in this group. Group II-3 infants developed the onset of G.I. signs 15, 20 and 28 days following initiation of feeding, but had other intercurrent problems. Group III-3 infants never fed formula. These had no x-ray or autopsy evidence of pneumatosis. In these 24 patients with N-E, 75% developed the disease related to the onset of feeding. The remainder appeared to develop their disease in relationship to other problems. Formula feeding in this series is very closely associated with the development of N-E, particularly over-aggressive feeding. Feeding is not the sole cause of N-E but is closely enough related to its development to warrant delayed and cautious feeding of infants at risk of N-E.