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Mechanical ventilation of newborn infants has been employed in many centers. Because methods for selection of infants and technique and pattern of ventilation have varied, comparisons of results are difficult. This report reviews the history of mechanical ventilation of the neonate and describes a scoring system developed for the selection of newborn infants for intermittent positive-pressure ventilation (IPPV/I). The clinical diagnosis and management of 204 neonates prior to selection for mechanical ventilation are outlined. All infants were hypercapnic, hypoxie, acidotic and/or apneic prior to initiation of IPP/I. Survival of these infants following mechanical ventilation is discussed in relation to the scoring system used for selection for mechanical ventilation.

Five infants with intolerance to lactose or sucrose and one infant with intolerance to both lactose and sucrose have been studied. These infants were symptomatic with fermentative diarrhea, vomiting, and failure to gain weight. The tolerance of these patients to disaccharides was measured, and the sugar or sugars to which they were intolerant were removed from their diets. The infants began to gain weight as their diarrhea abated. After they were asymptomatic and thriving for a period of time, they were re-examined and were found to respond normally to the ingestion of disaccharides. Disacchariduria was detected in 5 of the 6 infants during the acute period of their disorders, but not at the time of their reexamination. This finding is probably correlated to the amount of disaccharide ingested and the activity of the specific intestinal disaccharidase at the time of the test. The clinical symptoms and signs of these patients with acquired intolerance to disaccharides were identical to those of patients with congenital absence of intestinal disaccharidases.

The activities of intestinal sucrase and isomaltase are not detectable in rats before 15-16 days of age, but administration of corticosteroids precociously induces the activities of these two alpha-glucosidases. 9-day old rats were removed from their mothers, warmed in an incubator, and fed by constant infusion through gastrostomies. The basic diet was a soya preparation to which various sugars were added. When the diet contained 2% sucrose, diarrhea ensued for 48 hr, but subsided when intestinal sucrase and isomaltase appeared precociously. In animals fed sucrose, the activities of sucrase and isomaltase were markedly increased as compared to animals on carbohydrate-free diets (sucrase 2.41+/-0.23 vs. 0.63+/-0.13 U, isomaltase 3.43+/-0.42 vs. 0.78+/-0.18 U). Maltase activity was doubled, while lactase was not altered significantly. The mitotic index of crypt cells, the depth of crypts, and incorporation of thymidine-(3)H into DNA were increased. In adrenalectomized rats, activities of sucrase and isomaltase were not detected nor induced by sucrose. Steroids given to adrenalectomized rats caused appearance of the enzymes; but if cortisone and sucrose were given together, there was synergism evidenced by a marked increase in activities (sucrase 7.2+/-1.1 vs. 0.68+/-0.12 U). In contrast to observations in adult animals, the effect of sucrose on alpha-glucosidases in developing animals demands the participation of the adrenal gland.

A 9-year-old girl with vomiting, changes in behavior, coma, and evidence of hepatic dysfunction at 3½ years of age was found to have hyperammonemia and decreased activity of liver ornithine transcarbamylase. When her dietary protein was reduced, she had improvement in her clinical condition and a return to normal of all hepatic function indices. Despite a defect in an enzyme of ornithine metabolism, she did not have hyperaminoacidemia, specifically hyperornithinemia, even when she had hyperammonemia. When she ingested a large amount of ornithine (300 mg/kg) she developed hyperornithinemia and hyperornithinuria. She also had orotic aciduria despite having normal activities of red cell orotidylic decarboxylase and pyrophosphorylase. Treatment with a low protein diet and citric acid supplements has been successful in preventing hyperammonemia and promoting growth and development.

Litters of 10-day-old rats and their mothers were placed in specially designed cages which enabled the pups to continue to suckle, not to have access to water, solid foods, or feces, and to ensure that their sole dietary carbohydrate was lactose. The animals were killed at intervals and intestinal β-galactosidases, α-glucosidases, and cellular proliferation were measured. Although the specific activity of intestinal lactase followed the usual decline observed during development, the enzyme was maintained at a significantly higher activity than that of control rats. These animals were also able to hydrolyze lactose more readily as demonstrated by their having a significantly higher concentration of glucose in blood after ingestion of lactose. When segments of intestine were incubated with lactose, glucose plus galactose, sucrose, mannitol, or saline, the decline in the activity of lactase was much less in the presence of lactose than in any of the other media. Thus, the substrate had a stabilizing or protective effect on the enzyme. The developmental pattern of the intestinal a-glucosidases and the "acid" β-galactosidases, and the normal morphological maturation of the intestine were not altered by prolonged nursing and elimination of carbohydrates other than lactose.

There was a significant depression of the activities of intestinal lactase, invertase, and alkaline phosphatase in rats given drinking water containing 2.5 mg of colchicine per 100 ml. Activities of intestinal maltase, aspartate transcarbamylase, and dihydroorotase were not affected by the drug. Injection of colchicine (1 mg/kg) caused depression of intestinal invertase activity within 8 hr. Investigation of the effect of colchicine on the disaccharides in vitro demonstrated that invertase and maltase were not affected by concentrations up to 125 mg/100 ml. Intestinal lactase was inhibited by concentrations exceeding 5 mg/100 ml. Calculation of the concentration of colchicine present in the intestine, after a single injection, indicated that the in vivo effect of colchicine was not due to simple enzyme inhibition. Histological examination showed an increase in crypt cells but no decrease in the length of the villi. Cellular migration along the villi, as well as activity of uridine kinase in intestinal mucosa, was increased in colchicine-treated rats. It was concluded that colchicine did not depress intestinal invertase, lactase, and alkaline phosphatase by decreasing cellular renewal, but rather it exerted its effect directly on the differentiated cells of the villus.

Because of the relative paucity of data on the epidemiology and management of perinatal herpes simplex virus (HSV) infections, the following recommendations represent the best current judgments of the Committees on Fetus and Newborn and Infectious Diseases of the American Academy of Pediatrics. HSV infection of the newborn is associated with a case fatality rate of 60% and at least half of the survivors have significant neurologic or ocular sequelae, or both. Approximately 75% of isolates from affected neonates are HSV-2 and 25% are HSV-1. Although preliminary data suggest that antiviral chemotherapy is effective in reducing mortality and morbidity resulting from neonatal HSV infections, measures designed to prevent infection of newborns are currently the most important means of controlling neonatal infections. A maternal source of infection can be found in about 90% of neonatal cases. Maternal HSV infection is usually caused by type 2 strains and involves the labia, cervix, and/or vagina. The majority of genital infections are asymptomatic and difficult to recognize on clinical examination, making identification of women whose infants are in jeopardy very difficult. EPIDEMIOLOGY Maternal Infection Primary HSV infection during pregnancy may be associated with spontaneous abortion, prematurity, and rarely with congenital anomalies. The risk of infection to the newborn appears to be the highest in primary genital infection of the pregnant woman, but is also high in recurrent infection. Women with a history of recurrent genital HSV infection, those with active disease during the current pregnancy, and those whose sexual partners have proven genital HSV infection should be monitored with virologic or cytologic studies, or both, at least twice during the last six weeks of pregnancy.

The effects of pasteurization, lyophilization, and freezing on immunoglobulin and lymphocytes in human milk was studied. We found a significant decrease in total lymphocyte count after all three processing methods. Pasteurization and lyophilization caused a significant decrease in immunoglobulin concentration and in specific antibody titer to Escherichi coli . Freezing specimens up to four weeks resulted in no significant alteration of IgA content or in E. coli antibody titer. Since a major advantage of human milk is the transference of passive local immunity, these quantitative changes may have clinical importance.

Thirty-nine critically ill infants with pulmonary disease received tolazoline because of severe hypoxemia refractory to administration of 100% O2 and mechanical ventilation. Twenty-seven (69%) of the infants responded with an increase in PaO2 greater than or equal to 20 torr in the first umbilical arterial gas after completion of the initial ten-minute infusion (1 to 2 mg/kg) of the drug. A response was not correlated with survival. The overall survival was 46%, essentially unchanged from our previous report (44%). Infants with hyaline membrane disease had the poorest survival rate (33%). Complications associated with the use of tolazoline occurred in 82% of the infants. A hypotensive reaction, defined as a 25% decrease in mean arterial pressure from the pre-tolazoline level, occurred in 67% of the infants, and more commonly in the infants with RDS (87%). In 11 infants who did not respond to the initial dose of tolazoline, the dose was increased up to 10 mg/kg/hour; only one infant responded, and eight (73%) had a hypotensive reaction.

A prospective study of 377 premature infants (less than or equal to 1500 gm) was undertaken to delineate the natural history of subependymal/intraventricular hemorrhage (S/IVH) and its complications using ultrasound (US) and computed tomography (CT). Low grade (I, II) S/IVH had a low mortality while higher grades (III, IV) still had elevated mortality rates. The addition of intraparenchymal hemorrhage (IPH) to S/IVH incrementally increased the incidence of death and other complications, suggesting IPH hemorrhage should be categorized separately. When a specific day could be identified, S/IVH had its onset in the first 7 days of life with peak incidence occurring on day 3. S/IVH appeared to be an event limited to less than 24 hours in all but 5% of infants in whom progression of hemorrhage was documented over a 24-hour period. The mortality rate of these progressive hemorrhages was high, 50%. The benign phenomenon of late S/IVH was detected in 5% of infants. These hemorrhages were clinically silent and of minor severity. Several complications of S/IVH were detected. Hydrocephalus was a significant complication only for higher grades of S/IVH. When present, severe hydrocephalus had an early onset and reached a maximum at around 3 weeks of age. "Atrophic change" of a cerebral hemisphere was detected in 30% of all S/IVH infants, while this was not seen in nonS/IVH infants. This "atrophic" abnormality had a marked predilection for the left hemisphere, independent of the site of the S/IVH. Periventricular leukomalacia (PVL) was documented by US in 2% of infants and could be detected in the first week of life. PVL presented in the first week of life as an echogenic lesion which developed "cystic" changes at approximately 3-4 weeks of age. This complication should be categorized separately from S/IVH.

6. Enhorning G, Grossman G, Robertson B: Tracheal deposition of surfactant before the first breath, Am Rev Respir Dis 107:921, 1973. 7. Fujiwara T, Chida S, Watabe Y, Maeta H, Morita T, and Abe T: Artificial surfactant therapy in hyaline membrane disease, Lancet 1:55, 1980. 8. King R J, and Clements JA: Surface active materials from dog lung. !L Composition and physiologic correlations, Am J Physiot 223:715, t 972. 9. Hallm'an M, Schneider HA, and Gluck L: Human fetus, a potential surfactant donor: isolation of lung surfactant from amniotic fluid, Pediatr Res 15:663, 1981. 10. Pearson D J, Mentnech MS, Gamble M, Taylor G, and Green FHY: Acute pulmonary injury induced by immune complexes, Exp Lung Res 1:323, 1'980. 11. King RJ and Macbeth MC: Physicochemical properties of dipalmitoyl phosphatidylcholine after interaction with an apolipoprotein of pulmonary surfactant, Biochim Biophys Acta 557:86, 1979.

Sodium nitroprusside was administered to 58 neonates, including 11 with severe respiratory distress syndrome, 15 with persistent pulmonary hypertension of the newborn, 28 with clinical shock, three with systemic hypertension, and two with pulmonary hypoplasia, all refractory to conventional intensive therapy. Nitroprusside was infused at 0.2 to 6.0 μg/kg/min for periods of 10 minutes to 126 hours. Infants with severe respiratory distress syndrome had increased Pa o 2 and decreased Pa co 2 or peak inspiratory pressure, and nearly all (82%) survived. Infants with persistent pulmonary hypertension of the newborn had variable responses; improvement did not correlate with survival, but survival (47%) was identical to that in an earlier series of infants given tolazoline. Infants in shock had improved perfusion, urine output, and serum bicarbonate levels, and these responses were significantly related to survival. Hypertension was controlled in all three hypertensive infants. Adverse effects were very uncommon. Toxic effects were not observed. Sodium nitroprusside is effective and can be used safely in circulatory disorders in the neonate.

Intestinal lactase declines to low levels in the postweaned mammal as an adaptation to normal termination of lactose ingestion. Although a well known phenomenon and presumably the basis of milk intolerance among most human adults, the mechanism of this decline has remained obscure. Evidence is presented to support a proposal that temporally related cytokinetic changes, which effect a generally corresponding reduction in enterocyte life-span, serve as the causal basis of lactase decline in the postweaned mammal.

Adult rats that were maintained on a low-carbohydrate intake showed rapid increase in the activities of sucrase, maltase, and lactase along the length of the small intestine when they were fed a high-starch diet. In the present study, we have identified these activity increases, and showed that they reflect proportional accumulations in enzyme-protein of sucrase-isomaltase (EC 3.2.1.10, 3.2.1.48), maltase-glucoamylase (EC 3.2.1.20), and neutral lactase (EC 3.2.1.23). It was determined that each of these enzymes exists in adult rat intestine in single immunoreactive form and accounts as a group for all sucrase, cellobiase, and most maltase and lactase activities. Dietary change from low to high carbohydrate (starch) resulted in an increase in [3H]leucine accumulation in each of the enzymes, without a change in the amount of label accumulation in total intestinal proteins. The increase in label accumulation in the brush-border carbohydrase pools was matched generally by proportional elevation in the pool concentrations of sucrase-isomaltase and lactase but not maltase. These studies suggest that the elevation of intestinal carbohydrase concentrations induced by high-carbohydrate feeding may involve selective stimulation of their synthesis.

Urea cycle function was evaluated in liver obtained from six patients with Reye's syndrome and from five control subjects. Reye's syndrome patients demonstrated normal activities for the extramitochondrial portion of the urea cycle, but showed marked abnormalities of the mitochondrial enzymes, i.e., carbamyl phosphate synthetase (CPS) and ornithine transcarbamylase (OTC) (Tables 2,3). CPS activity was reduced to less than 15% of control values in all four patients from whom tissues was obtained during the first 72 hr after the onset of encephalopathy. Two patents from whom tissue was not obtained until after 9 days of symptoms showed no reduction in CPS activity. The OTC activity was also reduced (3-67% of control values) in the four patients from whom tissue was obtained early in the illness. In addition, greater than 60% reduction in Vmax and Km for carbamyl phosphate was noted in all four patients in whom sample size permitted kinetic analysis, including both patients in whom CPS and OTC activity were not markedly reduced. The same kinetic abnormality as well as decreased CPS activity were experimentally produced in normal rate liver incubated in the presence of 1.0 mM 4-pentenoic acid, a short chain fatty acid and known hepatic mitochondrial toxin (Table 4).

The enteric epithelium of suckling rat undergoes dramatic functional and cytokinetic changes (redifferentiation) with maturation. Ileal epithelial maturation was studied in infant rats subjected to 60% proximal enterectomy at age 10 d in an effort to examine redifferentiation mechanisms. Two months after resection the residual ileal remnant was increased in diameter, weight, total protein, and DNA per unit length compared with ileal segments from control littermates that had laparotomy without resection. The residual ileum demonstrated increased sucrase activity per unit length but was indistinguishable from control ileal segments in activity per unit DNA or villus distribution. Lactase activity was negligible in all segments of the residual intestine. Villus height and crypt depth were increased in the residual ileum with slight increases in cell turnover and cell-migration rates. These results show the presence of an intrinsic program for regulation of ileal epithelial maturation and its resistance to alteration by a major stimulus applied before its expression.

Eighteen newborn infants who were moribund secondary to respiratory insufficiency were treated with prolonged mechanical breathing by an anesthetic endotracheal tube; 11 survived. On removal of the endotracheal tube laryngeal and tracheal obstruction did not develop. The longest period of successful respirator treatment was nine days. The birth weight of the smallest surviving infant was 2.2 lb (1,020 gm). Tracheal intubation with a soft plastic tube is quicker and simpler than tracheostomy, and even if maintained for many days, may be less traumatic. It deserves wider and probably earlier trial in the treatment of respiratory inadequacy of the newborn. Attention to detail is essential for airway preservation and for continuance of satisfactory ventilation. Nutrition is best managed by feeding through a gastrostomy tube.

Jejunal biopsies were obtained from five iron-deficient infants 24 to 32 hours after an intramuscular injection of iron-dextran. Newly produced cells at the base of the villus appeared to have a higher cytochrome-oxidase activity compared to the older cells at the tip which were produced during a period of iron deficiency. These results in man, similar to those previously described in the rat, suggest that the repair of intestinal cytochrome-oxidase activity which accompanies treatment of iron deficiency is limited by the rate of new cell production. In the iron-deficient rat histochemical evidence of cytochrome-oxidase repair corresponds closely to the extent of migration of new cells up the villus as indicated by autoradiography, between 8 and 48 hours following simultaneous administration of tritiated thymidine and iron-dextran. Colchicine, which arrests cell division at metaphase, interferes with cytochrome-oxidase repair when administered simultaneously with iron-dextran. Enzymes not known to contain iron or require it as a cofactor were assayed in jejunal scrapings from iron-deficient and control rats. Aspartate transcarbamylase, alkaline phosphatase, sucrase, and maltase activities were normal in the intestinal mucosa of the iron-deficient rat. No intestinal malfunction was demonstrated in the iron-deficient rat by determination of fecal fat excretion, I131 PVP excretion, and transport of glucose and galactose in everted sacs of the jejunum and the ileum.

Cord sera were obtained from 5,006 infants. There were 135 sera with IgM values greater than 20 mg. per cent. Of these, 60 per cent probably were due to a placental leak, 13 per cent were in a questionable category, and 27 per cent were considered to be due to production of abnormal amounts of IgM in utero. Although such determinations were of some value in discovering clinically significant, inapparent congenital infections, certain premature and full-term infants with infections recognized in the immediate postnatal period had normal levels of IgM. Long-term follow-up in 27 of the 37 infants with definitely abnormal IgM in their cord serums revealed all of them to be normal.

Summary Active chronic hepatitis, confirmed by biopsy, is reported in an infant who was 10 months of age when she had the onset of recurrent jaundice, fever, and malaise. She had laboratory evidence of liver injury, hypergammaglobulinemia, and, on one occasion, hemolytic anemia. A sister of the patient died at 46 months of age and had postnecrotic cirrhosis at postmortem examination. This is the youngest patient described in the literature with active chronic hepatitis.

CELLULAR proliferation in the small intestine and the rapid renewal of intestinal epithelium have been investigated before1–3. A number of techniques have been used to measure the rate of proliferation and the migration of the cells of intestinal epithelium, but only adult animals have been investigated. The morphology4,5 and enzyme6–9 pattern of the small intestine in the suckling differ from that of the adult rat, and therefore we decided to compare the rate of cellular migration at these different ages by means of incorporation of tritiated thymidine and histo-autoradiography.

Extract: At 15 days after birth, the small intestine of the rat showed a striking increase in relative weight, an increased depth of intestinal crypts, an elevation of the mitotic and the labeling index of crypt cells, and a decrease in the ratio of height of the villi to depth of the crypts. Metabolically, the biological half-life of 14C phenylalanine incorporated into protein was decreased in the intestine of 21-day-old rats compared with that of the 32-day-old rat. With autoradiography, a decreased half-life of 3H-leucine in crypt cells was noted in rats 5 and 21 days of age, compared with fully weaned rats 32 days of age. These observations indicated that protein turnover is not completely dependent on cellular turnover in suckling rats. Artificial feeding of suckling rats from 9 to 15 days of age produced an increase in the relative weight, mitotic index, depth of crypts, and activity of invertase in the jejunum. Prolonged administration of hydrocortisone to newborn rats resulted in similar changes in the duodenum and in the jejunum, but not in the ileum. These changes could be related to an increased rate of cellular migration along the villi of the duodenum and the jejunum. It was concluded that both diet and hormones were important factors in the marked changes in intestinal cell proliferation and differentiation observed at weaning. Speculation: The usual changes in cellular proliferation and differentiation of the intestinal mucosa of the weanling rat and the observation that these changes can be stimulated precociously suggest that the intestinal tract of suckling rats could be used to investigate further those factors important to the control of cell differentiation. Since cell turnover increases to adult levels after 15 days of age, the observed increase in protein turnover in suckling and in weanling rats, compared with that of adult rats, suggests that at these ages protein turnover is not coordinated with cell turnover.

1. The developmental pattern and effect of cortisone on acid beta-galactosidase and neutral beta-galactosidase were studied in postnatal rats by a recently proposed method for their independent determination. 2. After birth the acid beta-galactosidase activity increases in the ileum, whereas it decreases slightly in the jejunum. On day 16 after birth the activity in the ileum decreases and in 20-day-old rats activity in both parts of the intestine decreases to adult values. In suckling animals the activity in the ileum exceeds the jejunal activity severalfold and in adult animals the activity in the jejunum is slightly higher than that in the ileum. 3. Neutral beta-galactosidase activity is high after birth and decreases in both jejunum and ileum after day 20 after birth. In 12-20-day-old rats activity in both parts is essentially the same, but in adult animals jejunal activity exceeds ileal activity four-to five-fold. 4. Cortisone (0.5, 2.0 or 5.0mg/100g body wt. daily for 4 days) does not influence the activity of either enzyme in 60-day-old rats. Acid beta-galactosidase activity is decreased after cortisone treatment in 8-, 12-, 16-and 18-day-old rats, with sensitivity to cortisone increasing with the approach of weaning. No effect of cortisone on acid beta-galactosidase is seen in 8-day-old rats. Neutral beta-galactosidase activity is increased in the ileum of 8-, 12-, 16- and 18-day old rats, but only in the jejunum of 8-and 12-day-old rats.

We have described an infant with neonatal thyrotoxicosis who developed supraventricular tachycandia, goiter, and periorbital edema. Both the baby's and mother's sera contained the long-acting thyroid stimulator (LATS). While the level of LATS remained unchanged in the serum of the mother, it rapidly fell in the serum of the infant. The biological half-life of LATS in the infant's serum was calculated to be 6 days, and by the age of 21 days no LATS activity could be detected. Based on these findings, antithyroidal treatment which had been instituted soon after birth was discontinued on the thirty-eighth day without recurrence of signs or symptoms of thyrotoxicosis. In addition to conventional antithyroid therapy for thyrotoxicosis, exchange transfusion and prenatal corticosteroid therapy of the mother may be considered when neonatal or maternal serum LATS titers, respectively, are very high.

Two enzymes of the de novo pathway of pyrimidine biosynthesis, aspartate transcarbamylase and dihydroorotase, and two enzymes of the salvage pathway, uridine kinase and thymidine kinase, were assayed in crypts, villi, and whole intestinal mucosa of the rat during development. Elevated activities of these enzymes could be correlated with active cellular proliferation. The activities of the enzymes were greatest in crypts and decreased as cells migrated along the length of the villi. Also, changes in cellular proliferation during development of intestinal mucosa mirrored changes in enzymatic activities of both the de novo and salvage pathways. In colonic mucosa, where cellular turnover does not increase at weaning, there was no change in activities of these enzymes, offering a biochemical basis for determination of cellular turnover in the intestine.

Pups of both the California and Stellar sea lions have no intestinal enzymes for hydrolysis of sucrose, lactose, cellobiose, or trehalose. If these animals were given lactose or sucrose, they developed severe fermentative diarrhea and weight loss similar to the clinical syndrome encountered in infants with either hereditary or acquired intolerance to disaccharides. quired intolerance to disaccharides.

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.

The Center for Disease Control (CDC), after consultation with a panel of experts, has revised its recommendations for prevention of gonococcal ophthalmia neonatorum. These recommendations now state, "ophthalmic ointment or drops containing tetracycline or erythromycin or a 1% silver nitrate solution" are effective and acceptable.1-3 This is a change from previous recommendations which highlighted silver nitrate as the primary agent for prophylaxis.4 The American Academy of Pediatrics' committees support these recommendations. The prevalence of largely asymptomatic genital gonococcal infection in pregnant women and the occurrence of gonococcal ophthalmia in untreated infants (estimated at 28%)5 born to infected women indicate the need for continued prophylaxis for all newborn infants.

The concept of a regionalized system encompassing three broadly defined levels of neonatal care is now well recognized and increasingly practiced in the United States. The American Academy of Pediatrics has described, in some detail, a system of classifying nurseries as Levels I, II, or III, based on the type of care they are capable of providing for the newborn infant.1 There has been little question about the composition of care in Level I or Level III units, but the committee recognizes that there is considerable diversity of opinion about the definition of Level II units and the functions these units should perform. The concept of the Level II neonatal unit has, in general, been supported by most pediatricians and neonatologists; however, there is little factual information available about Level II units, how they function, and how they contribute to perinatal outcome. The committee sent 300 questionnaires to the directors of all neonatal training programs, to the Chairmen of all Academy Chapters, and to 70 other practicing pediatricians. Responses were received from 114 Level III centers, 46 Level II centers, and 7 Level I hospitals. The responses came from 45 states and five Canadian provinces. According to the responses and the thoughtful comments received, the functions of Level II units are of considerable interest and concern to many pediatricians; but, obviously, it is impossible to suggest universal solutions for all regions which will cover all possible occurrences. The committee has considered all the opinions expressed and the information available regarding the functioning of Level II units and makes the following recommendations

To the Editor.— We recently reported an improved outcome for infants with birth weight in the 751-to 1,000-g range; the prognosis for infants weighing 750 g or less at birth was equivocal.1 Since the publication of this report, further interesting data on the very low-birth-weight infants cared for in the Stanford University Hospital Intensive Care Unit have become available. We would like to add these data to those already published. In the original paper,1 we reported a 28% neonatal mortality for 751-to 1,000-g birth weight infants born during 1977 to 1980.

INTRODUCTION It is cautioned that there is an element of risk in early discharge insofar as medical supervision during the infant's transitional period must, of necessity, be intermittent rather than continuous. With this in mind, the following guidelines are suggested. CRITERIA FOR EARLY INFANT DISCHARGE 1. Attendance at prenatal childbirth education and infant care classes where problems of the first three to five days of life are included. 2. Identification of a supporting person to assist with care at home in the neonatal period. 3. Identification of physician-directed source of continuous medical care following hospital discharge. This should include an appointment at 2 to 3 days of age. 4. Uncomplicated antepatum, intrapartum, and postpartum course of both mother and infant. 5. Term infant (38 to 41 completed weeks) who is normally growrn (2,500 to 4,500 gm) and who is examined by a physician prior to discharge and found normal. 6. A minimum of six hours of hospitalization during which time the infant has achieved thermal homeostasis and fed successfully (demonstrated a normal suck and swallowing mechanism). 7. Laboratory data: (a) maternal or cord blood serologic test for syphilis; (b) cord blood (or infant blood) type and Coombs if mother Rh negative or type O. A Coombs test should be performed on all infants if a screening test for irregular antibodies was not performed during pregnancy; and (c) hemoglobin and blood sugar determinations as clinically indicated. 8. Maternal skill and demonstrated ability with: (a) feeding technique; (b) skin care, including cord care; (c) temperature assessment and measurement with thermometer and (d) assessment of infant well being and recognition of illness.

Growth charts based on data from normal children are commonly used to assess the growth of children who were premature. We examined the growth of 62 infants (EGA 30±2 wks and birthweight 1205±198 gm) who were born in 1975-77, followed prospectively for 3 years and who had normal developmental histories, physical exams and no apparent sequelae of prematurity at age 3 years: Number in parentheses= National Center for Health Statistics percentile of mean. We concluded that growth charts prepared from data from normal children are not appropriate for children who had birthweights ≤ 1500 gm (except perhaps for head circum.) and that little catch-up growth occurs between one and 3 years in such infants. What factors are operative and whether this pattern is significant or whether there will be later catch-up growth is unknown.

1340 TRANSCUTANEOUS OXYGEN MONITORING, HYPOXIC RANGE AND CORRELATION WITH PROSTAGLANDIN E 1

57 THE EFFECT OF INTERHOSPITAL TRANSPORT VARIABLES ON THE SURVIVAL OF CRITICALLY ILL NEONATES WITH RDS

The enteric epithelium of the suckling rat undergoes dramatic functional and cytokinetic changes at the time of weaning. Evidence suggesting that this redifferentiation is preprogrammed and intrinsic has been obtained by surgical transplants of fetal intestines. In an attempt to alter this redifferentiation a 60% proximal intestinal resection was performed on suckling rats at 10 days of age. Animals surviving for 2 months were compared with sex and weight matched littermates who had undergone laparotomy or laparotomy with transection. The residual intestine was increased in diameter and weight per unit length, but not significantly lengthened. The segmental increase in weight was primarily accomplished by hyperplasia as evidenced by parallel increases in total protein and DNA content. This increase in cell number was associated with a modest increase in the segmental sucrase and maltase activities in the residual ileum. However, when expressed as activity per unit DNA, sucrase and maltase concentrations in the residual ileum were indistinguishable from control ileal segments. Lactase activity virtually disappeared from all segments of the residual intestine in resected animals. These results lend in vivo support to the concept of a fixed intrinsic program of enteric redifferentiation.

High molecular weight precursor forms of various intestinal brush border enzymes have been demonstrated by pulse-labelling of intestinal explants maintained in culture. In the present study we have examined in vivo precursor forms of rat intestinal lactase. Fasted infant rats were injected (IP) with [35S]-methionine and killed after 0.5, 2, 4, and 18 H. The short fast was necessary to maximize incorporation of label. Lactase forms were isolated from Triton X-100 extracts of the intestinal homogenates by immunoprecipitation techniques using highly selective antisera. The isolated enzyme forms were separated by SDS-electrophoresis and examined by fluorography. Labelling within 30 min occurred in precursor forms of apparent mol. wts of 170, 125, and 90 Kd. A further precursor form of 200 Kd appeared within 2 H. All labelled precursor forms were no longer evident by 4 H. Apparent labelled brush border forms of lactase of 220, 130, and 95 Kd were evident by 2 H and were still present after 18 H. Using similar methodology, we have examined precursors of sucrase-isomaltase, with confirmation of existence of mature and immature precursor forms of 250 and 240 Kd respectively. Demonstration of lactase precursor forms determined in vivo provides confirmation of similar in vitro findings. These studies are consistent with the initial intra-cellular synthesis of high molecular weight precursor forms of lactase with subsequent transfer to brush border sites.