Management of Esophageal and Pharyngeal Perforation in the Newborn Infant

PEDIATRICS ◽  
1982 ◽  
Vol 70 (4) ◽  
pp. 592-596
Author(s):  
Dana E. Johnson ◽  
John Foker ◽  
David P. Munson ◽  
André Nelson ◽  
Pakshir Athinarayanan ◽  
...  

Perforation of the esophagus or pharynx may occur during placement of endotracheal or nasogastric tubes in the newborn infant. Controversy exists, however, whether medical or surgical therapy is better in the management of these perforations. Nine patients who had esophageal or pharyngeal perforation in the neonatal period and were treated medically with antibiotics, nutritional support, and closed chest-tube drainage of pneumothoraces are described. All perforations healed without surgical repair. No mortality or morbidity occurred secondary to these perforations. This study, together with a review of the 73 patients described in the literature, indicate that perforations of the pharynx and esophagus can be satisfactorily managed medically. There is no apparent advantage to routine early surgical exploration. Only complications such as mediastinitis and mediastinal mass formation seem to require surgical treatment. Medical therapy with close observation for signs of sepsis and/or mediastinal changes will enable most newborn infants to avoid an operation and will identify those infants for whom surgery is definitely indicated.

PEDIATRICS ◽  
1967 ◽  
Vol 39 (2) ◽  
pp. 294-296
Author(s):  
RONALD L. SEARCY ◽  
J. EDWARD BERK ◽  
SHINICHIRO HAYASHI ◽  
BRUCE D. ACKERMAN

The presence of measurable quantities of amylase in the serum of newborn infants or in serum derived from cord blood may be demonstrated through the use of a sensitive saccharogenic procedure that permits analysis of small quantities of serum. Serum amylase levels are highly variable during the early part of the neonatal period, but they usually tend to be close to or below the lower limits of normal established for adults. The origins of the serum amylase in the newborn infant remain to be elucidated.


PEDIATRICS ◽  
1956 ◽  
Vol 18 (4) ◽  
pp. 594-594

Newborn infants of diabetic mothers commonly develop remarkably low concentrations of sugar in the blood within a few hours after birth. This has led many to believe that the high morbidity and mortality in these infants might be due to hypoglycaemia. The present study concerns 90 infants born to diabetic women. The frequent occurrence of hypoglycaemia in the newborn of diabetic mothers was confirmed. However, it was found that there was no relationship between the development of a morbid neonatal course and the concentration of sugar in the blood at time, or the extent and rapidity of the decrease in concentration. No correlation existed between the degree of hypoglycaemia and abnormal incidents in the first 2 weeks of life. The authors agree with the opinion held by most investigators, that there is no need to administer glucose to infants born of diabetic women. In these infants, oral administration of glucose is hazardous and administration of glucose solutions subcutaneously or intravenously only serves to increase the abnormal volume of body water, and may embarrass the heart. The authors advise that all fluid should be withheld from these infants until time fourth or fifth day of life. They found no evidence that the period of hypoglycaemia in the neonatal period was followed by subnormal intelligence in later childhood.


PEDIATRICS ◽  
1957 ◽  
Vol 20 (4) ◽  
pp. 590-600
Author(s):  
Simon Kove ◽  
Stanley Goldstein ◽  
Felix Wróblewski

Measurements of transaminases in the serum have proven of value in the diagnosis of hepatic diseases in adults. It therefore seemed of interest to apply these techniques to the newborn infant. To establish the normal range of the activity of these enzymes in the serum for the neonatal period, studies were made of glutamic pyruvic transaminase (GPT) in 63 normal newborn term infants for the first week of life. It was found that values for the activity of GPT up to 90 units must be considered physiologic for this early neonatal period. This compares to a physiologic neonatal range of activity up to 120 units for glutamic oxaloacetic transaminase (GOT), found in a previous investigation on these same infants. Thus the range of activity for these two enzymes in newborn infants is somewhat greater than that of adults in whom values up to 45 units for both enzymes are considered normal. In neonatal physiologic jaundice the degree of hyperbilirubinemia did not affect the activity of GPT, as was also the case, from previous studies, with respect to GOT. Serial determinations of the activity of GOT and GPT were also made in a small number of infants with jaundice due to pathologic conditions to determine the value of this test in the differential diagnosis of jaundice of unknown origin in the newborn infant. It was found that in hemolytic disease of the newborn, activity of these enzymes usually remains within the normal neonatal range. In very severe hemolysis, activity of GOT may be increased to about 300 to 400 units, temporarily, although activity of GPT remains within the normal neonatal range. In neonatal biliary obstruction there is a sustained increase of activity of transaminase in the serum which may reach values up to about 800 units for the duration of the obstruction, whether it be temporary, as in the "inspissated bile syndrome" or protracted, as in atresia of the bile ducts. It would appear that serial measurements of the transaminases in the serum may be of distinct diagnostic value in jaundice of unknown origin in the neonatal period, and it is suggested that this procedure be included in the investigation of a clinical problem involving this syndrome.


PEDIATRICS ◽  
1974 ◽  
Vol 53 (2) ◽  
pp. 211-216
Author(s):  
Allen Erenberg ◽  
Dale L. Phelps ◽  
Robert Lam ◽  
Delbert A. Fisher

Radioimmunoassay measurements of serum concentrations of thyroxine (T4), triiodothyronine (T3), free T4 (FT4), free T3 (FT3), and thyroxine binding globulin (TBG) were conducted in full-term newborn infants between birth and 5 days of age. The mean concentrations of T4 and FT4 increased from cord blood levels of 11.9 µg/100 ml and 2.9 ng/100 ml to peak values of 16.2 µg/100 ml and 7 ng/100 ml by 24 to 48 hours of age. Mean serum total and free T3 concentrations increased from cord blood levels of 50.5 ng/100 ml and 146 pg/100 ml to peak values of 419 ng/100 ml and 1,260 pg/100 ml by 24 hours of age. Mean T3/T4 and FT3/FT4 ratios increased from 1/238 to 1/39 and from 1/20 to 1/6, respectively, during this period. By 72 to 126 hours, both the T4 and T3 concentrations had fallen somewhat. Mean serum TBG concentrations were unchanged and approximated 5.0 mg/100 ml during the first 5 days of life. These data confirm earlier reports that the normal newborn infant rapidly becomes chemically hyperthyroid in the neonatal period due to increased thyroid hormone secretion; this neonatal hyperthyroid state is due more to T3 than to T4. The data also confirm earlier reports that the fetus is T3 deficient due to a decreased capacity to monodeiodinate T4 to T3 in extrathyroidal tissues. The rapid increase in serum T3 after delivery at a time when the capacity to convert T4 to T3 is reduced suggests that the increment in serum T3 is due, predominantly, to increased T3 secretion from the thyroid gland stimulated by the neonatal TSH surge. Thus with parturition, the newborn infant is transformed from a state of chemical T3 deficiency to a state of chemical T3 thyrotoxicosis.


1980 ◽  
Vol 43 (02) ◽  
pp. 099-103 ◽  
Author(s):  
J M Whaun ◽  
P Lievaart ◽  

SummaryBlood from normal full term infants, mothers and normal adults was collected in citrate. Citrated platelet-rich plasma was prelabelled with 3H-adenine and reacted with release inducers, collagen and adrenaline. Adenine nucleotide metabolism, total adenine nucleotide levels and changes in sizes of these pools were determined in platelets from these three groups of subjects.At rest, the platelet of the newborn infant, compared to that of the mother and normal adult, possessed similar amounts of adenosine triphosphate (ATP), 4.6 ± 0.2 (SD), 5.0 ± 1.1, 4.9 ± 0.6 µmoles ATP/1011 platelets respectively, and adenosine diphosphate (ADP), 2.4 ± 0.7, 2.8 ± 0.6, 3.0 ± 0.3 umoles ADP/1011 platelets respectively. However the marked elevation of specific radioactivity of ADP and ATP in these resting platelets indicated the platelet of the neonate has decreased adenine nucleotide stores.In addition to these decreased stores of adenine nucleotides, infant platelets showed significantly impaired release of ADP and ATP on exposure to collagen. The release of ADP in infants, mothers, and other adults was 0.9 ± 0.5 (SD), 1.5 ± 0.5, 1.5 ± 0.1 umoles/1011 platelets respectively; that of ATP was 0.6 ± 0.3, 1.0 ± 0.1,1.3 ± 0.2 µmoles/1011 platelets respectively. With collagen-induced release, platelets of newborn infants compared to those of other subjects showed only slight increased specific radioactivities of adenine nucleotides over basal levels. The content of metabolic hypoxanthine, a breakdown product of adenine nucleotides, increased in both platelets and plasma in all subjects studied.In contrast, with adrenaline as release inducer, the platelets of the newborn infant showed no adenine nucleotide release, no change in total ATP and level of radioactive hypoxanthine, and minimal change in total ADP. The reason for this decreased adrenaline reactivity of infant platelets compared to reactivity of adult platelets is unknown.Infant platelets may have different membranes, with resulting differences in regulation of cellular processes, or alternatively, may be refractory to catecholamines because of elevated levels of circulating catecholamines in the newborn period.


1976 ◽  
Vol 35 (03) ◽  
pp. 712-716 ◽  
Author(s):  
D. Del Principe ◽  
G Mancuso ◽  
A Menichelli ◽  
G Maretto ◽  
G Sabetta

SummaryThe authors compared the oxygen consumption in platelets from the umbilical cord blood of 36 healthy newborn infants with that of 27 adult subjects, before and after thrombin addition (1.67 U/ml). Oxygen consumption at rest was 6 mμmol/109/min in adult control platelets and 5.26 in newborn infants. The burst in oxygen consumption after thrombin addition was 26.30 mμmol/109/min in adults and 24.90 in infants. Dinitrophenol did not inhibit the burst of O2 consumption in platelets in 8 out of 10 newborn infants, while the same concentration caused a decrease in 9 out of 10 adult subjects. Deoxyglucose inhibited the burst in O2 consumption in newborn infant and adult platelets by about 50%. KCN at the concentration of 10−4 M completely inhibited basal oxygen consumption but did not completely inhibit the burst after thrombin. At the concentration of 10−3 M, it inhibited both basal O2 consumption and the burst in infants and adult subjects.


Neonatology ◽  
2021 ◽  
pp. 1-8
Author(s):  
Nestor E. Vain ◽  
Florencia Chiarelli

Neonatal hypoglycaemia is a common metabolic disorder presenting in the first days of life and one potentially preventable cause of brain injury. However, a universal approach to diagnosis and management is still lacking. The rapid decrease in blood glucose (BG) after birth triggers homeostatic mechanisms. Most episodes of hypoglycaemia are asymptomatic, and symptoms, when they occur, are nonspecific. Therefore, neonatologists are presented with the challenge of identifying infants at risk who might benefit from a rapid and effective therapy while sparing others unnecessary sampling and overtreatment. There is much controversy regarding the definition of hypoglycaemia, and one level does not fit all infants since postnatal age and clinical situations trigger different accepted thresholds for therapy. The concentration and duration of BG which cause neurological damage are unclear. Recognizing which newborn infants are at risk of hypoglycaemia and establishing protocols for treatment are essential to avoid possible deleterious effects on neurodevelopment. Early breastfeeding may reduce the risk of hypoglycaemia, but in some cases, the amount of breast milk available immediately after birth is insufficient or non-existent. In these situations, other therapeutic alternatives such as oral dextrose gel may lower the risk for NICU admissions. Current guidelines continue to be based on expert opinion and weak evidence. However, malpractice litigation related to neurodevelopmental disorders is frequent in children who suffered hypoglycaemia in the neonatal period even if they had other important factors contributing to the poor outcome. This review is aimed to help the practicing paediatricians and neonatologists to comprehend neonatal hypoglycaemia from physiology to therapy, hoping it will result in a rational decision-making process in an area not sufficiently supported by evidence.


2014 ◽  
Vol 30 (6) ◽  
pp. 662-665
Author(s):  
Tomoyuki Ono ◽  
Yusuke Ando ◽  
Koji Fukae ◽  
Takashi Kajiwara ◽  
Masahiro Oe ◽  
...  

PEDIATRICS ◽  
1963 ◽  
Vol 31 (6) ◽  
pp. 946-951
Author(s):  
Samuel O. Sapin ◽  
Leonard M. Linde ◽  
George C. Emmanouilides

Angiocardiography from an umbilical vessel approach was performed in 10 critically sick newborn infants. The umbilical vein route was successfully employed up to the eighth day of life, while the umbilical artery was safely used as late as age 5 days. This approach has advantages over other methods of catheterization and angiocardiography. Angiocardiographic quality was satisfactory for accurate interpretation.


PEDIATRICS ◽  
1952 ◽  
Vol 9 (5) ◽  
pp. 534-543
Author(s):  
LYTT I. GARDNER

Three cases of newborn tetany are described, pointing out the relationship between dietary phosphate load and the manifestations of this disease. An additional three newborn infants are described who showed other symptomatology than tetany in association with dietary phosphate load. [See Table 1 in Source Pdf]. Data concerning diet, cause of death and degree of parathyroid hyperplasia are tabulated in eight newborns who were found to have parathyroid hyperplasia at autopsy. Similar data are tabulated on eight newborns and five older children who were found to have normal parathyroid glands at autopsy. Several other factors possibly involved in newborn tetany and newborn parathyroid hyperplasia are discussed. The importance of measuring serum inorganic P in the differential diagnosis of neonatal distress is pointed out.


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