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Clinical notes

The Journal of Pediatrics December 1978

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Figure. A, The left femoral triangle in the unabducted position. (Adapted from Gray's Anatomy of the Human Body, with permission). B, Technique for greater saphenous vein venipuncture with femoral triangle highlighted. the needle, it is necessary to compress the venipuncture site for several minutes to ensure complete venous stasis. In the authors' experience, this technique was successful in 225 of 300 (75%) attempts with no complications. DISCUSSION The reasons for selecting this particular venipuncture site are several: (I) The size of the greater saphenous vein allows removal of large quantities of blood relatively rapidly. (2) After preparing the skin surface for blood cultures, there is no need to contaminate the skin by palpating for venous location. (3) The possible complications with femoral artery puncture, including thrombosis, arteritis, excessive hemorrhage, and secondary injury to the hip or lower extremity, are avoided." (4) With the sick neonate on a ventilator, in whom the use of external jugular venipuncture is limited or impossible, the greater saphenous vein offers a reliable alternative. (5) Finally, having consistently reproducible anatomic landmarks, repetition of the procedure becomes a simple and a rapid means of venipuncture. David T. Plaxico, M.D. Richard L. Bucciarelli, M.D. Box J 296 Department of Pediatrics University of Florida College of Medicine Gainesville, FL 32610 REFERENCES 1. Gray H: in Goss CM, editor: Anatomy of the human body, ed 29, Philadelphia. 1973, Lea & Febiger Publishers, p 717.

2. Gray H: In Goss CM, editor: Anatomy of the human body, ed 29, Philadelphia, 1973, Lea & Febiger, Publishers, P 656. . .. . 3. Asnes RS, and Arendar OM: Septic arthritis of the hlp: A complication of femoral venipuncture, Pediatrics 38:837, 1966.

Hyponatremia in very low-birth-weight infants and human milk feedings We report two infants of very low-birth-weight who developed low-serum sodium concentration while being fed with human milk. CASE REPORTS Case 1. Patient D.D., a 960 gm infant girl, was born at 26 weeks' gestation. after a pregnancy complicated by severe preecclampsia. The infant developed severe hyaline membrane disease. Because of multiple maternal medications, she was given human milk from a milk bank; transpyloric feedings were begun on the fifth day of life. Although the infant initially gained weight appropriately. at the age of 37 days she was noted to have had no weight gain for several days despite an adequate caloric intake (210 nil/kg/day). Serum sodium concentration was 122 mEgll. Urinary excretion of sodium was I mfiq/l, and of potassium 4 mfiq/l, Sodium chloride, 6 mEq/kg/day, was added to the 0022-3476/78/121026 +02$00.2010

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1978 The C. V. Mosby Co.

Clinical notes

Volume 93 Number 6

feedings. Within three days the serum sodium concentration had returned to normal levels. Sodium supplementation was continued for a total of 17 days. Case 2. Patient B.D., a \,080 gm female infant, was born at 27 weeks' gestation after an uncomplicated pregnancy. The infant developed severe hyaline membrane disease. Transpyloric feedings with her mother's milk were begun on day 7. By age 26 days the infant was gaining 25 gm/day. On the twenty-seventh day she was noted to have an increasing frequency of apneic spells. Serumelectrolyte values were: sodium 110 mEq/l, chloride 73 mllq/l, potassium 5.5 mEq/I, bicarbonate 28 mEq/1. Urine sodium concentration was 19 mEq/l, and potassium IS mEq/1. Serum osmolality was 230 mosmolll, urine osmolality was 143 mosmollJ. She was taking 165 rnl/kg/day of human milk at that time and was receiving theophylline orally for apnea. The infant was initially treated with saline intravenously, then by the addition of sodium chloride to the milk. Three days later the electrolyte values were normal. Sodium supplementation was eventually discontinued. The infant was breast fed for six months and at the age of one year growth and development are normal.

DISCUSSION The usual maintenance intake of2 to 3 mEq/kg/day of sodium chloride is rarely sufficient in the extremely premature infant. Low-birth-weight infants cannot adequately conserve urinary sodium.' As much as 4 to 8 mEq/kg/day may be needed to keep up with sodium needs in these infants.' The sodium content of human milk is approximately 6 mEq/l, much lower than that of most proprietary formulas. A lowbirth-weight infant getting a maximum of 1&0 to 200 mllkg of human milk per day will fail to get maintenance requirements of sodium. Episodic hyponatremia has been reported as a complication of low sodium content formulas.' Although theophyl1ine is a mild diuretic. the role it played in enhancing or producing hyponatremia in our second patient is unclear. Hyponatremia should be added to the short list of possible complications of the feeding of human milk to low-birth-weight infants.' Savitrt P. Kumar, M.D. Staff Neonatologist Department of Pediatrics University of Pennsylvania 271 Administration Building Hospital of the University of Pennsylvania 3400 Spruce St. Philadelphia, PA 19104 Linda M. Sacks. M.D. Fellow in Neonatology Department of Pediatrics University of Pennsylvania

REFERENCES 1. Siegel SR, and Oh W: Renal function as a marker of human 2.

3.

fetal maturation, Acta Paediatr Scand 65:481, 1976. Usher RH: Special problems of the premature infant, in Avery GB, Editor: Neonatology, Philadelphia, 1975, JB Lippincott Company p 178. Roy RN, Chance GW, Radde lC, Hill DE, Willis DM, and Sheepers W: Late hyponatremia in the very low birth

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weight infants « 1.3 kilograms), Pediatr Res 10:516, 1976. 4. Davies DP: Adequacy of expressed breast milk for early growth of pre-term infants, Arch Dis Child 52:296, 1977.

Chorioangioma Of the placenta and intrauterine growth failure Chorioangioma is the most frequent benign tumor of the human placenta and may be present in as many as 1% of all pregnancies.' Numerous compromises of pregnancy including polyhydramnios, premature labor, toxemia, abruptio placenta, fetal cardiac failure, and microangiopathic hemolytic anemia, as well as congenital anomalies, are more frequently observed in pregnancies complicated by chorioangiomas.': 2

CASE REPORT Pregnancy progressed uneventfully and specifically and was not complicated by toxemia, prematurity, or polyhydramnios. A 2,180 gm girl was delivered at term with moderate meconium staining and a nuchal cord; Apgar scores of 7 and 9 were recorded at 1 and 5 minutes, respectively. Three vessels were present in the umbilical cord. The placenta was 19.5 X 17 X 3 em. A 6 em cauliflower-shaped mass was found protruding from the fetal surface of the placenta. The mass was firm on cut section and appeared to arise from a single vascular stalk. Microscopically the peripheral portions of the tumor were composed of small capillary vessels with plump endothelial cells. The central portion of the specimen was much more cellular with only a suggestion of vascular channels. Histologically a diagnosis of chorioangioma of the placenta was made. Changes compatible with toxemia, inflammation, infection, or infarction of the placenta were not present. The neonatal course was unremarkable and physical examination was compatible with that of a term infant. At 22 months of age, she does not have dysmorphic features. The physical examination is normal except for an alternating exotropia. Height (73 ern) is at the tenth percentile. Weight (6.4 kg) and head circumference (43 em) have been parallel to, but below, the third percentile. Psychologic and neurologic development are delayed to approximately the eight-month level. Laboratory studies were normal.

DISCUSSION Pregnancies complicated by chorioangioma of the placenta more frequently end with low-birth-weight infants'? and other pregnancy complications, particularly if lesions of 5 em or greater are present.' Benson and Joseph' suggested that shunting of placental blood through the chorioangioma was the central pathogenetic error created by this lesion. Certainly infants from such pregnancies with cardiomegaly, cardiac failure, hydrops fetalls, or even fetal death may be explained by this mechanism. Supported by a grant for a clinical Genetics Program (lOH 820004 08) and a Mental Retardation Training Program (No. 920) from the National Institutes of Health. 0022-34761781121027+02$00.20/0

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1978 The C. V. Mosby Co.

Hyponatremia in very low-birth-weight infants and human milk feedings.

1026 Clinical notes The Journal of Pediatrics December 1978 SII/l"r{rrtt/! iliac "i':'!'' ';!--+- c/rculllf/cx ccucu r--';W:O:t-~-llItIClIf Figure...
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