Hyperviscosity Syndrome Associated With Necrotizing Enterocolitis Rosemary D. Leake, MD; Basil Thanopoulos, MD; Roberta Nieberg,
\s=b\ 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 Child 129:1192-1194, 1975)
Although
a
few
MD
sporadic
case re-
ports had appeared linking in¬ dividual symptoms with high hemato-
Xi
crit values, Baum1 was the first to examine the overall problem of hy¬ perviscosity secondary to increased red blood cell mass in the newborn pe¬ riod. With the development of an ac¬
viscometer,- syndromes in in¬ fants and adults'" have been defined. The symptom complex for infants includes plethora, respiratory dis¬
curate
tress, hypoglycemia, hyperbilirubin¬
emia, lethargy, seizures, jitteriness, and thrombocytopenia.7 Coagulation defects have been described." Cardiomegaly and cyanosis occur com¬ monly." The case of a newborn infant with gangrene of an extremity sec¬ ondary to hyperviscosity has been re¬
ported.10 No previous reports have linked hy¬ perviscosity with necrotizing entero¬ colitis (NEC). We are, therefore, presenting the case of a newborn, presumed to be the infant of a dia¬ betic mother, with verified hyper¬ viscosity, islet cell hypertrophy, hy-
Received for publication July 23, 1974; acNov 26. From the departments of pediatrics (Drs. Leake and Thanopoulos) and pathology (Dr. Nieberg), University of California at Los Angeles School of Medicine, Harbor General Hospital, Torrance. Reprint requests to Department of Pediatrics, Harbor General Hospital, 1000 W Carson St, Torrance, CA 90509 (Dr. Leake).
cepted
perinsulinemia, hypoglycemia, and NEC. REPORT OF A CASE A baby was the product of the full-term pregnancy of a gravida 2, para 1, O-positive, Coombs-negative, 37-year-old mother whose mother and sister had insulin-de¬ pendent diabetes. Birth weight of the mother's previous baby was 4,082 gm (9.0 lb). The mother received prenatal care from the fourth month of pregnancy on¬ ward. No glucosuria was noted during the pregnancy; however, a glucose tolerance test was not performed. The only maternal medication administered during preg¬ nancy was a thiazide for chronic hyperten¬ sion. Spontaneous rupture of membranes occurred 18 hours before delivery. Fetal monitoring showed no abnormal patterns. First stage of labor was 12 hours; second stage was 17 minutes. Medications given during labor were meperidine (Demerol)
hydrochloride, promethazine hydrochloride (Phenergan), and oxytocin. Delivery was spontaneous. Birth weight was 2,835 gm (6.2 lb). Cord clamping was accomplished within 15 seconds of delivery. One-minute Apgar score was 9. Initial physical exami¬ nation disclosed plethora and slight meco¬ nium staining. Results of laboratory studies during the first 19 hours of life included the following: cord hemoglobin level, 18.6 gm/100 ml; hematocrit value, 57%; peripheral hemoglo¬ bin level at 11 hours of age, 28 gm/100 ml, and hematocrit value, 83%. Platelet count 87,000/cu mm. Serum bilirubin level mg/100 ml, and calcium level was 6.6 mg/100 ml. Chest roentgenogram
was
was
9.9
Downloaded From: http://archpedi.jamanetwork.com/ by a UNIVERSITY OF ADELAIDE LIBRARY User on 09/18/2017
showed diffuse cardiomegaly and changes consistent with mild meconium aspiration. The infant was transferred to Harbor General Hospital at 19 hours of age be¬ cause of increasing jitteriness and periph¬ eral cyanosis. An umbilical venous catheter was inserted for partial exchange transfu¬ sion. An abdominal x-ray film taken imme¬ diately after catheter placement showed the catheter to be at the level of the dia¬ phragm and the presence of widespread pneumatosis intestinalis without portal venous gas. Umbilical venous samples for determination of hematocrit value and vis¬ cosity were obtained. Dextrose, 1 gm/kg, in a 50% solution was infused for two min¬ utes via the umbilical venous catheter. Twenty minutes following the glucose bolus, a plasma sample was drawn for in¬ sulin assay; 25 ml plasma was substituted for an equal volume of whole blood as a partial exchange transfusion, the umbilical catheter was removed, and an infusion of 10% dextrose in water was begun in a pe¬ ripheral vein. Laboratory data at Harbor General Hos¬ pital included a blood glucose level on ad¬ mission of 0 mg/100 ml, using a glucose oxidase method (Dextrostix). Central venous hematocrit reading was 75% prior to the exchange transfusion and 58% two hours following the partial exchange transfusion. Insulin level, determined by the method of Morgan and Lazarow, was 52uU/ml (mean ± SE 19 ± 2.9 for seven full-term, healthy infants 20 minutes after an identical glucose bolus). Viscosity, measured at 37 C by microcone-plate viscometer within 20 minutes of sampling =
(from a free-flowing venous site), was 31, 23, 15, 9, and 5 centipoises at a shear rate of 22.5, 45, 90, 225, and 450 per second, re¬ spectively (greater than 2 SD from nor¬ mal). Bacterial cultures of cerebrospinal fluid, blood, urine, nasopharynx, and cathe¬ ter tip specimens proved sterile. A fecal
specimen was inoculated into cell cultures of rhesus monkey kidney, HeLa, and Wl38 (human fibroblast); no virus was isolated. Repeated abdominal roentgenograms at 29 hours of age showed air in the portal venous system and pneumatosis intestinalis. Despite bowel rest, nasogastric drainage of bile-stained fluid, intra¬ venous ampicillin sodium and intramuscu¬ lar kanamycin sulfate therapy, the infant became distended and anurie, and passed grossly bloody stools. He died at 52 hours. Postmortem examination disclosed necro¬ tizing enterocolitis involving the ileum and large bowel. On microscopic examination, patchy zones of acute transmural colitis were noted, more severe in the large bowel. Associated with these extensive zones of inflammation were foci of pneumatosis in-
testinalis. The air was seen in the subserosal tissues. Although bowel specimens were not cultured for pathogens, Gram stain for invasive bacteria, including clostridia, was unremarkable. Occasional gan¬ glion cells were seen in Auerbach plexus; these appeared shrunken and pyknotic, possibly as a consequence of hypoxia. Submucosal hemorrhage was noted in both large and small bowel sections, while the latter had foci of extensive intramural hemorrhage. The adjacent mesenteric ves¬ sels were severely dilated and congested with a scattering of acute inflammatory cells seen in the surrounding adipose tis¬ sue. Minute foci of hemorrhage were noted in most organs, while extensive hemor¬ rhage occurred in the lungs and adrenals. Microscopic examination of the brain showed no abnormalities. No evidence of large vessel thrombosis was seen. Special stains for detection of fibrin thrombi were unremarkable; hence there was no histo¬ logie evidence of disseminated intravascular coagulopathy. An additional finding was hyperplasia of the islets of Langer¬ hans.
COMMENT
Although many cases of hypervis¬ cosity are unexplained, the singleton infants most commonly affected are
diabetic progeny,11 infants with tri¬ somy syndromes,'2 and infants with intrauterine growth retardation.13 Twin-to-twin transfusion syndromes occur as well,11 and maternal-to-in¬ fant transfusions are noted occasion¬ ally. 1· > Our newborn was most likely the infant of a prediabetic mother, in view of the maternal family history, beta cell hypertrophy, hyperinsulinism, and hypoglycemia. Our infant had the usual signs of NEC—a "septic" appearance, leth¬ argy, abdominal distention, and bloody stools. Classic roentgen¬
ographic findings
were
present
at 19
hours of age, whereas the usual onset is the second to 60th day of life."'' Fur¬ thermore, this was a full-term infant, whereas most cases occur in prema¬ ture infants.17 The presence of thrombocytopenia in nine of 16 patients with NEC has been reported.1* Our infant had thrombocytopenia and widespread pulmonary and adrenal hemorrhages, but died before further hématologie studies were obtained. Hypoglycemia occurs in one third
of hyperviscous infants,7 but no previ¬ ous reports have linked hyper¬ viscosity with NEC. With the microcone-plate viscometer, the torque produced by a small sample of blood (0.5 ml) rotated at various speeds can be analyzed. In this case, severe hy¬ perviscosity was noted. Although the cause of NEC has not yet been elucidated, current thought suggests an ischemie basis for the le¬ sions. Hyperviscosity, coupled with the poor microcirculation of the mes¬ enteric vascular bed, an area of end arterioles with very limited collateral supply, might have led to hypoxic tis¬ sue changes in the bowel wall and re¬ sultant NEC. Such nonocclusive is¬ chemie changes in the mesentery have been reported in adult patients with high hematocrit readings.19 Other factors could contribute to the development of NEC. Thrombosis of the mesenteric vessels can lead to an NEC-like picture."1 Also, NEC has been linked to Hirschsprung disease,1" some types of bowel obstruction, and exchange transfusions.-"·'-' Infectious agents have been described.18 Patent ductus arteriosus at times produces a reduction in systemic cardiac output and NEC." In the neonatal piglet, as¬ phyxia has been shown to decrease mesenteric perfusion by 35% in the proximal part of the colon and by 50% in the distal part of the jejunum, and to produce a picture of focal hemor¬ rhage and vascular engorgement not unlike that found in NEC." Oral for¬ mula feedings have been postulated as a precipitating factor.24 Our infant, however, had no evi¬ dence for any of these mechanisms. There were no thromboses, asphyxie episodes, or infectious agents. No pat¬ ent ductus was identified. Ganglion cells were present throughout the co¬ lon, thus eliminating the possibility of Hirschsprung disease. No oral feedings were given to the infant. He did undergo partial exchange trans¬ fusion when the hyperviscous state was identified, but widespread pneu¬ matosis intestinalis was present prior to transfusion. This abnormal finding persisted in the same area of the bowel throughout the next 24 hours, making the iatrogenic introduction of air at the time of catheterization un-
Downloaded From: http://archpedi.jamanetwork.com/ by a UNIVERSITY OF ADELAIDE LIBRARY User on 09/18/2017
likely and the diagnosis of NEC prob¬ able. Postmortem findings confirmed widespread intestinal involvement
with NEC. This case is presented in the hope that we may alert others to the possi¬ bility that the mesenteric circulation can be compromised in the neonatal
hyperviscosity syndrome. Early inter¬ vention in the face of a very high hematocrit reading may be indi¬ cated.
Nonproprietary Names and Trademarks of Drugs Oxytocin—Pitocin, Syntocinon, Uteracon. Ampicillin sodium—Alpen-N, Amcill-S, Omnipen-N.
Dr. Thanopoulos is supported by Investigative Group Research Support grant (470)G3 from the Los Angeles Heart Association.
References
Hyperviscous blood and perinatal Pediatr Res 1:288-290, 1967. 2. Wells RE, Denton R, Merrill EW: Measurement of viscosity of biologic fluids by cone plate viscometer. J Lab Clin Med 57:646-656, 1961. 3. Wells R: Syndromes of hyperviscosity. N Engl J Med 283:183-186, 1970. 4. Gatte RA, Muster A, Cole R, et al: Neonatal polycythemia with transient cyanosis and cardiorespiratory abnormalities. J Pediatr 69:10631072, 1966. 5. Kontras SB: Polycythemia and hyperviscosity syndromes. Pediatr Clin North Am 19:919-933, 1972. 6. MacKintosh TF, Walker CH: Blood viscosity in the newborn. Arch Dis Child 48:547-553, 1973. 7. Gross GP, Hathaway WE, McGaughey HR: Neonatal hyperviscosity in the neonate. J Pediatr 82:1004-1012, 1973. 8. Komp DM, Sparrow AW: Polycythemia in cyanotic heart disease: A study of altered coagulation. J Pediatr 76:231-236, 1970. 9. Wood JL: Plethora in the newborn infant associated with cyanosis and convulsions: A review of postnatal erythropoiesis. J Pediatr 1. Baum RS:
pathology.
54:143-151, 1959.
10. Papageorgiou A, Stern L: Polycythemia and gangrene of an extremity in a newborn infant. J Pediatr 81:985-987, 1972. 11. Pildes RS: Infants of diabetic mothers. N Engl J Med 289:902-904, 1973. 12. Lappalainen J, Kouvalainen K: High hematocrits in newborns with Down's syndrome. Clin Pediatr 11:472-474, 1972. 13. Humbert JR, Abelson H, Hathaway EE, et al: Polycythemia in small for gestational age infants. J Pediatr 75:812-819, 1969. 14. Minkowsky A: Acute cardiac failure in connection with neonatal polycythemia in monovular twins and single newborn infants. Biol Neonate 4:61-74, 1962. 15. Michael AF Jr, Mauer AM: Maternal-fetal transfusion as a cause of plethora in the neonatal period. Pediatrics 28:458-461, 1961. 16. Bell RS, Graham CB, Stevenson JK: Roentgenologic and clinical manifestations of neonatal necrotizing enterocolitis. Am J Roentgenol Radium Ther Nucl Med 112:123-134,1971. 17. Hopkins GB, Gould VE, Stevenson JK, et al: Necrotizing enterocolitis in premature infants: A clinical and pathologic evaluation of au-
Advice From
a
topsy material. Am J Dis Child 120:229-232,
1970. 18. Wilson SE, Woolley MM: Primary necrotizing enterocolitis in infants. Arch Surg 99:563\x=req-\ 566, 1969. 19. Fogarty TJ, Fletcher WS: Genesis of nonocclusive mesenteric ischemia. Am J Surg 111:130-137, 1966. 20. Orme RE, Eades SM: Perforation of bowel in newborn as complication of exchange transfusion. Br Med J 4:349-351, 1968. 21. Touloukian RJ, Berdon WE, Amoury RA, et al: Surgical experience with necrotizing enterocolitis in infants. J Pediatr Surg 2:389-401,1967. 22. Kitterman JA, Phibbs RH, deLorimier AA: Necrotizing enterocolitis: Evidence for ischemia as the cause. Clin Res 22:241A, 1974. 23. Touloukian RJ, Posch JN, Spencer R: The pathogenesis of ischemic gastroenterocolitis of the neonate: Selective gut mucosal ischemia in asphyxiated neonatal piglets. J Pediatr Surg 7:194-205, 1972. 24. Book LS, Herbst JJ, Jung AL: Necrotizing enterocolitis in infants fed an elemental formula. Pediatr Res 8:105, 1974.
Successful Author
'The main rule of a writer is never to pity your manuscript. If you see something is good, throw it away and begin again. A lot of writers have failed because they have too much pity. They have already worked so much, they cannot just throw it away. But I say that the wastepaper basket is a writer's best friend. My wastepaper basket is on a steady diet.' "
no
"
Isaac Bashevis Singer
Reprinted
from Reichek MA:
Storyteller.
The New York Times
Magazine,
March 23, 1975, pp 16-33.
Downloaded From: http://archpedi.jamanetwork.com/ by a UNIVERSITY OF ADELAIDE LIBRARY User on 09/18/2017
\s=b\ 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 Child 129:1192-1194, 1975)
Although
a
few
MD
sporadic
case re-
ports had appeared linking in¬ dividual symptoms with high hemato-
Xi
crit values, Baum1 was the first to examine the overall problem of hy¬ perviscosity secondary to increased red blood cell mass in the newborn pe¬ riod. With the development of an ac¬
viscometer,- syndromes in in¬ fants and adults'" have been defined. The symptom complex for infants includes plethora, respiratory dis¬
curate
tress, hypoglycemia, hyperbilirubin¬
emia, lethargy, seizures, jitteriness, and thrombocytopenia.7 Coagulation defects have been described." Cardiomegaly and cyanosis occur com¬ monly." The case of a newborn infant with gangrene of an extremity sec¬ ondary to hyperviscosity has been re¬
ported.10 No previous reports have linked hy¬ perviscosity with necrotizing entero¬ colitis (NEC). We are, therefore, presenting the case of a newborn, presumed to be the infant of a dia¬ betic mother, with verified hyper¬ viscosity, islet cell hypertrophy, hy-
Received for publication July 23, 1974; acNov 26. From the departments of pediatrics (Drs. Leake and Thanopoulos) and pathology (Dr. Nieberg), University of California at Los Angeles School of Medicine, Harbor General Hospital, Torrance. Reprint requests to Department of Pediatrics, Harbor General Hospital, 1000 W Carson St, Torrance, CA 90509 (Dr. Leake).
cepted
perinsulinemia, hypoglycemia, and NEC. REPORT OF A CASE A baby was the product of the full-term pregnancy of a gravida 2, para 1, O-positive, Coombs-negative, 37-year-old mother whose mother and sister had insulin-de¬ pendent diabetes. Birth weight of the mother's previous baby was 4,082 gm (9.0 lb). The mother received prenatal care from the fourth month of pregnancy on¬ ward. No glucosuria was noted during the pregnancy; however, a glucose tolerance test was not performed. The only maternal medication administered during preg¬ nancy was a thiazide for chronic hyperten¬ sion. Spontaneous rupture of membranes occurred 18 hours before delivery. Fetal monitoring showed no abnormal patterns. First stage of labor was 12 hours; second stage was 17 minutes. Medications given during labor were meperidine (Demerol)
hydrochloride, promethazine hydrochloride (Phenergan), and oxytocin. Delivery was spontaneous. Birth weight was 2,835 gm (6.2 lb). Cord clamping was accomplished within 15 seconds of delivery. One-minute Apgar score was 9. Initial physical exami¬ nation disclosed plethora and slight meco¬ nium staining. Results of laboratory studies during the first 19 hours of life included the following: cord hemoglobin level, 18.6 gm/100 ml; hematocrit value, 57%; peripheral hemoglo¬ bin level at 11 hours of age, 28 gm/100 ml, and hematocrit value, 83%. Platelet count 87,000/cu mm. Serum bilirubin level mg/100 ml, and calcium level was 6.6 mg/100 ml. Chest roentgenogram
was
was
9.9
Downloaded From: http://archpedi.jamanetwork.com/ by a UNIVERSITY OF ADELAIDE LIBRARY User on 09/18/2017
showed diffuse cardiomegaly and changes consistent with mild meconium aspiration. The infant was transferred to Harbor General Hospital at 19 hours of age be¬ cause of increasing jitteriness and periph¬ eral cyanosis. An umbilical venous catheter was inserted for partial exchange transfu¬ sion. An abdominal x-ray film taken imme¬ diately after catheter placement showed the catheter to be at the level of the dia¬ phragm and the presence of widespread pneumatosis intestinalis without portal venous gas. Umbilical venous samples for determination of hematocrit value and vis¬ cosity were obtained. Dextrose, 1 gm/kg, in a 50% solution was infused for two min¬ utes via the umbilical venous catheter. Twenty minutes following the glucose bolus, a plasma sample was drawn for in¬ sulin assay; 25 ml plasma was substituted for an equal volume of whole blood as a partial exchange transfusion, the umbilical catheter was removed, and an infusion of 10% dextrose in water was begun in a pe¬ ripheral vein. Laboratory data at Harbor General Hos¬ pital included a blood glucose level on ad¬ mission of 0 mg/100 ml, using a glucose oxidase method (Dextrostix). Central venous hematocrit reading was 75% prior to the exchange transfusion and 58% two hours following the partial exchange transfusion. Insulin level, determined by the method of Morgan and Lazarow, was 52uU/ml (mean ± SE 19 ± 2.9 for seven full-term, healthy infants 20 minutes after an identical glucose bolus). Viscosity, measured at 37 C by microcone-plate viscometer within 20 minutes of sampling =
(from a free-flowing venous site), was 31, 23, 15, 9, and 5 centipoises at a shear rate of 22.5, 45, 90, 225, and 450 per second, re¬ spectively (greater than 2 SD from nor¬ mal). Bacterial cultures of cerebrospinal fluid, blood, urine, nasopharynx, and cathe¬ ter tip specimens proved sterile. A fecal
specimen was inoculated into cell cultures of rhesus monkey kidney, HeLa, and Wl38 (human fibroblast); no virus was isolated. Repeated abdominal roentgenograms at 29 hours of age showed air in the portal venous system and pneumatosis intestinalis. Despite bowel rest, nasogastric drainage of bile-stained fluid, intra¬ venous ampicillin sodium and intramuscu¬ lar kanamycin sulfate therapy, the infant became distended and anurie, and passed grossly bloody stools. He died at 52 hours. Postmortem examination disclosed necro¬ tizing enterocolitis involving the ileum and large bowel. On microscopic examination, patchy zones of acute transmural colitis were noted, more severe in the large bowel. Associated with these extensive zones of inflammation were foci of pneumatosis in-
testinalis. The air was seen in the subserosal tissues. Although bowel specimens were not cultured for pathogens, Gram stain for invasive bacteria, including clostridia, was unremarkable. Occasional gan¬ glion cells were seen in Auerbach plexus; these appeared shrunken and pyknotic, possibly as a consequence of hypoxia. Submucosal hemorrhage was noted in both large and small bowel sections, while the latter had foci of extensive intramural hemorrhage. The adjacent mesenteric ves¬ sels were severely dilated and congested with a scattering of acute inflammatory cells seen in the surrounding adipose tis¬ sue. Minute foci of hemorrhage were noted in most organs, while extensive hemor¬ rhage occurred in the lungs and adrenals. Microscopic examination of the brain showed no abnormalities. No evidence of large vessel thrombosis was seen. Special stains for detection of fibrin thrombi were unremarkable; hence there was no histo¬ logie evidence of disseminated intravascular coagulopathy. An additional finding was hyperplasia of the islets of Langer¬ hans.
COMMENT
Although many cases of hypervis¬ cosity are unexplained, the singleton infants most commonly affected are
diabetic progeny,11 infants with tri¬ somy syndromes,'2 and infants with intrauterine growth retardation.13 Twin-to-twin transfusion syndromes occur as well,11 and maternal-to-in¬ fant transfusions are noted occasion¬ ally. 1· > Our newborn was most likely the infant of a prediabetic mother, in view of the maternal family history, beta cell hypertrophy, hyperinsulinism, and hypoglycemia. Our infant had the usual signs of NEC—a "septic" appearance, leth¬ argy, abdominal distention, and bloody stools. Classic roentgen¬
ographic findings
were
present
at 19
hours of age, whereas the usual onset is the second to 60th day of life."'' Fur¬ thermore, this was a full-term infant, whereas most cases occur in prema¬ ture infants.17 The presence of thrombocytopenia in nine of 16 patients with NEC has been reported.1* Our infant had thrombocytopenia and widespread pulmonary and adrenal hemorrhages, but died before further hématologie studies were obtained. Hypoglycemia occurs in one third
of hyperviscous infants,7 but no previ¬ ous reports have linked hyper¬ viscosity with NEC. With the microcone-plate viscometer, the torque produced by a small sample of blood (0.5 ml) rotated at various speeds can be analyzed. In this case, severe hy¬ perviscosity was noted. Although the cause of NEC has not yet been elucidated, current thought suggests an ischemie basis for the le¬ sions. Hyperviscosity, coupled with the poor microcirculation of the mes¬ enteric vascular bed, an area of end arterioles with very limited collateral supply, might have led to hypoxic tis¬ sue changes in the bowel wall and re¬ sultant NEC. Such nonocclusive is¬ chemie changes in the mesentery have been reported in adult patients with high hematocrit readings.19 Other factors could contribute to the development of NEC. Thrombosis of the mesenteric vessels can lead to an NEC-like picture."1 Also, NEC has been linked to Hirschsprung disease,1" some types of bowel obstruction, and exchange transfusions.-"·'-' Infectious agents have been described.18 Patent ductus arteriosus at times produces a reduction in systemic cardiac output and NEC." In the neonatal piglet, as¬ phyxia has been shown to decrease mesenteric perfusion by 35% in the proximal part of the colon and by 50% in the distal part of the jejunum, and to produce a picture of focal hemor¬ rhage and vascular engorgement not unlike that found in NEC." Oral for¬ mula feedings have been postulated as a precipitating factor.24 Our infant, however, had no evi¬ dence for any of these mechanisms. There were no thromboses, asphyxie episodes, or infectious agents. No pat¬ ent ductus was identified. Ganglion cells were present throughout the co¬ lon, thus eliminating the possibility of Hirschsprung disease. No oral feedings were given to the infant. He did undergo partial exchange trans¬ fusion when the hyperviscous state was identified, but widespread pneu¬ matosis intestinalis was present prior to transfusion. This abnormal finding persisted in the same area of the bowel throughout the next 24 hours, making the iatrogenic introduction of air at the time of catheterization un-
Downloaded From: http://archpedi.jamanetwork.com/ by a UNIVERSITY OF ADELAIDE LIBRARY User on 09/18/2017
likely and the diagnosis of NEC prob¬ able. Postmortem findings confirmed widespread intestinal involvement
with NEC. This case is presented in the hope that we may alert others to the possi¬ bility that the mesenteric circulation can be compromised in the neonatal
hyperviscosity syndrome. Early inter¬ vention in the face of a very high hematocrit reading may be indi¬ cated.
Nonproprietary Names and Trademarks of Drugs Oxytocin—Pitocin, Syntocinon, Uteracon. Ampicillin sodium—Alpen-N, Amcill-S, Omnipen-N.
Dr. Thanopoulos is supported by Investigative Group Research Support grant (470)G3 from the Los Angeles Heart Association.
References
Hyperviscous blood and perinatal Pediatr Res 1:288-290, 1967. 2. Wells RE, Denton R, Merrill EW: Measurement of viscosity of biologic fluids by cone plate viscometer. J Lab Clin Med 57:646-656, 1961. 3. Wells R: Syndromes of hyperviscosity. N Engl J Med 283:183-186, 1970. 4. Gatte RA, Muster A, Cole R, et al: Neonatal polycythemia with transient cyanosis and cardiorespiratory abnormalities. J Pediatr 69:10631072, 1966. 5. Kontras SB: Polycythemia and hyperviscosity syndromes. Pediatr Clin North Am 19:919-933, 1972. 6. MacKintosh TF, Walker CH: Blood viscosity in the newborn. Arch Dis Child 48:547-553, 1973. 7. Gross GP, Hathaway WE, McGaughey HR: Neonatal hyperviscosity in the neonate. J Pediatr 82:1004-1012, 1973. 8. Komp DM, Sparrow AW: Polycythemia in cyanotic heart disease: A study of altered coagulation. J Pediatr 76:231-236, 1970. 9. Wood JL: Plethora in the newborn infant associated with cyanosis and convulsions: A review of postnatal erythropoiesis. J Pediatr 1. Baum RS:
pathology.
54:143-151, 1959.
10. Papageorgiou A, Stern L: Polycythemia and gangrene of an extremity in a newborn infant. J Pediatr 81:985-987, 1972. 11. Pildes RS: Infants of diabetic mothers. N Engl J Med 289:902-904, 1973. 12. Lappalainen J, Kouvalainen K: High hematocrits in newborns with Down's syndrome. Clin Pediatr 11:472-474, 1972. 13. Humbert JR, Abelson H, Hathaway EE, et al: Polycythemia in small for gestational age infants. J Pediatr 75:812-819, 1969. 14. Minkowsky A: Acute cardiac failure in connection with neonatal polycythemia in monovular twins and single newborn infants. Biol Neonate 4:61-74, 1962. 15. Michael AF Jr, Mauer AM: Maternal-fetal transfusion as a cause of plethora in the neonatal period. Pediatrics 28:458-461, 1961. 16. Bell RS, Graham CB, Stevenson JK: Roentgenologic and clinical manifestations of neonatal necrotizing enterocolitis. Am J Roentgenol Radium Ther Nucl Med 112:123-134,1971. 17. Hopkins GB, Gould VE, Stevenson JK, et al: Necrotizing enterocolitis in premature infants: A clinical and pathologic evaluation of au-
Advice From
a
topsy material. Am J Dis Child 120:229-232,
1970. 18. Wilson SE, Woolley MM: Primary necrotizing enterocolitis in infants. Arch Surg 99:563\x=req-\ 566, 1969. 19. Fogarty TJ, Fletcher WS: Genesis of nonocclusive mesenteric ischemia. Am J Surg 111:130-137, 1966. 20. Orme RE, Eades SM: Perforation of bowel in newborn as complication of exchange transfusion. Br Med J 4:349-351, 1968. 21. Touloukian RJ, Berdon WE, Amoury RA, et al: Surgical experience with necrotizing enterocolitis in infants. J Pediatr Surg 2:389-401,1967. 22. Kitterman JA, Phibbs RH, deLorimier AA: Necrotizing enterocolitis: Evidence for ischemia as the cause. Clin Res 22:241A, 1974. 23. Touloukian RJ, Posch JN, Spencer R: The pathogenesis of ischemic gastroenterocolitis of the neonate: Selective gut mucosal ischemia in asphyxiated neonatal piglets. J Pediatr Surg 7:194-205, 1972. 24. Book LS, Herbst JJ, Jung AL: Necrotizing enterocolitis in infants fed an elemental formula. Pediatr Res 8:105, 1974.
Successful Author
'The main rule of a writer is never to pity your manuscript. If you see something is good, throw it away and begin again. A lot of writers have failed because they have too much pity. They have already worked so much, they cannot just throw it away. But I say that the wastepaper basket is a writer's best friend. My wastepaper basket is on a steady diet.' "
no
"
Isaac Bashevis Singer
Reprinted
from Reichek MA:
Storyteller.
The New York Times
Magazine,
March 23, 1975, pp 16-33.
Downloaded From: http://archpedi.jamanetwork.com/ by a UNIVERSITY OF ADELAIDE LIBRARY User on 09/18/2017
