DISSEMINATED INTRAVASCULAR COAGULATION

IN THE NEWBORN
William E. Hathaway, M.D., Marilyn M. Mull, M.D., and Giselle S. Pechet, M.D.
Departments of Ped#{252}itrics and Pathology, Universitj of Colorado Medical Center, Denver, Colorado

ABSTRACT. Eleven of 19 sick newborn infants without evidence of DIC. Diagnosis of DIC in the
were shown to have either laboratory and/or newborn is best made by reliance upon specific
pathologic evidence of disseminated intravascular clotting factor assays (platelets, fibrinogen, and
coagulation (DIC ) during an observation period of factors V and VIII ) rather than nonspecific screen-
8 months. Three
of the affected infants had severe ing tests or presence of fibrin degradation prod-
viral diseases ( rubella, cytomegalic inclusion virus, ucts. DIC may be a more common complication of
and herpes simplex). Seven of the infants had se- severely ifi newborn infants than is generally real-
vere idiopathic respiratory distress syndrome ized. Pediatrics, 43:233, 1969, NEWBORN INFANTS,
(IRDS ), and one infant (the product of a severely INTRAVASCULAR COAGULATION, RESPIRATORY DIS-

toxemic mother ) had transient respiratory distress. TRESS SYNDROME, DEFIBRINATION SYNDROME, NEW-

The remainder of the sick infants had mild IRDS BORN DISEASES.

D ISSEMINATED intravascular coagulation sures were studied for derangements of the

( DIC ) has been documented as an coagulation and hemostatic mechanism.
intermediate pathologic mechanism in The diagnosis of idiopathic respiratory cbs-
many children’s diseases. These disorders tress syndrome (IRDS) was established by
include bacterial infections,1 viral diseases,’ clinical and laboratory data which included
cancer,’ hemolytic-uremic syndrome,4 pur- Silverman scoring, blood gas and pH deter-
pura fulminans,’ and giant hemangiomata.6 minations, and chest films. Treatment for
Defibrination syndrome7 and pathologic this disorder in this nursery consists of (1)
evidence of fibnn thromboembolism’ have oxygen therapy and assisted ventilation as
been described in newborn infants who indicated to keep the arterial P02 and pCO2
did not have any of the above diseases. near the normal range; (2) intravenous
Two recent case reports suggested that glucose in water with added sodium bicar-
DIC has been rarely described in the neo- bonate to correct the base deficit as deter-
natal period.9’10 Prompted by these reports mined by the Astrup nomogram; (3) anti-
and the current interest in DIC, the follow- biotic therapy, usually with penicillin and
ing preliminary clinical and pathologic ob- kanamycin; and (4) other supportive care
servations from our experience with DIC in as needed. All infants received vitamin K,
the neonatal period are presented. oxide ( 1 mg) intramuscularly. Infants had
initial blood, nasopharyngeal, and stool cul-
MATERIALS AND METHODS
tures. No bacterial pathogens were isolated
During the past 8 months sick infants ad- in any of the study infants.
mitted to the University of Colorado Medi- In addition, 20 normal, full-term and 20
cal Center intensive care nursery who sur- normal, premature infants were studied
vived longer than 4 hours and who had during the first 48 hours of life (blood ob-
umbilical venous and arterial catheters in- tamed by venipuncture).
serted for diagnostic and therapeutic mea- Whenever possible the following studies

(Received May 22; revision accepted for publication September 5, 1968.)

Supported by grants from the Easter Seal Research Foundation and the U.S. Public Health Service
( #HD 01965-02).
G.S.P. is a Clinical
Investigator of the Veteran’s Administration.
ADDRESS: Department of Pediatrics, University of Colorado Medical Center, 4200 East Ninth Avenue,
Denver, Colorado 80220.

PEDIATRICS, Vol. 43, No. 2, February 1969

233

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234 IV. COAGULATION

TABLE I
CLINICAL AND LABORATORY FINDINGS IN STUDY INFANTS

Thrombelastogram
Birth Weight Platelet B.T.
Case Number Age Sex Diagnosis
(ym) Count (mm) r+k Ma
(mm) (mm)

Normal adult 200,000- 10.5-1 30-60

450,000
0 infants <4 hr term normal full term 200,000- *54 11-16.5 50-61
400,000
0 infants <24 hr I ,500-,500 normal premature 2-6 8-16 37-58
10 da M disseminated herpes 62,500 no clot no clot
infection >30
0 hr M 990 rubella syndrome 2,500 >30 >120 10
3 6 hr ,90 cytomegalic inclu- 11,000 >30
sion disease 50
4 14 hr F 1,470 severe IRDS 57,000 134
5 3 hr M 1,640 severe IRDS low5 16 52
6 14 hr M I ,630 severe IRDS 100,000 9
7 3 hr F 1,390 severe IRDS 375,000 18l 42
0 hr 260,000 54 184
8 4 hr M I ,90 severe IRDS; intra- 187,500 3 15 44
cranial bleed
9 0 hr M ,350 severe IRDS low5 10 17 48
10 0 hr M 1,600 severe IRDS 250,000 16l 28
11 6 hr F 1,470 mild IRDS; abruptio 57,000 74 224 22
placenta
3 hr M ,900 mild IRDS 280,000 4 11
13 18 hr F ,360 mild IRDS 250,000 15 51
14 1 hr M ,660 mild IRDS 230,000 44 1 52
15 18 hr M ,900 suspected intra- 245,000 4
uterine infection
16 hr F 1,250 neonatal asphyxia Average 34 13 60
17 1 hr F 1,410 mild IRDS 20.2,500 3 214 40
18 10 hr M 2,270 mild IRDS 179,000 44
19 16 hr M 1,400 prolonged apneic 150,000 64
spells

B.T. =bleeding time. Low indicates decreased platelets on peripheral blood smear.

were done on venous blood obtained in an from the first syringe ( two-syringe tech-
amount of 0.1 M sodium citrate anticoagu- nique) was collected in a proteinase inhibi-
lant determined according to the hemato- tor (Trasylol) and thrombinized. The
cnt: ( 1 ) thrombelastogram (TEG), (2) serum obtained was assayed for fibrin split
one-stage prothrombin time (PT), (3) kao- products ( FSP) by a quantitative precipi-
lin partial thromboplastin time (PTT),11 tin technique after Claman and Merrill;15
( 4 ) factor VIII ( antihemophilic factor) the agar contained rabbit antifibrinogen an-
assay according to P001,12 (5) factor V tisera instead of anti-immunoglobulins.
( proaccelerin) assay according to Borch- The autopsies of infants who died were
grevinck and others,” and (6) fibrinogen reviewed by one of us ( G.P. ) for evidence
determination according to Ratnoff and of ante mortem fibrin depositions, micro-
Menzie.14 In addition, bleeding times ( Ivy) thrombi, and hemorrhages. In addition to
and phase platelet counts were done. Blood routine hematoxylin and eosin histologic

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 ARTICLES 235

staining, PAS, and PTAH stains were used dence for a severe consumption coagulopa-
when indicated. thy, including low platelets, low fibrinogen,
and low factors V and VIII. By histologic
RESULTS
examination, both infants showed evidence
Tables I and II summarize the results of of fibrin thrombi (Fig. 1 and 2) as well as
the clinical and pathologic findings in the diffuse hemorrhagic lesions. The in
findings
infants studied. The range of values for the Case 3 were equivocal. Platelets were low;
coagulation tests in the normal full-term fibrinogen and factor V were only slightly
and premature infants are also shown in low; factor VIII was elevated; thrombin
Table I. Cases 1 and 2 had excellent cvi- time was 28 seconds (normal 7 to 9 sec-

TABLE II
LABORATORY AND PATHOLOGIC FINDINGS IN STUDY INFANTS

F SP Factor
Case PT PTT Factor Factor
(mg/1 (mg/100 Pathological Findings
Number (see) (see) V (%) VIII (%)
ml) ml)

Normal
adult 12-14 37-50 70-150 60-150 neg. 190-420
S
20infants 12-16 41-70 65-146 65-147
20infants 12-17 60-100 64-100 S

1 no clot no clot 0 3 neg. 0 Microthrombi-lungs, liver, kidney, brain;

moderate pulmonary hemorrhage.
2 no clot no clot 0 Microthrombi-myocardium, lungs, pan-
creas, kidney and liver; diffuse hemor-
rhages; moderate hyaline membranes.
3 23.3 103.5 42 190 neg. 172 hemorrhage in skin, kidney, and brain.
4 8 17 15 100 Microthrombi-lungs; hemorrhages in
myocardium, lungs, brain, kidney; se-
vere hyaline membranes.
5 14.5 126.5 36 50 Microthrombi in liver and lungs; severe
hyaline membranes; alveolar hemor-
rhages
6 15 63.8 40 50 neg. Fibrin in heart and liver; hemorrhages in
brain, heart, liver, lung, duodenum; se-
vere hyaline membranes.
7 44 45 Severe hyaline membranes; alveolar hem-
56 40 p05. orrhages.
8 0 1.2 neg. 200 Living.
9 44 53 neg. Living.
10 16.0 89.0 32 45 p05. Living.
11 100 55 15 141 Livmg.
12 12 82 64 75 pos. Living.
13 72 72 75 p05. Living.
14 16 81 60 100 p05. Living.
15 16 90 92 105 p05. Living.
16 13 90 54 83 p05. Living.
17 14 88 88 90 Living.
18 14 57 74 100 Living.
19 15 127 58 63 neg. Living.

S Fibrin split products assayed in 45 normal newborns revealed 8 positive and the remainder negative.
p05. (positive) means from 1 to 5 mg/i#{174} ml.
PT=prothrombin time; PTT=partial thromboplastin time; FSP=fibrin split products.

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236 I.v. COAGULATION

This 1atie1t was treated for 20 hours prior

to death with intravenous heparin, which
may have altered the subsequent findings
by preventing further DIC.
The infants with severe IRDS ( Cases 4
through 10 ) showed variable thrombocy-
topenia, prolongation of the r + k value on
the TEG, and distinct decreases in factors
V and VIII. Serum FSP were occasionally
positive. Hemorrhage was the predominant
pathologic finding in addition to pulmonary
hyaline membranes; in addition, Cases 4, 5,
and 6 did show evidence of fibrin thrombi
(Fig. 3and4).
Case 11 showed definite evidence for
DIG (low platelets, abnormal TEG, low
factor VIII, low fibrinogen, and greatly in-
creased FSP ) , although he recovered with-
out specific therapy. This case is similar to
the case of defibrination syndrome follow-
Fic. 1. Case 1. Fibrin
( arrows ) ,
tlirombi
PAS
in
stain.
glomerular tuft ing
and
abruptio
others.1#{176}
Bleeding times were
placenta

prolonged in the
reported by Edson

onds). Fibrin thrombi were not demon- most severely affected infants, who were
strated at postmortem examination, al- also the most thrombocytopenic ( Cases 1,
though diffuse hemorrhages were present. 2, 3, 9, and 1 1 ) . The infants with mild
IRDS or other illnesses studied ( Cases 12
through 19) did not show any coagulation
abnormalities except mild prolongation of
the r + k ( TEG ) in
case 17 and increased
amounts of FSP in most of the cases.

COMMENT

Severe viral infections are often asso-

ciated with evidence of DIC.2 Therefore, it
was not surprising to find disseminated intra-
vascular coagulation in the infant with ac-
quired herpes infection and in the infant
with an intra-uterine infection with rubella
virus. To our knowledge, this is the first re-
port of severe DIG associated with an in-
tra-uterine infection. The baby with cy-
tomegalic inclusion disease had only
suggestive clinical evidence for dissemi-
nated intravascular coagulation.
More interesting is the observation that
the patients with severe IRDS had labora-
tory signs of varying degrees of consump-
FIG. 2. Case 2. Platelets and fibrin aggregate in
lion coagulopathy without evidence of asso-
lumen of small pulmonary vessel ( arrow ) . H and
E stain. ciated infection. These findings were not

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 ARTICLES 237

seen in the patients with mild IRDS. Histo-

logic confirmation of disseminated intravas-
cular coagulation was less striking in the
severe IRDS infants; the consumption of
fibrinogen was less than that seen in the pa-
tients with the viral infections ( Gases
1 and
2 ) . However, hemorrhages, a constant fea-
ture of DIG, were frequently seen in the in-
fants with severe IRDS.
The diagnosis of DIG in the neonatal pe-
nod is not without difficulty. Goagulation
tests which are often used to screen for de-
pletion of clotting factors may be mildly to
moderately abnormal in the normal infant.
These tests include the one-stage prothrom-
bin time, partial thromboplastin time, and
thrombin time. Fortunately, of the factors
which are most commonly depleted in DIG
( fibrinogen, platelets, prothrombin, and
factors V and VIII ), fibrinogen, factor \7,

and factor VIII are within the normal adult

Fic. 3. Case 4. Platelets and fibrin aggregate at-
range in normal premature and full-term tached to wall of small pulmonary vessel. H and
infants. Prothrombin may be low physiolog- E stain.
ically;16 platelets can be below normal in
“normal” premature infants.1 Therefore,
ucts of fibrin. The significance of increased
unless the screening tests are markedly ab-
FSP in IRDS remains to be clarified.
normal, specific assays for those factors af-
fected in DIG may be necessary in order to
confirm the diagnosis. Our cases with sus-
pected or proven DIG ( Gases 1 through
11 ) almost uniformly showed decreased
levels of factors V and VIII. In other
studies investigators18 have demonstrated
decreased levels of proaccelerin and AHF
in premature infants dying with
IRDS.
Degradation products of fibrinogen or
fibrin split products are frequently in-
creased in DIG.’9 Other studies,2021 as vell
as our own, have demonstrated FSP in
“normal” infants and in mildly ill infants
without other evidence of DIG. It is of in-
terest that, of the cases of probable DIG in
this report, only three out of eight showed
FSP while most of the infants with mild ill-
ness and no evidence for DIG did demon-
strate FSP. Markarian and others22 have
shown that fibrinolysins may be “depleted”
in severe IRDS, and therefore these infants Fic. 4. Case 5. Fibrin thrombi with attached ervth-
may be unable to form degradation prod- rocytes in hepatic venule ( arrow ) H and
. E stain.

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238 I.V. COAGULATION

SPECULATION 9. Leissring, J. C., and Vorlicky, L. N. : Dissemi-

nated intravascular coagulation in a neonate.
The purpose of this report is to empha- Amer. J. Dis. Child., 115:100, 1968.
size the rather common occurrence of DIG 10. Edson, J. R., Blaese, R. M., White, J. C., and
in severely ill newborn infants. It is inter- Krivit, W. : Deflbnnation syndrome in an in-
fant born after abruptio placentae. J. Pc-
esting to note the evidence for DIG in se-
diat., 72:342, 1968.
vere IRDS and to consider the therapeutic 11. Proctor, R. R., and Rapaport, S. I.: The partial
implications, i.e., the possible use of hepa- thromboplastin time with kaolin. Amer. J.
rin. However, a trial of heparin in these in- Clin. Path., 36:212, 1961.
fants has failed to show improvement in 12. Pool, J. G. : Preparation and testing of anti-
hemophiliac globulin (factor VIII) sources
survival statistics, although infants with
for transfusion therapy in hemophilia.
IRDS were more “resistant” to hepariniza- Scand. J. Clin. Lab. Invest. ( Suppi. 84),
tion than normal premature infants.2’ The 17:70, 1965.
relationship of DIC to the pathogenesis of 13. Borchgrevink, D. F., Pool, J. C., and Stor-
morken, H. : A new assay for factor V
systemic hemorrhages and IRDS remains to
( proaccelerin-accelerin ) using Russell’s
be elucidated.
viper venom. J. Lab. Clin. Med., 55:625,
1960.
SUMMARY
14. Ratnoff, 0. D., and Menzie, C.: A new method
Disseminated intravascular coagulation for the determination of fibrinogen in small
( DIG ) occurs more often than previously samples of plasma. J. Lab. Clin. Med.,
37:316, 1951.
recognized in the newborn period. Labora-
15. Claman, H. N., and Merrill, D. : Quantitative
tory and/or pathologic evidence of DIG
measurement of human gamma-2, beta-2A,
was demonstrated in 11 of 19 sick infants in and beta-2M serum immunoglobulins. J.
this study. Infants with intra-uterine or Lab. Clin. Med., 64:685, 1964.
postnatal infections (viral or bacterial), 16. Aballi, A. J., and DeLamerens, S. : Coagulation
changes in the neonatal period and in early
severe idiopathic respiratory distress syn-
infancy. Pediat. Clin. N. Amer., 9:785, 1962.
drome, or those born to high risk mothers
17. Medoff, H. S. : Platelet counts in premature in-
( toxemia or abruptio placenta ) should be fants. J. Pediat., 64:287, 1964.
suspected of developing manifestations of 18. Markarian, M., Lindley, A., Jackson, J. J., and
intravascular coagulation. Bannon, A. : Coagulation
factors in pregnant
women and premature infants with and
REFERENCES without the resphatory distress syndrome.
1. McKay, D. G., and Wahle, C. H. : Epidemic Thromb. Diath. Haemorrh., 17:585, 1967.
gastroenteritis due to Escherichia col:0111B. 19. Merskey, C., Kleiner, G. J., and Johnson, A. J.:
Arch. Path., 60:679, 1955. Quantitative estimation of split products of
2. McKay, D. C. : Disseminated intravascular co- fibrinogen in human serum, relation to diag-
agulation in virus disease. Arch. Intern. nosis and treatment. Blood, 28:1, 1966.
Med., 120:129, 1967. 20. Stiehm, E. R. : Split products of fibrinogen in
3. McMillan, C. W., Gaudry, C. L., and Hole- cord serum. (Abst. ) Pediat. Res., 1:221,
mans, R. : Coagulation defects and meta- 1967.
static neuroblastoma. J. Pediat., 72:347, 21. Bonifaci, E., Baggio, P., and Gravina, E.:
1968. Demonstration of split products of flbrino-
4. Pie!, C. F., and Phibbs, R. H. : The hemolytic- gen in the blood of normal infants. Biol.
uremic syndrome. Pediat. Clin. N. Amer., Neonat., 12:29, 1968.
13:295, 1966. 22. Markarian, M., Githens, J. H., Jackson, J. J.,
5. VanDerHorst, R. L.: Purpura fulminans in a Bannon, A. E., Lindley, A., Rosenblut, E.,
newborn baby. Arch. Dis. Child., 37:436, Martorell, R., and Lubchenco, L. 0. : Fibrin-
1962. olytic activity in premature infants. Amer.

6. Hillman, R. S., and Phillips, L. L. : Clotting-fl- J. Dis. Child., 113:312, 1967.

brinolysis in a cavernous hemangioma. 23. Markarian, M., Jackson, J., Bamion, A.,
Amer. J. Dis. Child., 113:649, 1967. Rosenbl#{252}t,E., Martorell, R., Lubchenco, L.
7. Reerink-Brongers, E. E., and De Koningh, 0., and Githens, J. H. : A clinical trial of hep-
M. J. : Acute fibrinolysis in a newborn infant. arm in premature infants with and without
Lancet, 1 :985, 1964. the respiratory distress syndrome (RDS).
8. Boyd, J. F. : Disseminated fibrin thromboembo- Program and Abstracts, thirty-sixth Annual

lism among neonates dying within 48 hours Meeting the Society

of for Pediatric Re-
of birth. Arch. Dis. Child., 42:401, 1967. search, p. 123, 1966.

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 ARTICLES 239

APPENDIX-CASE REPORTS

Case 1 care nursery at age 4 hours where he was noted to

be in moderate respiratory distress, jaundiced, and
A 2,270 gm, Caucasian male infant was the
covered with a petechial rash. Liver and spleen
product of a normal pregnancy, labor, and dcliv-
were enlarged. Chest film showed cardiomegaly
cry. The 1-minute Apgar score was 8; at 5 minutes
and pneumonia. Laboratory studies were: hemato-
the infant became apneic and required intubation
crit, 40%; hemoglobin, 13.0 gm; WBC, 8,300 with a
and assisted ventilation. For the next 2 days the
normal differential; and 68 nucleated RBC’s per
infant had respiratory distress which was treated by
100 WBC’s. Blood smear showed decreased plate-
oxygen and intravenous sodium bicarbonate. The
lets and increased numbers of “burred” red cells.
infant showed marked improvement and was ready
The infant developed convulsions and apneic
for discharge by the eighth hospital day when he
spells. Disseminated intravascular coagulation was
developed lethargy, jaundice ( total biirubin 14.4
suspected and the patient was given intravenous
mg/100 ml. ), and respiratory distress. Chest x-ray
heparin 100 U/kg every 4 hours until time of death
showed bilateral pneumonia. Antibiotics (penicillin
at age 24 hours. Postmortem examination revealed
and kanamycin ) were started, although cultures of
diffuse hemorrhages the skin, kidneys,
in and pen-
blood, cerebrospinal fluid, urine, and throat failed
ventricular areas of the brain. The lungs showed
to grow any bacteria. The infant’s condition be-
thickened alveolar walls with eosinophilic material
came worse, and on the tenth day he developed
in the air spaces. Alveolar lining cells were hyper-
apneic episodes and
convulsions. Prolonged bleed-
plastic and some contained large intranuclear baso-
ing was noted from needle puncture sites. When
philic inclusions characteristic of cytomegalovirus.
the laboratory data indicated intravascular coagu-
Liver showed foci of erythropoiesis and cholestasis.
lation, intravenous heparin ( 150 U/kg) and fresh
Bile duct cells contained intranuclear inclusions.
plasma ( 10 mI/kg) were given. Bleeding subsided
Cytomegalovirus was isolated from the brain, kid-
but the infant expired 6 hours later. Postmortem
ney, and lungs.
findings included fibrin thrombi in the lungs, liver,
glomeruli, and cerebellum. Micro hemorrhages
were seen in the lungs and renal parenchyma. The Case 4
liver showed parenchymal cell necrosis and multi- A 1,470gm female, Caucasian infant was the
nucleated giant cells compatible with viral hepatitis. product of a normal pregnancy complicated by a
Lungs showed thickening of alveolar walls due to difficult breech delivery. The infant was apneic at
mononuclear cell infiltrates. Viral cultures of lungs, birth, was resuscitated, and was transferred to the
kidney, brain, liver, and spleen grew herpes sim- University of Colorado
Medical Center at age 4
plex virus. hours. The infant noted to have severe respira-
was
tory distress; the
chest x-ray was compatible with
Case 2
hyaline membrane disease. The infant deteriorated
A 990 gm, Caucasian male infant (classified as rapidly; increasing cyanosis and hypoxia were cvi-
small for gestational age-SGA) was the product of dent while on assisted ventilation. She expired at
a pregnancy complicated by rubella in the mother 18 hours of age. Autopsy showed pulmonary
at approximately 8 weeks’ gestation. Soon after changes of hyaline membrane disease. Focal hem-
birth the infant developed moderate respiratory orrhages were present in the myocardium, pulmo-
distress and a generalized petechial rash. Sple- nary alveoli, kidney, and brain. Fibnin micro-
nomegaly was present. Chest film revealed bilateral thrombi were seen in small vessels in the lungs.
bronchopneuinonia. The infant was treated with
prednisone and antibiotics
but showed rapid dete-
rioration and expired at 27 hours of age. Autopsy Case 5
showed hyaline membranes in the lungs and eryth- A 1,640 gm, male, Caucasian infant (twin of
ropoiesis in the liver. Hemorrhages were present Case 7 ) was the product of a pregnancy compli-
in the pulmonary parenchyma, pericardium, my- cated by mild toxemia. Birth was uncomplicated.
ocardium, pancreas, liver, kidneys, and small One-minute Apgar was 7; the infant rapidly devel-
bowel. Fibrin and platelet thrombi were present in o_ severe respiratory distress. Chest film was
the small vessels of the lungs, pancreas, kidney, compatible with hyaline membrane disease. The
and liver. The infant’s antibody studies were posi- infant showed rapid progression of his disease and
tive for rubella. required assisted ventilation on a respirator. In-
tractable cyanosis appeared and he expired at age
Case 3 16 hours. Autopsy showed hyaline membranes lin-
A 2,290 gm, SGA, Caucasian male infant was ing the ixnmaturely formed air spaces. Hemor-
noted to have generalized petechiae and hepato- rhages were present in the pulmonary alveolar
splenomegaly at birth. Prenatal history was unre- walls and in several alveoli. Severe visceral conges-
vealing. The infant was transferred to our intensive tion was present.

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240 I.V. COAGULATION

Case 6 gradual improvement and was discharged at age

41 days. He was a slow feeder and continued to
A 1,630 gm, Caucasian male infant was born to
show poor muscular tone without localizing neuro-
an unwed mother who had no prenatal care. De-
logical signs.
livery was uncomplicated; Apgar ( 1 minute ) was
4. The infant developed typical findings of severe
IRDS within a few hours of birth. Hypotension Case 9
and anemia ( hematocnit 35% ) were noted during A 2,350 gm, SGA, Caucasian male infant was
his course. Assisted ventilation was required and the product of an uncomplicated pregnancy termi-
progressive deterioration was noted. The infant ex- nating by pitocin induction
and normal delivery.
pired at age 40 hours. Autopsy revealed severe He was transferred to the
University of Colorado
hyaline membrane disease. Microthrombi were Medical Center nursery at age 3 hours where the
seen in the small vessels of the heart and liver. diagnosis of severe IRDS was made. The patient
Hemorrhages were found in the lateral cerebral was extremely ill and required assisted ventilation
ventricles, myocardium, lungs, liver, and duode- on a respirator for 8 days. Intermittent seizures
num. were noted and intracranial bleeding was sus-
pected. At age 30 days the infant remained lethar-
Case 7 gic and showed impaired neurological develop-
A 1,390 gm, female infant ( twin of Case 5) de- ment.
veloped severe IRDS. In spite of treatment with
sodium bicarbonate, oxygen, assisted ventilation, Case 10
and antibiotics, the infant’s course was progres- A 1,600 gm, Caucasian male infant was deliv-
sively downhill to death at age 31 hours. Autopsy ered without difficulty following a breech presenta-
revealed severe pulmonary hyaline membranes. tion. Prenatal course was uncomplicated. The in-
Fibrin thrombi were seen in a few pulmonary fant was transferred to the University of Colorado
veins and in the liver sinusoids. Hemorrhages were Medical Center nursery at age 4 hours in moderate
noted in the alveolar spaces, pleura, bowel muco- respiratory distress. The infant developed severe
sae, and pancreas. IRDS which required assisted ventilation for a
brief time. He gradually recovered and was dis-
Case 8
charged in good condition at age 45 days.
A 1,920 gm, male, Caucasian infant was the
product of a pregnancy complicated by mild toxe- Case 11
mia. Delivery was uncomplicated; 1-minute Apgar
was 7. The patient was transferred to the Univer- A 1,470 gm, Caucasian
female infant was the
product of a primigravida who had severe toxemia
sity of Colorado Medical Center at age 12 hours
because of respiratory distress. The infant devel- of pregnancy. Delivery was by Cesarean section.
oped moderately severe IRDS which lasted for 5 Apgar was 4. The infant showed lethargy, pallor,
days. During this time the infant showed marked hypotension, hypothermia, and mild respiratory
flaccidity and intermittent convulsions. Intracranial distress for 8 hours after delivery; however, grad-
hemorrhage was suspected. Bacterial cultures of ual recovery was noted following symptomatic
blood and spinal fluid (cerebrospinal fluid was therapy and the patient was discharged at age 22
grossly bloody) were negative. The infant showed days in good condition.

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 DISSEMINATED INTRAVASCULAR COAGULATION IN THE NEWBORN
William E. Hathaway, Marilyn M. Mull and Giselle S. Pechet
Pediatrics 1969;43;233

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 DISSEMINATED INTRAVASCULAR COAGULATION IN THE NEWBORN
William E. Hathaway, Marilyn M. Mull and Giselle S. Pechet
Pediatrics 1969;43;233

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the World Wide Web at:
http://pediatrics.aappublications.org/content/43/2/233

Pediatrics is the official journal of the American Academy of Pediatrics. A monthly publication, it has
been published continuously since 1948. Pediatrics is owned, published, and trademarked by the
American Academy of Pediatrics, 141 Northwest Point Boulevard, Elk Grove Village, Illinois, 60007.
Copyright © 1969 by the American Academy of Pediatrics. All rights reserved. Print ISSN: 1073-0397.

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