CT Detection
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CAROL
and Course of Intracranial in Premature Infants
M. RUMACK,1
MARILYN
M. McDONALD,2 AND
JEFFREY
Hemorrhage
OWEN P. O’MEARA,2 C. RUDIKOFF1
BOB
B. SANDERS,1
Twenty neonates with a suspected intracranial hemorrhage were studied by computed tomography (CT). The exact site and extent of the hemorrhage in all infants were clearly demonstrated on serial CT scans. In intraventricular hemorrhage, a dense subependymal halo lined the ventricular system and could be recognized for up to 2 weeks. Discrete hemorrhage adjacent to the ventricular system also appeared as discrete nodules rather than as a diffuse hemorrhage. Blood in the ventricular system could be recognized up to 2 weeks when there were blood-cerebrospinal fluid levels. Hydrocephalus was a common sequeia and was readily detectable before a measurable change In head size.
concur with previous reports [6-10]. Nineteen of the infants weighed less than 2,000 g; 17 were less than 32 weeks gestation. The one common denominator seemed to be a major anoxic episode. In fact, 1 1 of the 20 infants
Intracranial hemorrhage in premature infants is the most common central nervous system abnormality in neonatal autopsies [1]. The incidence is estimated at 1 .1 per 1000 live births [2]. Since more premature infants are supported by intensive medical therapy, there has been an increased incidence of intraventniculan hemorrhage [3]. It has been shown that the diagnosis of hemorrhage by computed tomography (CT) is as reliable as pathologic data [4-7]. This study of 20 neonates with intracranial hemorrhage concurs with the known association of anoxia, prematurity, and low birth weight as the most commonly associated factors [1 2, 8].
tenocoiitis
had
only
Premature
infants
with
and
suggestive
hypoxia solved
heaters.
resuscitate required
A pediatrician
neonates during
on intensive
was
the acute
present. hemorrhage
care
Sedation
of intracranial
because
nurse
was
trained
to
very
rarely
the infants
were
Neurologic
evaluations
were
obtained
at discharge
and
was
and
Another
had
an
with only
disseminated
had pla-
infant,
isolated
the
subarach-
severe meconium infant without major
intravascular
were obtained in four infants
reen-
coagulation
within 24 hr of a clinical and within 72 hr in 13. Of 14
TABLE Summary
1
of Clinical
Findings No. Patients
on
Gestational
examinations.
age 35
weeks
19
Binthweight,2,000g
19
Age at suspected tem
central
hemorrhage,
Drop in hematocrit, Metabolic acidosis,
Findings
Twenty neonates hemorrhage. The
delivery.
postterm,
seven abruptio
Findings
CT scans hemorrhage
Results Clinical
breech
another previa,
had mild hyaline membrane disease, which at 6 days of age, then developed necrotizing
Radiologic
so lethargic. As the infant improved, sedation was occasionally necessary on follow-up scans. We attempted to scan all infants within 48 hr, so there would be no resolution of the blood. However, a few infants whose intracranial hemorrhage was not suspected until the development of complications were scanned weeks later. Lumbar puncture on all infants confirmed the presence of blood. A few very low birth weight infants who deteriorated rapidly were scanned immediately after death. follow-up
who
and
to placenta
and died. Traditionally, ventricular hemorrhage was felt to occur as a delayed phenomenon 24-48 hr after a hypoxic incident [11, 12]. Half of our babies bled within the first 24 hn, although significant clinical deterioration and demise was more commonly delayed beyond 2 days. In fact, six of the 20 neonates died after a prolonged clinical course of 1 week to 2 months. This differs from earlier experiences [2] of a rapid decline and may reflect the very vigorous support systems now available. In 13 of 20 babies, a hematocrit drop of 10% or more was documented. Transfusions of whole blood and packed red cells made it impossible to evaluate the hematocnit in others. Of the 20 babies, 17 demonstrated a metabolic acidosis of significant degree (13 with pH 7.20), although a few had a normal pH at the time of clinical suspected intracranial bleeding. None of our babies had a recorded serum sodium greater than 150 mEq/Iiter, although correlation between hypernatremia and intracranial hemorrhage has been reported [13].
hemorrhage (apnea, seizures, and resistant acidosis) were examined with a Delta 50 scanner, with a 21/4 mm scan time and a 256 x 256 matrix. Very critical infants could be evaluated while still on the respirator. Temperatures were kept stable with radiant
on difficult one
disease
due
noid hemorrhage associated plugging his bronchi. The
Methods
symptoms
membrane asphyxia
centa,
,
Subjects
hyaline
peninatal
were shown to have an intracranial clinical profiles (table 1) generally
nervous
48
sys-
hr
>10% pH 7.20
Downloaded from www.ajronline.org by 117.253.153.157 on 10/08/15 from IP address 117.253.153.157. Copyright ARRS. For personal use only; all rights reserved
CAROL
and Course of Intracranial in Premature Infants
M. RUMACK,1
MARILYN
M. McDONALD,2 AND
JEFFREY
Hemorrhage
OWEN P. O’MEARA,2 C. RUDIKOFF1
BOB
B. SANDERS,1
Twenty neonates with a suspected intracranial hemorrhage were studied by computed tomography (CT). The exact site and extent of the hemorrhage in all infants were clearly demonstrated on serial CT scans. In intraventricular hemorrhage, a dense subependymal halo lined the ventricular system and could be recognized for up to 2 weeks. Discrete hemorrhage adjacent to the ventricular system also appeared as discrete nodules rather than as a diffuse hemorrhage. Blood in the ventricular system could be recognized up to 2 weeks when there were blood-cerebrospinal fluid levels. Hydrocephalus was a common sequeia and was readily detectable before a measurable change In head size.
concur with previous reports [6-10]. Nineteen of the infants weighed less than 2,000 g; 17 were less than 32 weeks gestation. The one common denominator seemed to be a major anoxic episode. In fact, 1 1 of the 20 infants
Intracranial hemorrhage in premature infants is the most common central nervous system abnormality in neonatal autopsies [1]. The incidence is estimated at 1 .1 per 1000 live births [2]. Since more premature infants are supported by intensive medical therapy, there has been an increased incidence of intraventniculan hemorrhage [3]. It has been shown that the diagnosis of hemorrhage by computed tomography (CT) is as reliable as pathologic data [4-7]. This study of 20 neonates with intracranial hemorrhage concurs with the known association of anoxia, prematurity, and low birth weight as the most commonly associated factors [1 2, 8].
tenocoiitis
had
only
Premature
infants
with
and
suggestive
hypoxia solved
heaters.
resuscitate required
A pediatrician
neonates during
on intensive
was
the acute
present. hemorrhage
care
Sedation
of intracranial
because
nurse
was
trained
to
very
rarely
the infants
were
Neurologic
evaluations
were
obtained
at discharge
and
was
and
Another
had
an
with only
disseminated
had pla-
infant,
isolated
the
subarach-
severe meconium infant without major
intravascular
were obtained in four infants
reen-
coagulation
within 24 hr of a clinical and within 72 hr in 13. Of 14
TABLE Summary
1
of Clinical
Findings No. Patients
on
Gestational
examinations.
age 35
weeks
19
Binthweight,2,000g
19
Age at suspected tem
central
hemorrhage,
Drop in hematocrit, Metabolic acidosis,
Findings
Twenty neonates hemorrhage. The
delivery.
postterm,
seven abruptio
Findings
CT scans hemorrhage
Results Clinical
breech
another previa,
had mild hyaline membrane disease, which at 6 days of age, then developed necrotizing
Radiologic
so lethargic. As the infant improved, sedation was occasionally necessary on follow-up scans. We attempted to scan all infants within 48 hr, so there would be no resolution of the blood. However, a few infants whose intracranial hemorrhage was not suspected until the development of complications were scanned weeks later. Lumbar puncture on all infants confirmed the presence of blood. A few very low birth weight infants who deteriorated rapidly were scanned immediately after death. follow-up
who
and
to placenta
and died. Traditionally, ventricular hemorrhage was felt to occur as a delayed phenomenon 24-48 hr after a hypoxic incident [11, 12]. Half of our babies bled within the first 24 hn, although significant clinical deterioration and demise was more commonly delayed beyond 2 days. In fact, six of the 20 neonates died after a prolonged clinical course of 1 week to 2 months. This differs from earlier experiences [2] of a rapid decline and may reflect the very vigorous support systems now available. In 13 of 20 babies, a hematocrit drop of 10% or more was documented. Transfusions of whole blood and packed red cells made it impossible to evaluate the hematocnit in others. Of the 20 babies, 17 demonstrated a metabolic acidosis of significant degree (13 with pH 7.20), although a few had a normal pH at the time of clinical suspected intracranial bleeding. None of our babies had a recorded serum sodium greater than 150 mEq/Iiter, although correlation between hypernatremia and intracranial hemorrhage has been reported [13].
hemorrhage (apnea, seizures, and resistant acidosis) were examined with a Delta 50 scanner, with a 21/4 mm scan time and a 256 x 256 matrix. Very critical infants could be evaluated while still on the respirator. Temperatures were kept stable with radiant
on difficult one
disease
due
noid hemorrhage associated plugging his bronchi. The
Methods
symptoms
membrane asphyxia
centa,
,
Subjects
hyaline
peninatal
were shown to have an intracranial clinical profiles (table 1) generally
nervous
48
sys-
hr
>10% pH 7.20
