NQ-044 Answer:
(D) This type of hemorrhage is most common seen in premature infants with
25 to 30 weeks of gestation.
Pathology of the case:
This is an immature fetal brain and judging from
the size and shape it should be less than 30 weeks of gestation.. The salient
pathologic change is a large hematoma that occupies the right side of the
lateral ventricles. Some small hemorrhages (arrow) are also present in
subependymal areas (corresponding to the germinal matrix microscopically).
This type of hemorrhage is
often seen as spontaneous hemorrhage without any relation to trauma in premature
infants between 22-30 weeks of gestation and the most common site of hemorrhage
is the germinal matrix at the median eminence (covering the basal ganglia).
Lesions in the white matter (periventricular leukomalacia)
are seen in premature babies after 28 weeks of gestations.
Hemorrhage from choroid plexus is extremely
uncommon in this age group.
Hemorrhage from the choroid
plexus is more commonly seen in term babies.
Body weight:
Intraventricular hemorrhages among infants weighing <1500
g and who come to necrospy ranges from 23 to 75%. The frequency drops
dramatically to 8% in babies weighing >2000g.
Origin of the hemorrhage:
The most common site is the periventricular matrix zone located between the
caudate nucleus and thalamus at the level of or slightly posterior to the
foramina of Monro. The next common site is the occipital lobe. The least common
site is the temporal horn of lateral ventricle. Hemorrhage may originate over
the head of the caudate. Some of the smaller hemorrhage may be confined to the
germinal matrix without rupture into the ventricle. In these cases, the
hemorrhage may be clinically asymptomatic and these hemorrhagic foci can be
found as incidental finding on autopsy.
Etiology:
By the
18th to 20th week of gestation, the neocortical ventricular wall is lined by a
prominent hypercellular well-vascularized zone known as the germinal matrix.
This germinal zone is composed of undifferentiated, differentiating and
migrating cells, radial glial fibers, polymorphous astrocytes, and thin-walled
blood vessels. The germinal cells have very little structural support and the
vessels are very fragile. A lot of angiogenesis and vessel remodeling is going
on during this period and this may be the reason why this area is so susceptible
to hemorrhage in younger premature infants. The control of blood pressure in the
brain is not well developed in these infants. The hemorrhage is usually resulted
of damage of the vessel wall. The mechanism may be damage of the endothelial
cells by acidosis secondary to hypoxia. Birth injury seems to play a role as
one-third of cases have difficult deliveries due to forceps rotations and breech
presentation.
Papile’s classification:
[Papile LA
et al., 1978]
Grade I: Subependymal hemorrhage
Grade II: Intraventricular hemorrhage (hemorrhage rupture into the ventricle)
Grade III:
Intraventricular hemorrhage with ventricular
dilation
Grade IV:
Intraventricular hemorrhage with ventricular
dilation and parenchymal extension.