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Posthemorrhagic
hydrocephalus
Posthemorrhagic
hydrocephalus results from obstruction of the cerebrospinal fluid
flow at the posterior fossa cisterns. The cerebrospinal fluid exits
the ventricular systems through the orifices of Luschka and Magendie.
These orifices are in the region of the medulla oblongata. The fluid
from this area must flow from the base of the cranium (posterior fossa)
to the convexity to drain through the Pachioni corpuscles. The
obstruction at the posterior fossa is due to obliterative arachnoiditis.
The clinical manifestations
of progressive posthemorrhagic hydrocephalus usually include an abnormal
increase in head circumference and a full fontanelle. Clinical manifestations
may not be present despite significant ventriculomegaly.
The diagnosis of posthemorrhagic
hydrocephalus is based on the presence of large ventricles and no
signs of cerebral atrophy. The distinction between ventricular distension
due to hydrocephalus and ventricular enlargement due to cerebral atrophy
can often be made based brain ultrasound (Figure 253.1). Computed
tomography or MRI may be needed to demonstrate atrophy or hydrocephalus.
Figure 253.1.— 
Characteristic ultrasonographic findings in brain
atrophy [A] and hydrocephalus [B]. The two ultrasounds on top [A]
demonstrate typical atrophic changes: large subarachoid spaces (green
arrows), prominent sulci (pink arrows), angular frontal horn of the
lateral ventricles (blue arrows), moderate to mild lateral ventricular
enlargement of the frontal horns (tan arrows), no enlargement of the
temporal horn of the lateral ventricle or third or fourth ventricle.
The two ultrasounds on the botton [B] demonstrate typical findings
of posthemorrhagic hydrocephalus: no subarachnoid space, thin sulci
(pink arrows), round frontal horns of the lateral ventricles (blue
arrows), large ventricles (tan arrows), periventricular echogenicity
(yellow arrows), large third and temporal horns of the lateral ventricles
(red arrows).
Posthemorrhagic
hydeocephalus has no treatment. Intraventricular fibrinolytic agents
such as urokinase, streptokinase, and tissue plasminogen activator
are not currently recommended. Posthemorrhagic hydrocephalus may require
shunting depending on its evolution.
Posthemorrhagic
hydrocephalus can arrest or become progressive. An arrested hydrocephalus
implies that the size of the ventricle remained the same from one
ultrasound to the next. Progressive hydrocephalus implies that the
ventricle increased in size from one ultrasound to the next. An arrested
hydrocephalus may become progressive and a progressive hydrocephalus
may arrest.
When
to conclude that arrested hydrocephalus will not progress?
There is no data
supporting an answer to this question. Two ultrasounds one week apart
that demonstrate no increase in ventricular size probably implies that
no further ventricular size increase will occur.
When
to conclude that progressive hydrocephalus will not spontaneously arrest
before producing brain damage?
There
is no data supporting an answer to this question. Probably, clinically
silent, slowly progressive hydrocephalus for one month or rapidly progressive
hydrocephalus for one week may produce brain damage. Hydrocephalus producing
clinical manifestation is also likely to produce brain damage. Human
studies using near-infrared-spectroscopy and Doppler ultrasound have
shown that even relatively small and slowly progressive increases in
ventricular size negatively affect brain metabolism in the periventricular
area. In animals, it has been documented that ventricular distension
results in periventricular damage (hypoperfusion, anaerobic metabolism,
and loss of high-energy phosphates).
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