Intracranial Haemorrhage
Intracranial haemorrhage is one of the most
frequent pathologies of the brain in infants. It occurs more often in preterm
infants than in term babies or older infants. Four main forms of haemorrhage can
be distinguished:
1.
Intracranial haemorrhage of
preterm infants
2.
Subdural haemorrhage
3.
epidural
haemorrhage
4.
Subarachnoid
haemorrhage
Intracranial Haemorrhage of Preterm Infants
Advances in modern neonatology
have caused the survival of more and more preterm infants. Today even preterm
infants, older than 22 or 23 weeks of gestation, can survive. However, many of
extremely preterm babies suffer from intracranial haemorrhage and may be more
or less severely neurologically handicapped.
Anatomical
Background
The high incidence of
intracranial haemorrhage is caused by some characteristics of the germinal matrix,
•
Germinal matrix is an immature
•
metabolically highly active
•
Richly vascularized layer of neuroepithelial cells.
•
very prominent between the 20th and 32nd gestational weeks.
•
After the 30th gestational week, the germinal matrix begins to
involute.
The proliferating neuroepithelial
cells of the germinal matrix are localised in the lateral wall of side
ventricles behind the foramen of Monro, lateral to the choroid plexus between
the developing head of the caudate nucleus and the thalamus.
Heubner’s
artery : The germinal matrix is perfused
by a branch of the anterior cerebral artery, the Heubner’s artery,
and small side branches of the lenticulostriate arteries. These vessels can be
displayed by cranial ultrasound in
sagittal and coronal sections . The size of Heubner’s artery
indicates that a major quantity of blood flow from the anterior cerebral artery
is determined for the perfusion of the metabolic active periventricular
germinal matrix. After the 32nd week of gestation, involution of
these vessels occurs simultaneously with involution of the germinal matrix.
The vessels of the germinal
matrix have a greater diameter,
thinner walls, less defined basement membranes and less perivascular support
than arteries of other brain regions .
Arterioles arising from Heubner’s artery,
terminal branches of the lateral striate arteries and callosal penetrating
arteries supply a capillary network and join a small vein. Some authors have
reported arteriolar-to-venous shunts or arteriolar-to-arteriolar anastomoses
without insertion of capillaries. Changes in blood pressure are directly
transmitted to the venous drainage causing rupture of the small veins and subependymal
haemorrhage which may rupture into the ventricle.
Frequency of Intracranial Haemorrhage
30-50 % In dependency on the gestational
age of the investigated preterm infants, intracranial haemorrhage could be
found in 30–50 % of all investigated patients (Kirks et al. 1986).
44
% : In older series of 742 infants
born before the 32nd week of gestation, Kirks et al. found intracranial
haemorrhages in 44 %.
20 % grade I
10 % grade II
7 % grade III
7 % grade IV (classification of Papile) could be found .
Nowadays the frequency of intracranial haemorrhage is lower.
Severe intracranial haemorrhage occurs more frequently in very immature babies with
severe asphyxia born before 28th week of gestation with a birth weight under
1,000 g .
Time of
Haemorrhage
Most intracranial haemorrhages
(90 %) occur within the first 72 h of life.
50 % are
diagnosed on the first day
25 % on the second
15 % are found on the third day
As 90 % of all intracranial haemorrhages occur
within the first 72 h of life, the first
sonographic investigation should be performed
within the first and third day of life ..
Protocol
of cranial Ultrasound scan
The first investigation should be
performed as early as possible to distinguish prenatal from postnatal lesions.
For forensic reasons this investigation should be performed and documented
within the first day of life.
The second investigation should be
performed after the vulnerable phase in which most bleedings occur, at the
third day of life.
The third investigation should be
performed at the end of the first week of life, to detect late bleedings and to
evaluate beginning posthaemorrhagic ventricular dilatation. In special cases
additional investigations can be performed, especially if the patient
deteriorates or severe haemorrhage is diagnosed.
Pathophysiology
About 80–90 % of all
intraventricular haemorrhages of preterm infants arise from the richly vascularised
periventricular germinal matrix. As mentioned above the germinal matrix has
relatively large vessels with only one endothelial layer.
This makes them especially
vulnerable to changes in blood pressure, acidosis, coagulation disorders, rapid
volume expansion and especially hypoxaemic-ischaemic injury.
Possible mechanical causes are
compression of the large draining sinuses and stretching of the capillaries
during reanimation.
High cerebral flow
Other reasons for the high
incidence of intracranial haemorrhages are an increase of intracranial
perfusion during apnoea (increase of pCO2 and decrease of pO2) and pneumothorax
(increase of pCO2 and venous pressure), during endo-tracheal suction and rapid volume
expansion. All these factors can cause rupture of the fragile capillaries and
lead to intracranial haemorrhage.
Decreased cerebral flow
A decrease of systemic blood
pressure and cardiac output during longer-lasting arterial hypotension associated
with asphyxia may cause a dramatic decrease of intracranial blood flow. This may
cause ischaemic damage of the metabolic highly active periventricular germinal
matrix. On the other hand, many hypertensive crises during reperfusion
(correction of acidosis and hypoxia) cause an increase of brain perfusion and rupture
of intracranial arteries.
The main risk factors for the
development of intracranial haemorrhage besides immaturity and asphyxia are
hypo- or hyperperfusion of the brain and especially of the germinal matrix.
Possible
risk factors for the development of intracranial haemorrhage
1.
Prematurity (≤28 weeks)
2.
Low birth weight (<1,000 g)
3.
Immature vascular bed of the periventricular germinal matrix
4.
Asphyxia/ischaemia
5.
Hypercapnia/hypocapnia
6.
Missing autoregulation of brain perfusion (blood pressure-passive
brain circulation)
7.
Decreased brain perfusion
a)
Low blood pressure
b)
Hypocapnia
c)
Low flow velocities in brain arteries
8.
Increased brain perfusion
a)
High blood pressure
b)
Rapid volume expansion
c)
Exchange transfusion
d)
Ligature of ductus
e)
Hypercapnia
f)
Pneumothorax (increased pCO2 and venous pressure)
g)
Endotracheal suctioning
h)
Cerebral seizures
i)
Longer handling of patient
9.
Increase venous pressure
a)
Difficult vaginal breech delivery
b)
Pneumothorax
c)
Problems with ventilation (obstruction of
d)
ventilation tube, increased PEEP, etc.)
e)
Asphyxia
10.
Coagulation disorders
11.
Fluctuating brain perfusion
12.
Breathing against ventilator
Most of the risk factors can lead to hypo- or hyperperfusion of the
brain which can be measured by Doppler sonography.
Hypoperfusion may cause
ischaemic injury. Hyperperfusion later may cause rupture of the previously
injured vessels of the germinal matrix.
Course of
Intraventricular Haemorrhage
80 % of all intracerebral haemorrhages rupture from the
periventricular germinal matrix into the lateral ventricles. From the lateral
ventricles, blood clots spread to the third and fourth ventricles and from
there through the foramina of Luschka and Magendie into the occipital
subarachnoid space. Within days or weeks, obliterative
fibrosing arachnoiditis may
develop which may cause posthaemorrhagic hydrocephalus .
In 15–25 % of all bleedings, the
haemorrhage is complicated by haemorrhagic infarction of the brain parenchyma.
The haemorrhagic infarction is located laterally to the side ventricle.
Haemorrhagic infarction is
usually associated with severe intraventricular haemorrhage on the same side.
Haemorrhage to the brain parenchyma is not merely an expansion of blood from the
ventricular space to the parenchyma as initially thought (Papile et al. 1978). Large
amounts of intraventricular blood may compress the
draining veins at the roof and
bottom of the lateral ventricle. This causes obstruction of the drainage of the
medullary veins, which form the terminal vein at the bottom of the lateral
ventricle .The result is a haemorrhagic
infarction within the
corresponding cerebral hemisphere .
2D Image
Ultrasonography of the brain is
the imaging modality of choice for the diagnosis of intracranial haemorrhage .
Haemorrhage appears as increased echogenicity within the germinal matrix, the
ventricular space and possibly in the parenchyma of the brain . The physical
basis for the echodense structure of intracranial bleeding is the dense network
of fibrin mesh that reflects ultrasound .
Intracranial bleedings of premature
babies can be categorised according to the location and amount of blood within
the brain.
Since the first report about the
classification of ICH by Lu Ann Papile, a lot of other classifications have
been described (Papile et al. 1978). All of these classifications are similar although
they differ in some important parts. In our point of view, the grading system
of Volpe and the suggestion of the paediatric section of the DEGUM are the best.
They differentiate three grades of severity:
• Grade I: germinal matrix haemorrhage
• Grade II: small intraventricular haemorrhage which fills
<50 % of the ventricular space
• Grade III: severe intraventricular haemorrhage which fills
>50 % of the ventricular space
This classification differs from
the initial classification of Lu Ann Papile, which is most frequently used
worldwide, in some points:
• It does not include haemorrhage within the brain parenchyma
(grade IV of Papile’s classification) and ventricular dilatation (a
characteristic of grade III in Papile’s classification).
• As ventricular dilatation and posthaemorrhagic hydrocephalus are
consequences of severe intracranial bleeding, the classification of Volpe and
the DEGUM does not include this in their grading system .
• Parenchymal haemorrhage is not a simple extension of blood from
the ventricular space to the parenchyma as Papile thought. It is a venous infarction
which is caused by a blockade of the terminal veins at the bottom of the
lateral ventricles and the subependymal veins at the roof of the ventricle.
This causes a cessation of the outflow from the medullary veins and leads to a haemorrhagic
infarction .
As mentioned earlier, 90 % of
all bleedings originate from the germinal matrix. If the bleeding does not rupture
through the ependymal walls and is confined to the germinal matrix, it is
classified as grade I haemorrhage .
Grade I haemorrhages may rupture
through the ependymal walls. If blood empties into the lateral ventricles, it
may cause moderate (grade II) or severe (grade III) intraventricular
haemorrhage.
If less than 50 % of ventricular
space is filled with blood clots, grade II is diagnosed .
If more than 50 % of the
ventricular space is filled with blood, grade III is diagnosed.
Parenchymal haemorrhage is an
own category, more similar to periventricular leucomalacia than to
intraventricular haemorrhage .
Doppler
Sonography
Most haemorrhages originate from
the germinal matrix which is supplied by small branches of the anterior
cerebral and the middle cerebral artery.
From the anterior cerebral
artery the Heubner’s artery and from the middle cerebral artery lenticulostriatic
branches and choroidal branches originate.
With colour-coded Doppler sonography, these arteries can be displayed in
parasagittal and coronal sections . With spectral Doppler flow velocities can
be measured. Perfusion changes in these arteries may cause intracranial
haemorrhage. Therefore, flow measurements in the anterior or middle cerebral artery
or their branches should be performed to study the evolution of intracranial
haemorrhage.
Risk
Factor: Low Blood Flow Velocities
We found very low flow
velocities in the anterior cerebral artery to be a major risk factor for the development
of severe intracranial haemorrhage .
Low birth weight infants with
very low flow velocities at the initial investigation developed significantly
more often severe intracranial haemorrhage (grade III or haemorrhagic infarction)
than infants with higher flow velocities
Other authors found that an ‘end-diastolic
block’ in cerebral circulation may predict intraventricular haemorrhage
in hypotensive extremely low birth weight infants . They found that infants
with an absent diastolic flow and an associated low mean arterial pressure
(MAP) <30 mmHg developed more often intraventricular haemorrhage than in infants
with MAP >30 mmHg. Absent diastolic flow was due to a haemodynamic-relevant
ductus arteriosus Botalli. The authors conclude that an end-diastolic block in
the cerebral circulation, together with a MAP of ≤30 mmHg or less and the presence
of PDA during the first 4 days of life, might be associated with IVH in
extremely low birth weight infants (Julkunen et al. 2008).
Low flow velocities may lead to low perfusion of the
germinal matrix and cause ischaemic injury. During reperfusion high velocities
and perfusion may occur. Especially during manipulation (endotracheal suction,
etc.), hypoxaemic-ischaemic injured arteries may rupture and cause intracranial
haemorrhage. The demonstration of low flow velocities may be a significant risk
factor for the development of severe intracranial haemorrhage .
Therefore routine measurement of
blood flow velocities in the anterior cerebral arteries after birth is recommended
to detect patients at risk for the development of ICH.
As low pCO2 levels cause a further reduction
of the flow velocities, hypocapnia should be avoided. We recommend a pCO2 level
of ventilated preterm infants at the upper normal range of 45 mmHg to prevent
an
iatrogenic fall of brain
perfusion.
After intracranial haemorrhage a
significant further decrease of the flow velocities could be shown . This may
be caused by intravascular blood loss and a temporarily increase of intracranial
pressure. Severe intracranial haemorrhage may lead to a significant reduction
of intravascular volume and cardiac output. Due to missing autoregulation of brain
perfusion, perfusion may fall under a critical limit and cause further
ischaemic lesions. Using Xe-133 clearance or positron emission tomography (PET),
Lou and Volpe could show that low cerebral
perfusion is a risk factor for
the development of intracranial haemorrhage .
In mature newborns who suffered
from severe intracranial hemorrhage significant lower flow velocities could be
found in comparison with a healthy control group . Although brain perfusion
cannot directly be measured by Doppler sonography, low blood flow velocities in
all greater intracranial arteries can be interpreted as low cerebral perfusion.
Risk
Factor: Missing Autoregulation
Immature preterm infants born
with a gestational age of 30 weeks or younger are not able to regulate
their brain perfusion such as
older infants or adults. These patients cannot maintain a stable cerebral
perfusion over a large range of blood pressure. Typical is a pressure-passive
cerebral circulation. If blood pressure increases, flow velocities
simultaneously increase which causes an increase of blood flow to the brain; if
blood pressure decreases, brain perfusion may drop under a critical limit . As mentioned
earlier fluctuating blood pressure may
lead to fluctuating brain flow,
which is associated with a higher incidence of severe intracranial haemorrhage.
47 % of patients with impaired cerebrovascular
autoregulation developed IVH.
13 % of patients with intact
autoregulation developed IVH .
Risk
Factor: Fluctuating Blood Flow Velocities
fluctuating blood flow
velocities are an important risk factor for the development of intracranial haemorrhage
in ventilated preterm infants when measuring blood flow velocities in the anterior
cerebral arteries within the first hours of life. Patients with stable flow
profiles did not develop severe intracranial haemorrhage.
Fluctuating flow was characterised
by a continuous change in systolic and diastolic peaks form beat to beat
whereas stable flow profiles resulted in stable peaks in systole and diastole
measured by Doppler sonography.
If fluctuations of flow
velocities were below 10 %, no statistically significant difference in the severity
of ICH could be found . As fluctuating
flow velocities are a significant risk factor for the development of ICH,
fluctuations
should be avoided. Study done
with treated a group of patients with pancuronium bromide they found
paralysed 72 premature
ventilated infants in the first 72 h of life. In this group, in which the
incidence of intraventricular haemorrhage was expected to be 90–100 %, only
7 % of the paralysed infants developed ICH . They induced stable blood pressure
and stable blood flow velocities within the cerebral arteries. In comparison
with the untreated control group, they found a significant decrease of severe intracranial
haemorrhage. Therefore, they suggests that all ventilated very preterm infants
should be treated with pancuronium. Other medications such as pethidine have
similar effects and can be used especially in the first 72 h where the majority
of intracranial haemorrhage
occurs . It has to be evaluated in greater prospective studies if other
sedative or
analgesic drugs, such as
fentanyl, are as effective.
Periventricular
Haemorrhagic Infarction of Preterm Infants
Severe intraventricular
haemorrhage may be complicated by bleeding into brain parenchyma.
Approximately 15–20 % of all
preterm infants with a gestational age below 28 weeks and a birth
weight below 1,000 g exhibit a
parenchymal lesion . It is usually
localised just dorsal and lateral to the external angle of the lateral ventricle
.
Parenchymal haemorrhage is
strikingly asymmetric.
In the largest series the lesion
was exclusively unilateral in about two thirds of the infants . The lesion may
be localised; in about one half
of the infants, the lesion was extensive and involved the periventricular
white matter from the frontal to
the parieto-occipital region . In the vast majority of patients, parenchymal
haemorrhages are associated with gross intraventricular bleeding . Parenchymal
bleeding usually could
be shown on the side with the
lager amount of intraventricular haemorrhage. Usually intraventricular bleeding
developed and progressed before parenchymal bleeding occurred . These data
suggest that severe intraventricular haemorrhage leads to obstruction of the
terminal and subependymal veins and impedes blood flow from the medullary
veins. Parenchymal bleeding therefore is a venous infarction and not a simple expansion
of blood from the ventricular space to the parenchyma .
In most classifications of
intracranial haemorrhage of preterm infants, including the first of Papile, bleeding
within brain parenchyma is included as grade IV haemorrhage . Papile and
co-workers thought that blood penetrates
from the ventricular cavity into
the brain parenchyma.
Newer investigations however
have shown that no merely extension of blood from the lateral ventricles to the
parenchyma occurs . Therefore Volpe and others excluded grade IV haemorrhage
from the grading system. Microscopic studies of the periventricular
haemorrhagic necrosis showed that the lesion is a haemorrhagic infarction . An
MRI study has shown intravascular thrombi and periventricular haemorrhage along
the course of the medullary veins within the area of infarction .
2D Image
features
Haemorrhagic infarction usually
occurs unilaterally, over and laterally to the side ventricle in association with
severe intracranial haemorrhage (usually grade III) . The bleeding can be shown
in coronal and parasagittal sections through the brain . Initially the haemorrhage
appears echogenic before cystic transformation occurs after 2–3 weeks .
The bleeding may be localised or
it may extend from the frontal to the occipital lobe. Haemorrhagic infarction
usually occurs associated with severe ipsilateral intraventricular bleedings
which have led already to dilatation of the corresponding ventricle.
Blood clots within the expanded
ventricle may compress terminal veins, which run at the bottom of both lateral
ventricles.
Doppler Sonography
As mentioned previously
periventricular haemorrhage is in its purest form a haemorrhagic infarction. The haemorrhagic component of the
infarction tends to be most concentrated near the ventricular angle where the
medullary veins, which drain the periventricular white matter, become confluent
and ultimately join the terminal
vein in the subependymal region .
In coronal sections the lesion appears as a unilateral, asymmetric,
globular, crescentic or triangular-shaped echodensity, radiating from the external
angle of the lateral ventricle.
On parasagittal projections, the full extension of the lesion is visualised
best. It may be classified as localised
(involving only the frontal,
parietal or parietooccipital region) or extensive (extending from frontal to the
parieto-occipital region)
80
% of parenchymal lesions were
observed in association with a large intraventricular haemorrhage. The
haemorrhagic lesion invariably occurred on the same side of the larger amount
of intraventricular blood . The haemorrhagic infarction usually developed and
progressed after the occurrence of a severe intraventricular haemorrhage .Large
intraventricular haemorrhages may impede the venous drainage from the medullary
veins. Colour Doppler and
especially power Doppler can display venous drainage of the periventricular
white matter . If high-resolution transducers are used, even smaller medullary veins which drain the periventricular white matter can be shown . Medullary veins gather at the lateral border of the side ventricle and form the subependymal veins which run at the roof and bottom of the lateral ventricle . The largest of the draining veins is the terminal vein, which runs at the bottom of the ventricle . With good ultrasound equipment (high-resolution transducers, high sensitivity of colour Doppler), these veins can easily be shown . In moderate intraventricular haemorrhages colour Doppler displays the veins within the echogenicity .
With pulsed Doppler sonography, a continuous flow with low flow velocities of 2–4 cm/s can be found .
Severe intraventricular
haemorrhages may compress the terminal vein and impede the drainage of the
medullary veins. According to the Bernoulli equation, flow velocities initially
increase within the vein . A further
increase of the compression may
lead to complete cessation of blood flow in the terminal and subependymal
veins and cause haemorrhagic
infarction of the periventricular region.
Doppler sonographic studies of
Taylor and Dean have shown a clear relationship between patency of the terminal
vein and development of periventricular haemorrhagic infarction .
Subdural
and Epidural Haemorrhage
Subdural and epidural
haemorrhages are usually caused by traumatic injury. They may also occur after
difficult delivery or traumatic injury in infancy and later childhood. Rare
causes of subdural or epidural haemorrhages are coagulation disorders such as
thrombocytopenia, haemophilia or disseminated intravascular coagulation
associated with severe infections.
Subdural haemorrhages usually
are caused by rupture of the bridging veins or tears within the large cerebral
sinuses. In neonates subdural haemorrhage may be caused by tentorial laceration
and rupture of the straight sinus, transverse sinus, the great vein of Galen
and infratentorial veins .
Epidural haemorrhages most often
are the result of a tear in branches of the middle meningeal artery. Epidural
haemorrhages however may also originate from major veins or venous sinuses. Epidural
haemorrhages are often associated with skull fractures which cross cerebral
sutures. Subdural haemorrhages are localised between
the surface of the brain and the
dura, whereas epidural haemorrhages are localised between the dura and the
periost of the inner surface of the skull. Rupture of greater intracranial
arteries may cause rapid deterioration of the condition of the child with
transtentorial herniation of the brain, whereas lesions of smaller cerebral
veins often are associated with only minimal symptoms, which may occur after
days or weeks.
2D Image
features
Fresh extracerebral haemorrhages
can be shown as echogenic space-occupying lesions between the hypoechoic brain
and the echogenic skull . Older intracranial haemorrhages get more and more
hypoechoic or echo-free .
Epidural haemorrhages have a convex, lentiform appearance,
whereas subdural haemorrhages are crescent shaped.
The distinction between sub- and
epidural haemorrhage is only academic. More important is the amount of blood,
which may displace intracranial structures and cause cerebral herniation. If
the fontanelle is open, conventional sagittal or coronal sections can be
performed . If the fontanelle is already very small or closed, transcranial
ultrasonography through the intact temporal bone can be performed . Depending
on the age of the
patient, a low transmission
frequency (<3 MHz) should be chosen. In older patients over 6 years, sometimes
low-
frequency transducers of 2 MHz with
better penetration have to be used for transcranial sonography.
• The first aim of 2D ultrasound is the detection and
location of a suspected haemorrhage.
• The second aim is the estimation of the amount of the
haemorrhage.
• The third aim is the detection of signs of
compression or displacement of normal structures: Larger haemorrhages may cause
compression of adjacent normal cerebral structures and midline shift and
transtentorial herniation.
• The fourth aim is to detect signs of increased intracranial
pressure: A greater haemorrhage leads to an increase of intracranial pressure and
a compression of cerebral vessels, which can be detected by spectral Doppler.
Doppler
Sonography
Doppler sonographic flow
measurements should be performed in all patients with intracranial haemorrhage.
As shown previously these measurements can be performed in the anterior
cerebral, the internal carotid arteries and the basilar artery by the
transfontanellar approach. If the transtemporal approach is used, additionally
both
middle cerebral arteries and the
anterior and posterior cerebral arteries can be measured.
Larger haemorrhages may lead to a compression of the intracranial arteries especially in the neighbourhood of the bleeding. Major haemorrhages may cause a significant increase of the intracranial pressure which may further compress the other intracranial vessels. This may lead to alterations of the diastolic amplitude in all intracranial arteries. The most sensitive method for the detection of increased intracranial pressure is the comparison of the flow velocities in the intra- and extracranial part of the internal carotid artery . In normal infants intracranial flow velocities do not differ significantly from extracranial flow velocities. In patients with increased intracranial pressure, the cerebral part of the artery is compressed, whereas the extracranial part is protected
by the petrosal bone. According to the Bernoulli equation in a compressed vessel, the flow velocities increase. An increase of the peak systolic velocity within the cerebral part of the internal carotid artery in comparison with the petrosal part is the most sensitive sign of an increased intracranial pressure .
A significant increase of the
intracranial pressure first may lead to an increase of all intracranial flow
velocities. A further increase leads to a decrease of the diastolic amplitude,
whereas the systolic peak further increases or is unchanged. In severe
haemorrhage the end-diastolic flow may be absent or even retrograde. In these
cases intracranial pressure is severely elevated. If the end-diastolic flow
velocity is zero, the intracranial pressure
corresponds to the diastolic blood pressure which can be measured non-invasively. In the case of retrograde diastolic flow, intracranial pressure exceeds the diastolic blood pressure .
As mentioned previously severe
subdural haemorrhage may also be caused by disseminated intravascular
coagulation. In these cases a midline shift can be found . The increase of intracranial
volume is caused by a significant amount of blood which may lead to herniation of
intracranial structures. Significant increase of the intracranial pressure
leads to compression of the intracranial arteries. Flow measurements may show a
significant decrease of the diastolic flow or even negative flow in all
intracranial arteries .
Diastolic zero flow or even backflow is a bad
prognostic sign, as cerebral perfusion may fall under a critical limit . Most of these patients die, due to longer-lasting bad
cerebral perfusion and following severe brain injury. If diastolic backflow is
found in cerebral arteries, haemodynamic causes of diastolic backflow (especially
a leakage of the aortic Windkessel) have to be excluded.
To rule out haemodynamic causes
of diastolic backflow, flow measurements in extracranial arteries such as the
celiac trunk or renal arteries should be performed. Normal flow in the
extracerebral arteries such as the celiac
trunk excludes a significant
leakage of the aortic Windkessel. In all other cases a thorough
echocardiographic
investigation has to be
performed to exclude congenital cardiac malformations with a defect in the
aortic Windkessel.
A patient with significant
intracranial haemorrhage and decreased diastolic blood flow velocities does not
need a thorough Doppler sonographic investigation but a rapid neurosurgical
intervention! The haemorrhage must immediately be surgically evacuated,
bleeding stopped and raised intracranial pressure decreased, to prevent
irreversible brain damage and severe handicap.
Subarachnoid
Haemorrhage
Primary subarachnoid haemorrhage
refers to a bleeding within the subarachnoid space. Subarachnoid haemorrhage is
not secondary to the extension of blood from the intracerebral, subdural,
epidural, cerebellar or intraventricular space. It is usually not the
consequence of bleeding from a tumour, coagulation disorder or vascular malformation
.
Subarachnoid haemorrhage is more
frequent in the premature infant than in the term neonate. It is almost always
benign. Many of subarachnoid haemorrhages relate to trauma or circulatory
events associated with prematurity.
Infants typically do well. They
show no neurological signs or come to evaluation with minimal .symptoms, such
as seizures.
In seldom cases with massive
subarachnoid haemorrhage, patients exhibit massive deterioration with sometimes
fatal course .
2D
Ultrasound features
Detection of subarachnoid
haemorrhage by ultrasound is difficult. As the periphery of the brain is echogenic,
haemorrhages can often not be differentiated from the brain surface for sure.
Thorough examination however may detect subarachnoid haemorrhage by increased
echogenicity of the corresponding brain surface . Greater haemorrhages may
distend the Sylvian fissure in the individual case. In fatal cases, further
investigations by two-dimensional ultrasound show hypoxaemic-ischaemic lesions
in the region where initially subarachnoid haemorrhage could be shown .
Doppler
Sonography
Small amounts of blood will not
change blood flow and blood flow velocities. Greater amounts of subarachnoid
blood may influence flow profiles and flow velocities. Due to vasospasm an increase
of the flow velocities can initially be found, which may be caused by
subarachnoid blood. In severe cases even decreased diastolic
amplitude and a decrease of the
end-systolic and end-diastolic flow velocities can be found . Prognosis in
these cases is very bad. Severe hypoxaemic-ischaemic lesions adjacent to the
initial bleeding can be found..