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Neonatal Intracranial Haemorrhage


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.

Heubners artery : The germinal matrix is perfused by a branch of the anterior cerebral artery, the Heubners 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 Heubners 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 Heubners 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 3050 % 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.



About 8090 % 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 1525 % 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 Papiles classification) and ventricular dilatation (a characteristic of grade III in Papiles 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 Heubners 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.




 There was a good correlation of fluctuating flow velocities with fluctuating blood pressure. Due to missing autoregulation of brain perfusion, alterations of blood pressure are directly transmitted to the brain. Low blood pressure causes low flow velocities and possibly low perfusion and vice versa.

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 90100 %, 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 1520 % 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 23 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 24 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..

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