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148
M. Riccabona
• Calcications—after infection and ischemia, particularly in basal ganglia.
• Residual choroid plexus or parenchymal lesions—posthaemorrhagic, postisch­emic, posttraumatic, etc.
Signs for increased intraventricular and/or intracranial pressure:
• Inhomogenous structure around ventricles, potentially some small hyperechoic cystic lesions—sign for either focal hypoxia or posthaemorrhagic or venous infarction (e.g. due to obstruction of draining periventricular veins during ven­tricular dilatation).
• Ballooning of temporal horn.
• Narrowing of external CSF spaces.
• Ventricles can be very narrow or slit like (e.g. in brain oedema after hypoxia).
• Extra-axial cause for increased brain pressure due to focal pathology (arachnoid cyst, subdural/epidural haemorrhage/effusion)—locally compressed paren­chyma, attened brain surface and potentially midline shift.
Differentiation epidural/subdural from subarachnoid space:
• Subarachnoid space—reaches into sulci, has network of crossing vessels and mildly echoic lines.
• Subdural space—does not reach into sulci, usually anechoic and only a few major bridging veins use aCDS.
Note In chronic and recurrent subdural effusion, multiple septae and layers of dif-
ferent echogenicity may occur.
Role of CDS in Increased Intracranial Pressure
Early phase, only slight increase in intracranial pressure—normal or slightly reduced resistive index (RI) (reactive diastolic hyperaemia), generally increased ow velocities.
Things change when pressure gets higher:
• Diastolic ow velocity decreasing—elevated RI:
– There may be tent-shaped antegrade diastoly in early phases—similar to
severe hypoxia.
• Systolic velocities decreasing—transient “pseudo-normal” RI.
• Diastole more affected reversed diastolic ow, RI>100%:
– Sometimes difcult to differentiate from other systemic reasons
such as PDA.
– Severely increased brain pressure—eventually leads to signicant reduction
of systolic ow velocity and signicant arterial perfusion decit (see also: brain oedema and brain death).
8 Neurosonography inNeonates, Infants andChildren
149
Other Techniques to Depict Increased Brain Pressure
Fontanellar pressure: apply gentle pressure on fontanel with nger while perform­ing DS of one of the major basal vessels (commonly MCA)—in case of signi­cantly increased brain pressure rst diastolic and then systolic ow velocities reduced during manoeuvre (Fig.8.9).
DS of ICA at extra- and intracranial portion from transfontanellar access (Fig.8.31):
fontanellar DS visualises ICA siphon cursing into head (both in coronal and parasagit­tal view)—place duplex gate for spectral trace in extracranial and intracranial ICA portion (Fig.8.32), calculate ratio between systolic intra- and extracranial velocities and RIs (equation=V
intracranially divided by V
syst max
extracranially):
syst max
• Normal—ow spectra do not differ, velocity ratio=1 (0.8–1.2).
• Slightly increased brain pressure (<10mmHg)—slight elevation of systolic ow velocity intracranially and only mild variation of diastolic ow, velocity ratio=>1.2.
• Signicantly elevated brain pressure (>10mmHg)=altered systolic+diastolic ow, velocity ratio<0.8.
US for Following Up Hydrocephalus With/Without Shunts
• All basic US criteria apply.
• Additionally try to visualise shunt drain: course, tip of drain and look for drain discontinuity.
Note Can be difcult, often transtemporal or transmastoid access necessary
(Fig. 8.33). Tip of shunt may be less echogenic than more peripheral part and missed, depending on US beam angle and access:
Fig. 8.32 Doppler in hydrocephalus. (a) Slightly elevated brain pressure, indicated by change of ow prole in intra-/extracranial ICA portion measured from fontanellar access in a coronal sec­tion. (b) TCI-Doppler for measuring ow response during fontanellar pressure (“druck”): no sig­nicant change in MCA ow pattern in this preterm baby with posthaemorrhagic hydrocephalus
150
Fig. 8.33 US/TCI in shunted hydrocephalus—mostly used in slightly older infants with (nearly) closed fontanel. (a) TCI: two drains, one in each lateral ventricle, with different ventricular disten­sion. Note a slight subdural effusion on the side with the smaller ventricle as a sign of overshunting. (b) TCI, axial view, 9month old infant: shunted hydrocephalus (shunt=arrow), still large ventricles
M. Riccabona
Fig. 8.34 US for assessing complications in shunted hydrocephalus. (a) Linear transducer, neck: disruption (++) of subcutaneous portion of shunt. (b) Fluid pouch in supercial subcutaneous soft tissue next to the drain (arrow) that is disconnected
• Always assess valve (effusion?).
• Try to follow extracranial partition of drain (subcutaneous track in skull, neck and chest easily seen)—disruption—focal uid effusions along drain path due to leakage/rupture (Figs.8.33a, b and 8.34).
• CDS: only useful if cellular components in CSF (if sound can penetrate— depending on material of shunt).
• Assess abdominal part of shunt: pseudocyst around intraabdominal tip may cause obstruction, free peritoneal/pleural uid helps to indicate drain function (but not a proof of proper drain function!), evaluate for peritonitis in children with pain, etc. (see respective chapter).
Note US may nd causes of obstruction or dysfunction and can depict size increase
of CSF space or perfusion deterioration due to increased brain pressure. However, US does not depict/rule out all causes of potential shunt complications, chronically or moderately increased brain pressure, stiff ventricle syndrome, etc.:
• CDS may show CSF flow in foramina of Monro, Magendie and Luschka and aqueduct—provided that there are reflectors in CSF (e.g. posthaemorrhagic particles, increased CSF protein levels and inflammatory cells) (Fig.8.35a, b).
ab
8 Neurosonography inNeonates, Infants andChildren
c
151
Fig. 8.35 Special applications of modern US in hydrocephalus. (a) Magnied fontanellar sagittal midline view: CDS demonstrates CSF ow in aqueduct. (b) Duplex Doppler trace conrms bidi­rectional undulating CSF ow. (c) 3DUS in hydrocephalus: three orthogonal views and rendered lateral ventricles (right lower box)
• Unusual access to extracerebral CSF spaces—use eye/orbit as US window. In increased intracranial pressure—optic nerve sheet dilatation and protrusion of papilla (see section/entry: US of eye).
• In CSF fistula: US may demonstrate fistula (if large enough and accessible) and show flow through fistula by aCDS if particles in CSF or relatively high flow velocities (cause some jet phenomenon, where one may find intermit­tent undulating jets that vary with respiration or with other forms of
152
M. Riccabona
increased thoracic pressure, such as, crying, breath hold and ventilation manoeuvres).
Note For any measurements of CSF spaces, standardised approach with reproduc-
ible measurements should be applied; CSF overdrainage can cause ventricular col­lapse and secondary subdural haemorrhage/effusion which may clinically mimic shunt dysfunction and increased brain pressure.
• 3DUS particularly valuable: complete documentation, reproducible measure­ment at comparable section and comparison to other sectional imaging (any desired section may be reconstructed from 3DUS data set) (Figs. 8.35c and respective chapter).
8.3.9 Cerebral Haemorrhage
Various forms of haemorrhage need to be differentiated in terms of location and aetiology: intra- and extracranial, intra- or extraventricular, parenchymal, extracere­bral (sub-galeal haematoma, subcutaneous haematoma, subdural, epidural, sub­arachnoid, etc.). etc. (Fig.8.36). Type of haemorrhage varies with age: preterms have different haemorrhages than term neonates or infants.
8.3.9.1 Haemorrhage inPreterm Babies: IVH Grades I–III, PVH
(Fig.8.37)
Typically occur in germinal matrix near head of caudate nucleus, where immature vessels tend to rupture with only mild trauma, unstable blood pressure and intravas­cular volume changes, etc.
IVH I: on US echogenic round or oval-shaped area below plexus and head of
caudate nucleus (intraventricular haemorrhage grade I = IVH I)—to be
Fig. 8.36 Scheme: cranial haemorrhages. Typical extra- (a) and intracranial (b) haemorrhages— site and respective appearance. Abbreviations: SEB/SEH subependymal bleed/haemorrhage, EDH epidural haematoma, SDH subdural haematoma, ICH intracerebral haemorrhage, IVH intraven­tricular haemorrhage, SAH subarachnoid haemorrhage and PVH periventricular haemorrhage (adapted from C. Roll / Datteln Germany)
de
8 Neurosonography inNeonates, Infants andChildren
153
a
b
c
fg
Fig. 8.37 Images and schematic drawings demonstrating classication and image appearance of brain (intraventricular) haemorrhage in preterms. (a) Scheme plexus bleed and IVH grade I° (sub­ependymal bleed/haemorrhage=SEB/SEH), IVH intraventricular haemorrhage. (b) Scheme IVH grade II°, III° and IVH+periventricular haemorrhage (=PVH, older term IHV IV°). (c) Parasagittal view: IVH I°/SEB, clot seen as somewhat echogenic nodular structure (may be difcult to differ­entiate from plexus haemorrhage). (d) Parasagittal view: IVH II°, huge clot in the plexus, a little bit of blood in the posterior horn. (e) Coronal view: fresh haemorrhage with blood lling the entire ventricle lumen=IVH grade III°. (f, g) Coronal view: haemorrhage with periventricular haemor­rhagic infarction/PVH on right (f) or left (g) (++) side
differentiated from swollen choroid plexus (also echogenic, but usually entire plexus affected) or choroid plexus bleeds (occur at any location of plexus, but commonly close to frontal attachment, located within plexus). For differentiation—axial sec­tion or axial 3DUS reconstruction helpful.
154
M. Riccabona
IVH II: if grade I haemorrhage increases, it ruptures into ventricle—some blood
seen in ventricle (grade II haemorrhage). Initially ventricles not dilated, only little blood or some clotting in ventricle.
IVH III: with progression of haemorrhage ventricles get dilated, increasingly
lled with blood (grade III haemorrhage). Blood also seen in third and fourth ventricle due to physiological CSF drainage pathways. Due to dilatation of ven­tricle paraventricular draining veins get compressed/obstructed/congested— cause venous infarction of periventricular respective areas haemorrhagic infarction.
IVH III + PVH: combination of periventricular haemorrhagic infarction with
grade III haemorrhage (initially called type IV haemorrhage, now classied as haemorrhage grade III + periventricular haemorrhage = PVH)—attributing new insight into aetiology and pathophysiology.
8.3.9.2 Haemorrhage inTerm Infants
Much rarer, usually do not occur as IVH but as intraparenchymal haemorrhages (intracerebral haemorrhage—ICH).
Typical locations: basal ganglia and locations of haemorrhagic venous infarc-
tions (Fig.8.38).
Rare other causes that dene locations—secondary haemorrhage into hypoxic
areas or trauma:
• Epidural haemorrhages—EDH (e.g. after forceps delivery or skull fractures), use TCI (Fig.8.39).
• Subdural haemorrhages—SDH (consider shaken baby syndrome), linear trans­ducer and TCI helpful (Figs.8.30 and 8.20d).
• Subarachnoid haemorrhages—difcult to see on US unless large; cause increased echogenicity between the sulci.
• Tentorial bleeds (e.g. after complicated foetal repositioning manoeuvres or breach delivery) (Fig.8.40).
• Direct impact (trauma), by caesarean section (e.g. cutting too deep, thus injuring brain through fontanel).
Unexplained haemorrhages in neonates and young infants raise suspicion of
Note
nonaccidental injury (NAI)—thorough workup.
US Appearance
All haemorrhages have similar US appearance and development:
• Hyperacute state: blood has similar echogenicity as surrounding tissue—not seen.
• (Sub)acute state: bright echogenic spot.
• Further course—sedimentation and resorption: inhomogenous with some hyper­echoic areas and clot formation—usually inhomogenously echogenic, tumour­like areas (Fig.8.41).
8 Neurosonography inNeonates, Infants andChildren
Fig. 8.38 Examples for other cerebral haemorrhages and DDx. (a, b) Basal ganglia haemorrhage (echogenic mass) in term infant (a) coronal and (b) (para-)sagittal section. (c, d) DDx in haemor­rhage: Echogenic swollen plexus (b, sagittal section) with hypervascularity on CDS (c, coronal view) in a plexus papilloma
155
Fig. 8.39 Epidural haemorrhage (++). Axial view—TCI, magnied section: subcalvarian complex ovaloid uid space-occupying lesion in terms of a subacute EDH
• Eventually resorbed—cystic remnants, hyperechoic ventricular wall and paren­chymal defects (Fig.8.20).
• Impairment of CSF circulation may cause hydrocephalus—careful monitoring and assess need for CSF drainage:
– Early phase: drainage sometimes achievable by repeated lumbar punctures. – Later phases: external drainage and shunt placement necessary.
156
M. Riccabona
ab
Fig. 8.40 Tentorial and cerebellar haemorrhage. (a) Coronal section, linear transducer: tentorial and cerebellar haemorrhage. (b) Same patient as in (a) tilted mastoid-axial view: superior demon­stration of bleed
Fig. 8.41 Clot and hydrocephalus after IVH III. (a) Coronal section demonstrating inhomoge- nously echogenic masses within lateral ventricles obstructing foramen of Monro. (b) Parasagittal view: demonstrates clots in dilated lateral ventricle after IVH III
Note Every term neonate and young infants with haemorrhage may suffer from
rare underlying disease, e.g. coagulopathies, venous thrombosis, vascular anoma­lies, underlying tumours, hyperviscosity, hypoxia, ischemia, dehydration, septicae­mia and meningoencephalitis. Differentiation by US often difcult or impossible (e.g. haemorrhagic infarction difcult to differentiate from haemorrhage without underlying infarction).
8.3.9.3 Role ofCDS inNeonatal Haemorrhage
Doppler and CDS does not help in dening aetiology or predicting haemorrhage, however, reduced ow velocities and large uctuation of ow spectra with repeated examinations (due to lack of autoregulation) associated with higher risk of haemorrhage:
• Only in severe active bleeding increased particularly diastolic ow with reduced RI seen in feeding vessel.
• Sometimes CDS depicts vascular anomaly that caused haemorrhage.
8 Neurosonography inNeonates, Infants andChildren
157
• CDS helpful for depiction of thrombosis of large venous pathways.
• aCDS is helpful to differentiate swollen choroid plexus (with existing perfusion) from choroid plexus bleed or clot.
8.3.9.4 Haemorrhage inInfants andOlder Children
After fontanel closure and increasing skull ossication, US possibilities decrease; particularly detailed assessment of small changes or exclusion of haemorrhage becomes increasingly difcult and eventually impossible. However, TCI can used as a rst orientation - but often CT and MRI are mandatory.
US Findings
• Haemorrhage as in transfontanellar view—initially echogenic, relatively sharp margins.
• As long as US access and penetration possible, large parenchymal bleeds and large SDH/EDH can be depicted, particularly if it causes some mass effect and distorts ventricles or midline structures.
Note Do not mistake repeating echoes from (contralateral) skull on transtemporal
images for haemorrhage.
• SDH may be recurrent—thus septae develop, with different echogenicity in vari­ous compartments. If chronic—hygroma.
Note Usually brain surface attened and sulci narrow in area of haematoma—in
atrophy sulci enlarged without attening of brain surface. If SDH of different age, always think of NAI, then try to assess near-eld cortex for depiction of typical teardrop lesion (resorbed focal venous infarctions) in (sub)cortical area—may be missed if only sector array used (Fig.8.20).
• Cerebellar and tentorial haemorrhages rare, also bleeds of brain stem and other posterior fossa structures. Difcult for US once skull ossied. Usually have poor prognosis.
• Transmastoid, -occipital and -temporal access mandatory when evaluating these potential pathologies.
In older children with appropriate history or symptoms, emergency imaging
Note
by CT and/or MRI indicated.
• Helpful application: assessment of skull and galea by high-resolution linear transducers. Haematoma seen, formation of seroma can be documented and measured, skull fractures—even if only subtle—usually nicely depicted by showing disruption of skull surface echo (Fig.8.42).
• Skull US also helpful for assessment of other skull or skin lesions; e.g. epithelial cysts, histiocytosis, eosinophilic granuloma, metastases, and in some places also applied for assessment of craniosynostosis.