Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5795_Библиотеки_им_академика_М_И_Перельмана.pdf
138
Fig. 8.21 PVL and white matter atrophy. Early PVL in coronal (a, b) and parasagittal (c) view—
seen as patchy bright focal periventricular echogenicities. Note enlarged extra-axial CSF space in
a. (d) Coronal view: preterm infant with patchy ocipital paraventricular echogenicities in bilateral
PVL with secondary haemorrahgic component (“haemorrhagic infraction”) (e) Coronal view:
Bilateral beginning cystic paraventricular defects in subacute PVL. (f) Parasagittal view: PVL with
multiple conuent cysts replacing destroyed white matter. (g) PVL in older infant with narrowed
occipital periventricular white matter on the left side, thus the sulci nearly reach the ventricular
wall of the clubbed and enlarged posterior horn of the lateral ventricle, as late sign of PVL (same
criteria as used in MRI)
M. Riccabona
8.3.5.2 Global or Diffuse Brain Oedema
Typical in severe conditions and mature brain—subdivided in global, cortical, brain
stem and basal ganglia hypoxia.
US Findings
• In periacute phase: brain looks completely normal.
• After 8–72h, brain becomes hyperechoic, with loss of cortico-medullary differentiation (“bright brain”), or inversed echogenicity of usually slightly hypoechoic
cortex from hyperechoic white matter (particularly in cortical ischemia). Due to
oedema, CSF spaces become narrowed, particularly obvious at lateral ventricles
(Fig.8.22). Often also just hyperechogenicity of stemm ganglia.
• Later, damaged and necrotic areas become cystic or gliotic, the latter difcult to
depict on US.
• Finally, brain atrophy—with widening of inner and outer CSF spaces, widening
of sulci and intrahemispheric ssure, disruption of cortico-medullary differentiation of brain parenchyma (Fig.8.23).
Note Grey scale US ndings very nonspecic; diagnoses and follow-up of brain
oedema relies on Doppler ndings, as increased intracranial pressure will impair
cerebral perfusion—discussed below.
8 Neurosonography inNeonates, Infants andChildren
Fig. 8.22 Brain US in asphyxia. (a) Coronal view: bright brain. (b) Linear transducer, coronal
view: cystic degeneration after severe asphyxia
139
Fig. 8.23 Brain atrophy. (a) Coronal view in brain atrophy: large intrahemispheric ssure (IHF)
and/extra-axial CSF space, somewhat prominent ventricles. (b) Coronal view with linear transducer: widened IHF, large extra- axial CSF space and lateral ventricles
8.3.5.3 Focal Hypoxemia andIschemia
US Findings
• Initially normal US.
• When oedema manifests—increasing echogenicity due to swelling and oedema
around affected area with some swelling as well as disruption of typical corticomedullary differentiation (Fig.8.24).
• Sometimes inversion of echogenicity of cortex and white matter.
• Potentially secondary haemorrhage—focal patchy echogenicities (Fig. 8.25),
sonographically indistinguishable from typical haemorrhagic infarction after
venous thrombosis (except for location—always also assess veins if unclear or
unusual).
• Small focal infarctions are sonographically difcult to detect, usually only
depicted in near eld when using high-resolution linear transducers.
140
ab cc
Fig. 8.24 US in infarction. (a) Coronal view: MCA infarction in subacute stage: increased echo-
genicity of affected left MCA territory. (b) Axial view by TCI: increased echogenicity indicating
infarction of ACA territory. (c) Parasagittal view: older stage of an MCA infarction with cystic
transformation
Fig. 8.25 Coronal view: haemorrhagic infarction
in early stage. Coronal view: echogenic,
somewhat triangular shaped defect in frontal area
in a baby with haemorrhagic infarction of the
right ACA territory
M. Riccabona
• Eventually focal infarctions form focal defects: cysts, gliosis (difcult to depict
on US), focal atrophy, etc.
• Haemorrhagic areas can form secondary calcications.
Note Infarctions will adhere to distributional areas—may affect either watershed
area or territory of major vessels. Sometimes steal phenomena may lead to more
diffuse or multifocal manifestation, e.g. in large vascular malformations with
shunt ow.
Infarction in Older Child
US not routinely used for diagnosis, but helpful for bedside follow-up (vessel
patency, perfusion state during neuro-resuscitation therapy, etc.). Usually no grey
scale ndings, just (a)CDS helpful.
Specic use of transcranial CDS: assessment of infarction risk by monitoring
children with sickle cell disease (see below).
8 Neurosonography inNeonates, Infants andChildren
141
8.3.5.4 (C)DS inBrain Hypoxia
General remarks: for spectral ow analysis, always consider potential inuence of
other systemic factors such as ventilation, medication, cardiac output, heart rate, etc.
Focal ischemia—aCDS may depict lack of ow signals in affected area:
• With some delay—reactive perifocal hyperaemia (“luxury perfusion”).
• If main vessels and large area affected—asymmetric ow proles on spectral
analysis of corresponding feeding arteries, or lack of ow on CDS if
vessel occluded.
Global/general hypoxia and brain oedema—typical phases (Fig.8.26):
• Phase I: normal vascular anatomy with normal ow spectra (up to 24 h
after event).
• Phase II—reperfusion and hyperaemic phase: increasing diastolic ow, poten-
tially also increased systolic velocity and decreased resistive index—these ndings usually associated with risk of only mild neurologic decit.
• Phase III—increasing brain pressure: if process cannot be controlled in stage II,
increasing oedema causes increasing peripheral resistance and rising intracranial
pressure. Initially leads to reduction of diastolic, then also systolic ow velocities.
Consecutively and constantly increasing RI values. In transition phase RI values
may become (pseudo-)normal, before they progress. If typical phase III pattern
with reduced systolic velocity and elevated RI due to signicantly reduced diastolic ow depicted—high probability of severe neurologic decits with worst
prognosis in those infants where these ndings persist longer.
Fig. 8.26 Flow spectra in brain oedema—
various stages. (a) Initial stage—normal ow.
(b) Hyperaemic phase, high diastolic ow.
(c) Beginning intracranial pressure, tent-shaped
diastolic ow. (d) Increasing intracranial
pressure, reversed diastolic ow. (e) Short spikes
without antegrade perfusion in brain death
142
M. Riccabona
Another typical pattern of phase III: tent-shaped diastolic ow spectrum with
lower end systolic and early diastolic velocity, higher velocity in mid-diastole
and again low end-diastolic velocity.
• Phase IV: with increasing intracranial pressure ow becomes increasingly pulsatile with reversed diastolic ow, increasingly reduced systolic ow velocities,
eventually only showing undulating signals with no sufcient antegrade perfusion—as all blood inow during systole ows out during diastole—constitutes
lack of peripheral brain perfusion and inevitably leads to brain death.
• Phase V—brain death: lack of parenchymal perfusion and no ow seen in major
vessels.
These phenomena apply also to older children in ICU for bedside monitoring.
Note Conrm severe ndings by (C)DS of cervical vessels and/or by ce-US; in
some countries persisting ndings of phase V-accepted for diagnosing brain
death (repeated examinations mandatory). Missing or reversed diastolic ow
with low systolic ow velocities or tent-shaped diastole indicates poor prognosis.
8.3.6 Other applications of (C)DS:
• (C)DS can be utilised to titrate optimal PCO2 for ventilation support at the bedside by performing duplex studies while altering respirator settings under constant PCO2 monitoring, thus dening PCO2 level which correlates with most
normal ow proles—to avoid perfusion decits and hyperperfusion (which
increases brain oedema risks).
• TCI-DS for monitoring sickle cell anaemia: screening for overt or silent infarction
and risk of (re-)infarction—high ow velocities = reliable predictor of stroke.
Measurements of time-averaged mean of maximum velocity velocities (TAMx) or
maximum systolic velocity of MCA most commonly performed in diseased children (not only with trait): normal <170cm/s, conditional=170–200cm/s (indicating closer follow-up), and abnormal >200 cm/s then (after conrmation with
repeated study within a week) indicating MR angiography for conrmation or
immediate treatment (Fig.8.27). Standardised assessment of all major intracranial
vessels essential, potentially include cervical arteries.
8.3.7 Inflammation
Introduction
US only shows indirect changes (signs that may be compatible with inammation)
or complication (e.g. abscess formation and haemorrhage). Final diagnosis always
needs other tests (lumbar puncture, blood samples, MRI, etc.).
ab
8 Neurosonography inNeonates, Infants andChildren
Fig. 8.27 Transcranial Doppler sonography (TCD) for monitoring sickle cell anaemia patients
with respective measurements: Note the difference between TAMx and TAMm—not to be confused to avoid wrong classications (a). Same patient without correction of automated Doppler
tracing (arrow)—this automated trace may be wrong and needs to be observed and corrected;
however, in this case only inuences TAMm and not TAMx or maximum systolic velocity (b)
143
MRI method of choice for evaluating central nervous system complications—
particularly in older children.
Note In spite of existing infection, US ndings may be completely normal.
8.3.7.1 Prenatal Intrauterine Infections andResiduals
Common causes for prenatal CNS infections are cytomegalovirus, herpes, toxoplasma, HIV and rubella (TORCH). Less common than in earlier times, but still
exist and lead to various postnatal US ndings.
Postnatal US Findings
• Hydro-, micro- and macrocephalus.
• Intracerebral calcications, band-like or stippled—most commonly in area of
basal ganglia (small echogenic foci, commonly without acoustic shadowing)
(Fig.8.28a).
• Non-calcifying vasculopathy as remnant of vascular involvement: band-like
echogenic stripes, particularly in basal ganglia along perforating arteries (not
specic, many other entities that affect vessels and perivascular bed)
(Fig.8.28b)—see also respective entry.
• Hemispheric calcication occurs, can be large—see also 8.3.9.
• Porencephalic defects, multicystic encephalopathy and atrophy.
144
Fig. 8.28 Intracranial/cerebral calcications. (a) Frontal coronal view: spotted multifocal cere-
bral calcications in the white matter after foetal TORCH infection. (b) Parasagittal view: noncalcifying vasculopathy (arrows)
M. Riccabona
Differentiation of metabolic causes, remnants of other prenatal CNS complica-
tions, remnants of prenatal haemorrhages, ischemic changes, etc. from (TORCH)
infections may be difcult.
8.3.7.2 Postnatal Inflammation
Meningitis
• Bacterial meningitis: widening of extra-axial CSF spaces with internal echoes,
may have debris/CSF layering (Fig.8.29a, brain).
• Some correlation of distribution of ndings with aetiology, e.g. tuberculous meningitis often manifests basally.
• Empyema may occur (Fig.8.29b).
Note Postinammatory hydrocephalus may develop—children should have fol-
low- up imaging.
Meningoencephalitis
• Commonly viral—ndings subtle.
• If brain involved: focally altered echogenicity similar to ndings in infarction or
ischemia.
• Secondary haemorrhage may occur, particularly in herpes encephalitis.
• Sequelae cannot be distinguished from other causes. Manifest as focal atrophy,
porencephalic and cystic defects, hydrocephalus and calcications.
• If calcication-like echoes seen in early stages of disease, consider rare or atypical aetiology (e.g. fungal infection and echinococcal abscess).
Ventriculitis and Brain Abscess
• Typical nding: thickened echogenic ependyma of ventricular wall with irregularly thickened swollen choroid plexus.
• CSF in ventricles shows echoes and sedimentation, which vary with brain positioning.
8 Neurosonography inNeonates, Infants andChildren
Fig. 8.29 Brain US in inammatory conditions. (a) Coronal view, near eld, linear transducer:
purulent meningitis—echogenic content in extra-axial CSF space, echogenic and thick arachnoid.
(b) Coronal view, sector transducer: frontoparietal empyema (++). (c) Coronal view: (sub-) cortical brain abscess (++)
145
• Complications: hydrocephalus, compartmentalisation of ventricular lumen and
isolated (fourth) ventricle (see hydrocephalus 8.3.7).
• Brain abscess: focal echogenicities with relatively sharp borders, surrounded
by hypoechoic oedematous rim and eventually central inhomogenously
hypoechoic space (central necrosis). With ongoing disease central necrosis
becomes larger, wall-like demarcation of abscess, eventually with thick capsule (Fig.8.29c, d).
• Haemorrhages or vascular malformations may initially be difcult to differentiate from abscess by US.Only by monitoring the imaging course of disease (with
better differentiation of necrosis and detritus as well as sedimentation) and with
clinical information the aetiology becomes evident.
Note Abscesses may connect with ventricular lumen.
CDS in Mening(oencephal)itis
May demonstrate hypervascularity of meninges as well as around capsule of
abscess.
• Flow spectrum exhibits diastolic hyperaemia with elevated diastolic ow velocity and low RI values (additional diagnostic hint).
8.3.8 Dilatation ofCSF Spaces: Hydrocephalus
Introduction and Definition
Hydrocephalus—dilatation of internal and/or external CSF spaces. Dilatation does
not mean increased intracranial pressure—there can be dilatation without increased
pressure and also increased pressure without dilatation.
Note Only increased intracranial pressure needs treatment.
146
M. Riccabona
Task of US
• Depiction of dilatation/widened ventricles or external CSF spaces.
• Potentially recognise cause of dilatation.
• Find signs that indicate elevated intracranial pressure.
The Most Common Causes
• Posthaemorrhagic or postinammatory.
• Associated with malformations.
• Secondary to obstruction of CSF drainage:
– Dysfunction of ventriculoperitoneal shunt, outow path stenosis, or space-
occupying lesion, adhesions, etc.
• Ex vacuo—atrophy:
– For example, after severe hypoxia, metabolic disease and postinfection.
• Normal variants (i.e. macrocephaly, ventriculomegaly and benign familiar external hydrocephalus/“frontal effusion”/familial benign macrocrania) (Fig.8.30a).
• After trauma (e.g. shaken baby syndrome).
• Increased CSF production (hypersecretory hydrocephalus):
– For example, after inammation or haemorrhage and choroid plexus
papilloma.
• Reduced resorbtion of CSF:
– For example, increased central venous pressure, venous sinus thrombosis, third space
phenomena, jugular vein obstruction and arachnoid granulation dysfunction.
US Appearance
Dilatation of CSF spaces which usually appear anechoic.
Extracerebral CSF spaces:
• Through fontanel—best seen with high-resolution linear transducers in coronal
section (widening of interhemispheric ssure) or when using sector array in
slightly angled coronal section (Fig.8.30a, b).
• Transtemporal/mastoid approach—allows visualisation of contralateral external
extra-axial CSF spaces—also useful for arachnoid cysts, CSF spaces of posterior
fossa and posterior horn of lateral ventricles (Fig.8.30c).
abc
Fig. 8.30 US in dilated extra-axial CSF space. (a) Linear transducer, coronal view: benign sub-
dural effusion/familial macrocephaly (DDx atrophy). (b) Coronal view: SDH after overshunting in
hydrocephalus. (c) Axial view by TCI: chronic, septated temporo-occipital SDH
ab c
8 Neurosonography inNeonates, Infants andChildren
147
US Findings in Dilated Ventricles
Conguration of ventricles helps differentiating supratentorial from infratentorial
or global hydrocephalus using following aspects:
• Foramen of Monro occlusion—dilated respective affected lateral ventricle with
small third and fourth ventricle.
• Aqueductal stenosis—lateral ventricles and third ventricle dilated (supratentorial
hydrocephalus) (Fig.8.31a–c).
• Obstructed foramina of Luschka and Magendie—all ventricles dilated, usually
combined with narrow extra-axial CSF spaces.
• Additional obstruction in subarachnoid space—dilated cisterns.
• Obstruction above and below fourth ventricle—isolated fourth ventricle (Fig.8.31d)—
only fourth ventricle dilated, particularly if supratentorial ventricular system shunted
and drained (rare condition, e.g. after infection, surgery or haemorrhage).
Other US Criteria
Signs that may allow differentiating aetiology:
• Echogenic content—haemorrhage or severe infection.
• Echogenic thickened ventricular wall—ependymitis (nonbacterial inammatory
reaction after haemorrhage due to resorptive phenomena, after ventriculitis, etc.),
with chronically increased pressure.
de
Fig. 8.31 Hydrocephalus. (a) Coronal view: supratentorial hydrocephalus, dilated lateral ventri-
cles (+ +
occluded. (c) Stenosed, but still patent aqueduct—fourth ventricle nicely lled. (d) Open aqueduct
with huge dilatation of forth ventricle on axial view by TCI. (e) Coronal view: dilated “isolated”
fourth ventricle (the supratentorial ventricular system is drained—otherwise one will have to consider severe hypoplasia of the cerebellum)
1,2
) and third ventricle. (b) TCI: Supratentorial hydrocephalus—aqueduct appears