10 yeras experience in paediatric spontaneus intracerebral haemorrhage

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  • 8/11/2019 10 Yeras Experience in Paediatric Spontaneus Intracerebral Haemorrhage

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    Original article S W I S S M E D W K LY 2 0 0 8 ; 1 3 8 ( 5 - 6 ) : 5 9 6 9 w w w . s m w . c h

    Peer reviewed article

    59

    A 10-year experience in paediatricspontaneous cerebral haemorrhage:

    which children with headache need morethan a clinical examination?

    Sandrine de Ribaupierrea, Bndict Rillieta,b, Jacques Cottingc, Luca Reglia

    a Service of Neurosurgery, Centre Hospitalier Universitaire Vaudois (CHUV), Lausanneb Service of Neurosurgery, Hpital Universitaire de Genve (HUG), Genvec Paediatric intensive care unit, Centre Hospitalier Universitaire Vaudois (CHUV), Lausanne

    Introduction: When a child is seen in a clinicwith a headache, stroke is certainly not the rst onthe list of differential diagnoses. In western coun-tries, stroke is typically associated with adults andthe elderly. Although rare, haemorrhagic strokesare not exceptional in the paediatric population,as their incidence is around 1/100 000/year.Prompt diagnosis is essential, since delayed treat-ment may lead to disastrous prognosis in thesechildren.

    Materials and methods: This is a retrospectivereview of paediatric cases with spontaneous cere-bral haemorrhage that presented in two universityhospitals in the last ten years. The experience ofthese primary and tertiary referral centres com-prises 22 consecutive cases that are analysed ac-cording to aetiology, presenting symptoms, treat-ment and outcome.

    Results: 77% of the children diagnosed withhaemorrhagic stroke presented with headaches.41% of them had a sudden onset, while 9% devel-oped headaches over a period of hours to weeks.

    While 9% presented only with headaches, themajority had either subtle (diplopia, balanceproblems) or obvious (focal decits, unilateral

    weakness and decreased level of consciousness)concomitant neurological signs. 55% had an arte-riovenous malformation (AVM), 18% had ananeurysm and 14% had a cavernous malforma-tion. In 14% the aetiology could not be deter-

    mined. The majority of haemorrhages (82%)were supratentorial, while 18% bled into the pos-terior fossa. All children underwent an emergencycerebral CT scan followed by specic investiga-tions. The treatment was dependent on the aeti-ology as well as the mass effect of the haematoma.In 23% an emergent evacuation of thehaematoma was performed. Two children (9%)died, and 75% had a favourable clinical outcome.

    Conclusion: Headaches in children are a com-

    mon problem, and a small minority may reveal anintracranial haemorrhage with poor prognosis ifnot treated promptly. Although characterisationof headaches is more difcult in a paediatricpopulation, sudden, unusual or intense headachesshould lead to imaging work-up.Any neurologicalnding, even one as subtle as hemianopsia or dys-metria, should alarm the physician and should befollowed by emergency imaging investigation. Ifthe cerebral CT reveals a haemorrhage, the childshould be referred immediately to a neurosurgicalreferral centre without further investigation. The

    outcome is grim for children presenting in comawith xed, dilated pupils. The long-term resultoverall for children after spontaneous intracranialhaemorrhage is not dismal and depends criticallyon specialised management.

    Key words: hemorrhagic stroke; pediatric; AVM;cavernoma; aneurysm; headache

    Summary

    Headaches regularly or occasionally occur in1525% of the paediatric population [24]. Whenthey occur, paediatricians or general practitionersare the rst to be consulted. Their clinical appre-ciation of the headache plays a major role in de-

    tecting a serious pathology such as intracerebralhaemorrhage, sinus thrombosis, tumour ormeningitis, as opposed to tension headache, mi-graine, or prodromal symptoms of u or viral dis-eases.

    Introduction

    59

    No financial

    support declared

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    Even though spontaneous cerebral haemor-rhages are rare in children, they must be consid-ered, and excluded rapidly in the differential diag-noses of headaches, as immediate treatmentmight be required in order to avoid devastatingdecits. Unlike benign headaches, serious in-tracranial pathologies are often accompanied bysymptoms, such as vomiting or focal neurological

    signs.Haemorrhagic strokes will, in a majority of

    cases, reveal themselves with an altered level ofconsciousness, but might also be less symptomatic

    with headaches, vomiting, seizures or focal neuro-logical decits [5, 6]. The average incidence ofhaemorrhagic stroke in the paediatric population

    is reported to be between 0.741.1/100000/year[68]. Their incidence is slightly lower than thatof ischaemic strokes; they represent between 27and 52% of paediatric strokes [6, 911].

    The purpose of this study is to analyse thesigns and symptoms of a consecutive paediatricseries presenting with spontaneous cerebralhaemorrhages in two primary and tertiary referral

    centres. The work-up and the treatment of thesechildren are reviewed. Main aetiologies are pre-sented as well as recommendations for follow-up.Differences in the management of haemorrhagicstroke between the paediatric and adult popula-tions will also be highlighted.

    60A 10-year experience in paediatric spontaneous cerebral haemorrhage

    Materials and methods

    We retrospectively reviewed the charts of paediatricpatients (

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    6161S W I S S M E D W K L Y 2 0 0 8 ; 1 3 8 ( 5 - 6 ) : 5 9 6 9 w w w . s m w . c h

    Table1

    Age

    Aetiology

    Grade

    Localisation

    Headaches

    Firsts

    ymptoms

    Signs/symptomsonarrivalatuniversityhospital

    NV

    Seizures

    GCS

    (years)

    1

    0,2

    Aneurysm

    FischerIV

    Lanteriorcereb

    ralartery

    ?

    Fewco

    nvulsions,syncope

    Cardiacarrestduringtransport,opistotonos,

    Yes

    3

    dilatedreactivepupils

    2

    1

    Aneurysm

    FischerIV

    Anteriorcommunicatingartery

    Sudden

    Criesh

    oldinghishead,vomit

    Reactivepup

    ils

    Yes

    Yes

    3

    3

    6

    AVM

    SpetzlerIII

    RParasplenium

    and

    Sudden

    While

    atschool,H

    Athen

    Symetricmo

    uvements

    910

    intraventricular

    decreasedlevelofconsciousness

    4

    6.5

    AVM

    Cerebellumand

    mesencephalon

    ?

    Equilibrium

    Ataxia

    15

    5

    6.5

    ?

    RFrontal

    Yes

    HA,leftsideparesis,memory

    Lsideparesis

    14

    difculties,coordination

    6

    8

    AVM

    SpetzlerIV

    LThalamic

    No

    Rightsideparesis

    Rsideparesis

    15

    7

    8

    AVM

    SpetzlerI

    LFrontal

    Sudden

    Leftey

    epainwithHA,pallor,

    GCS3then

    improvestoGCS11,vomit,desorientation

    ?

    3to11

    lossof

    consciousness,hypotonia

    8

    9.5

    AVM

    SpetzlerIII

    LThalamic

    ?

    Rsideparesis

    Rsideparesis

    15

    9

    9.5

    Cavernoma

    RCerebellum

    Yes

    Cerebellarsigns

    Cerebellarsyndrome

    15

    10

    10

    AVM

    SpetzlerIII

    RFrontal

    Sudden

    ComplainsofHAthenlossof

    Rxeddilatedpupil

    3

    consciousness

    11

    11

    AVM

    Cerebellum

    Sudden

    HAthendecreaselevelof

    Bilateralxeddilatedpupils

    7

    consciousness(10min)

    12

    11

    ?

    Suprasellar

    Progressive

    IncreaseinHA,v

    isualeldloss,

    Progressiveworsening,hypertension,bradycardia

    Yes

    12

    fewweeks

    thenvomiting

    13

    12

    AVM

    SpetzlerIII

    Ltrigoneandin

    traventricular

    Sudden

    HAwithNV

    HA

    Yes

    15

    14

    12

    ?

    RFronto-tempo

    ralandPallidum

    Sudden

    Complainsofheadachethenloss

    Bilateralxeddilatedpupils

    Yes

    3

    ofconsciousness

    15

    12

    Cavernoma

    RFronto-tempo

    ral

    Progressive

    HAthenvomitinginthemorning

    RthenLxeddilatedpupils,L

    Babinski

    Yes

    9

    fewhours

    16

    12

    Aneurysm

    RCarotidbifurcation

    Yes

    While

    watchingTV,H

    A,v

    isual

    Diplopia,desorientation

    Yes

    14

    difcultiesthenvomiting

    17

    12.5

    AVM

    SpetzlerII

    RSylvian,externalcapsule

    Sudden

    HAwh

    ileskiingthenrapidonset

    Lsideparesis

    15

    leftsideparesis

    18

    14

    AVM

    SpetzlerIV

    LThalamic

    ?

    Shortlossofconsciousness,

    Rsideparesis,aphasia

    14

    disorientationthenaphasia

    19

    15

    AVM

    ROccipital

    Sudden

    HA,vo

    mit,t

    hendecreasedlevel

    Rreactivedilatedpupil

    Yes

    13

    ofconsciousness

    20

    15.5

    ?

    LTemporo-Parietal

    Yes

    While

    skiing,HAthenvomiting

    Reactivepup

    ils

    Yes

    7

    21

    15.5

    Aneurysm

    FischerV

    LCarotidbifurcation

    Yes

    HAduringgym,t

    henvomiting

    HA

    Yes

    15

    22

    17.5

    Cavernoma

    LCerebellum

    Progressive

    Progre

    ssiveHA,N

    V,equilibrium

    Nystagmus,cerebellarsyndrome

    Yes

    15

    3days

    23

    18

    AVM

    SpetzlerI

    RParieto-Occip

    ital

    Yes

    Hemia

    nopsia2dayspriorthenHA

    Hemianopsia,GCSimprovedto15

    Yes

    15

    (wasat8inp

    eripherichospital)

    Table

    1

    L:

    left

    ,R:ri

    ght,

    AVM:art

    eri

    o-v

    enou

    sma

    lform

    ation

    ,HA:

    hea

    da

    che

    ,NV:nau

    seaan

    dv

    om

    iting

    ,GCS:

    Glasgo

    w

    Coma

    Sca

    le

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    mild neurological signs that were difcult to de-tect on general neurological examination (hemi-anopsia, moderate balance disorders), four (18%)had moderate neurological symptoms, includingcerebellar signs, diplopia or disorientation, and 15(68%) had severe symptoms ranging from clearmotor decit to altered state of consciousness.

    Three patients presented with onset of epileptic

    seizures (14%) (table 1).Nine (41%) of the children had a normal

    Glasgow coma score (GCS), three (14%) had aGCS of 14, four (18%) had a GCS between 8 and13, and six (27%) had a GCS less than 8 (table 1).

    62A 10-year experience in paediatric spontaneous cerebral haemorrhage

    Aetiology of haemorrhage

    Twelve (55%) of the children had an arterio-venous malformation (AVM) that bled (g. 14).Arteriovenous malformations are classied ac-cording to Spetzler-Martin grade by their func-tional localisation, size and drainage type (table 2).

    Two AVMs were classied as grade I, one grade II,four grade III, and three were grade IV. Two casescould not be classied due to incomplete work-up.

    Three patients (14%) had a cavernous an-gioma (g. 5), and four children (18%) had a rup-tured aneurysm (g. 6). In three patients (14%),the aetiology of the haemorrhage could not bedetermined. In two of them, an AVM destroyed bythe haemorrhage was suspected.

    Spetzler Grading System

    Size of AVM 6 cm 3

    Eloquent area yes 1

    no 0

    Deep veinous drainage yes 1

    no 0

    Add the points to obtain the Grade. The higher the grade,the higher the risk of microsurgical resection [1]

    Table 2

    Spetzler Grading

    System of arterio-

    venous malforma-

    tion.

    Figure 1

    Cerebral CT-scan demonstrating a frontal haemorrhage with intraventricular rupture

    caused by an AVM.

    Figure 2

    Sagittal FLAIR image showing an occipital haemorrhage

    after an AVM bleeding.

    Figure 3

    Right sylvian AVM.

    Left: Conventional

    angiogram revealing

    a right sylvian AVM

    fed by numerous

    small lateral

    branches.

    Right: Angio-MRI of

    the AVM.The haemor-rhage is visualised,

    and partially masks

    the nidus of the AVM.

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    63

    There were 18 supratentorial haemorrhages(82%), which could be subdivided into seven sub-cortical (considered supercial) and six deep (inthe basal ganglia or thalamus). There was one iso-lated intraventricular haemorrhage. Four patients

    with ruptured aneurysms had subarachnoidbleeding, 2 of which also had an associated intra-cerebral clot.

    There were 4 posterior fossa haemorrhages(18%): 3 involved only the cerebellum, while the

    fourth involved the cerebellum and the mesen-cephalon.

    In the supercial supratentorial haemor-rhages there were 4 AVMs, 1 cavernous malfor-mation and 1 haemorrhage of unknown aetiology.In the deep haemorrhages, there were 5 AVMsand 1 haemorrhage of unknown aetiology. Theintraventricular haemorrhage came from an AVMand the subarachnoid haemorrhages from rup-tured aneurysms.

    The aetiologies in the posterior fossa were2 cavernous malformations and 2 AVMs.

    InvestigationsAll children underwent an emergency cere-

    bral CT scan with and without contrast at admis-sion except those that had a CT scan at an outsidehospital.

    Life-threatening mass effect indicated needfor emergency surgical evacuation of the clot ordrainage of acute hydrocephalus without furtherinvestigations in 8 (36%) of the children. Addi-tional investigations were ordered dependant onthe aspect and localisation of the haemorrhage.

    When haemorrhage suggested aneurysm rup-ture, multislice CT-angiography was per-formed urgently. Intraarterial angiography

    was not necessary for aneurysm diagnosis. When an arteriovenous malformation was

    suspected, intraarterial cerebral angiography

    63S W I S S M E D W K L Y 2 0 0 8 ; 1 3 8 ( 5 - 6 ) : 5 9 6 9 w w w . s m w . c h

    Figure 4

    Large capsule-

    thalamic AVM.

    ab:T2-weighted MRI

    demonstrating a left

    capsule-thalamic

    AVM with a large

    draining vein going

    into the Galen vein.

    cd: Conventional an-

    giography showing

    the thalamic AVMwith deep venous

    drainage.

    Figure 5

    Cavernous malformation associated to a developmental anomaly.

    Left:T2-weighted MRI demonstrating a right cerebellar haemorrhage from a cavernous

    angioma (different signal intensities revealing different states of haemorrhage).

    Right: Associated developmental anomaly of the venous drainage, often present

    with the cavernoma seen on a sagittalT1-weighted MRI with gadolinium.

    Localization

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    was always necessary. Since, unlike adults,most of the children required general anaes-thesia for this investigation, endovasculartreatment of the AVM was planned during thesame procedure whenever feasible. All AVMs

    were managed by a multidisciplinary team in-volving the neurosurgeon, the interventionalneuroradiologist, and the radiation specialist.

    When a cavernous angioma was suspected,or when the aetiology remained unknown de-spite angiography, MRI was the examinationof choice.

    TreatmentManagement of cerebral vascular malforma-

    tions necessitates a multidisciplinary approachinvolving a vascular neurosurgeon, an interven-tional neuroradiologist, a radiation specialist, as

    well as a paediatric neurointensivist, and a paedi-atric neurologist. Multimodal treatment options

    are frequent and have to be planned from the startwhenever possible. The presence of life-threaten-ing mass effect necessitates immediate surgicaltreatment. An arteriovenous malformation maybe treated by microsurgery, by the endovascularapproach and with radiosurgery. A cavernous an-gioma typically needs microsurgical resection,

    whereas an aneurysm may be treated surgicallyand by endovascular approaches.

    Of the nine children with a mass effect, ve(23%) required emergency evacuation of theirhaematoma as a life saving treatment. In four ofthose patients, the cause of the haemorrhage(AVM) was treated at the same time (table 3). Onepatient with a cavernoma underwent primary ur-

    gent evacuation of the clot and then elective sur-gery for resection of the cavernous angioma.

    Two patients (9%) had hydrocephalus withincreased intracranial pressure requiring emer-gency external ventricular drainage; they had cur-ative surgery a few days later after stabilisation ofintracranial pressure. Both of them had an AVM.One patient (5%) had only an ICP monitor in-

    serted.Five other patients (23%) were treated surgi-

    cally, semi-electively, within the week followingthe haemorrhage; two patients had an aneurysm,two had cavernomas, and the last one had an

    AVM. Two other patients (9%) who had an AVMunderwent elective surgery at 1 month and at4 months.

    Two patients (9%) were embolised during thediagnostic angiography, one as the sole treatment,the other in a multimodality treatment plan fol-lowed by elective surgery. There was an attempt

    at embolisation in another patient with an AVM,but it was technically impossible to achieve, andhe had subsequent surgical cure.

    Three patients (14%) had elective radio-surgery as only treatment of their AVM, and twoothers in addition to their initial treatment (inone case surgery, in the other embolisation).

    One child (5%) beneted from multimodaltreatment with endovascular embolisation fol-lowed rst by microsurgery and then by radio-surgery.

    In one patient (5%) the causative lesion wasnot identied and no treatment was performed asthe haematoma had no mass effect.

    64A 10-year experience in paediatric spontaneous cerebral haemorrhage

    Figure 6

    Subarachnoid blood

    due to an anterior

    communicating ar-

    tery aneurysm.

    a Cerebral CT-scan

    without contrast

    showing a sub-

    arachnoid haemor-

    rhage, predomi-

    nantly in the basal

    cistern, as wellas in the Sylvian

    fissure.

    b The cause of the

    haemorrage was

    an anterior com-

    municating artery

    aneurysm which is

    here reconstructed

    in 3D from the

    angio-CT.

    c A sagittal recon-

    struction of the

    angio-CT showing

    the aneurysm

    d The same anterior

    communicating

    aneurysm this time

    with an angio-MRIseen from an ante-

    rior point of view.

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    65

    Follow-up and prognosis:The mean follow-up time of the 20 children

    who survived was 35 months (median 16 months)(table 3).

    Two children died (9%); both were intubatedbefore admission (GCS

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    and had to go into an institution. However, sincethis was the patient who had a second haemor-rhage, the causality of the symptoms between the

    radionecrosis and the second bleed is difcult toassess.

    From a radiological point of view, outcomeanalysis is easier to perform according to the aeti-ology:

    In the 4 (18%) patients treated for ananeurysm, follow-up consisted of multislice CT-angiography that conrmed complete occlusionin 3 patients (75%). In one patient (25%), a smallresidual dilatation (

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    67

    these 3 characteristics: sudden, unusual, worst. Ifheadache is associated with other neurologicalsigns and symptoms, urgent investigation is alsomandatory unless the clinical presentation is usualfor the child and has already been investigated inthe past.

    The average incidence of haemorrhagicstroke in the literature varies between 0.74

    1.1/100 000/year [68]. In our series, according toour recruitment population, it seems to be slightlylower with 0.66/100 000/year.

    Since this is a small series, we found no statis-tical difference in outcome resulting from eitherthe distance to the nearest hospital or whether thechild was treated rst in a peripheral hospital orin the university hospital.

    The aetiologies of spontaneous intracerebralhaemorrhages vary among the different publishedseries. However, AVM is the leading cause in chil-dren, unlike in adults, and accounts for 1456%

    [6, 7, 9, 1619], followed by cavernous angiomas(327% [7, 9, 16]) and intracranial aneurysms (629% [6, 9, 16, 18]). An additional aetiology forspontaneous intracranial haemorrhage in childrenis the vein of Galen malformation, no cases werefound in our series. It can reveal itself at birth,usually with cardiac failure, but in some rare casesit can lead, if undiagnosed, to haemorrhages inolder children. The localisation of the haemor-rhage depends upon the underlying lesion. Al-though AVMs are more common in the posteriorfossa in children than in adults, they remain morefrequent in the supratentorial space even inchildren [13, 20]. Aneurysmal ruptures are morefrequent in the anterior circulation than in theposterior circulation [21], and according toProust [22], they tend to be located on the inter-nal carotid artery bifurcation (36%), middle cere-bral artery (36%), anterior communicating artery(18%) or within the vertebrobasilar system (9%).Supratentorial localisation is also more commonfor cavernomas [23, 24].

    Improved management thanks to specialisedneurovascular teams and technological develop-ments has decreased morbidity and mortality of

    intracerebral haemorrhage in the last 50 years.However, the mortality of haemorrhagic strokesin children remains high, ranging between 6 and38% [10, 11, 1618, 25]. Mortality varies depend-ing on the primary lesion; it reaches 4042% for

    AVMs and increases to 4275% for posteriorfossa AVMs [20, 26, 27]. In our series, mortality

    was in the lower range: 8% for AVMs, and 9% intotal).

    This series conrms that morbidity and mor-tality depend mainly on the location of the haem-orrhage. While any clot leading to a signicant

    mass effect can threaten survival, a posterior fossableed has a comparatively higher risk, as it may di-rectly compress the brainstem. The following arepoor prognostic factors in the literature: coma-tose state (GCS

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    Cavernous angiomas are typically microsurgi-cal lesions and should be resected in totoif possi-ble [23, 36]. Cavernous angiomas are often asso-ciated with developmental venous drainageanomalies that increase the risk of surgical resec-tion and favor recurrence of a cavernous angioma.Radiosurgery did not show favourable outcomesand is not indicated [23, 24]. In our series only

    1 out of 3 children operated upon for a cavernousangioma were completely cured.

    Follow-up imaging is particularly importantin the paediatric population as recurrences can beobserved even after complete cure of an intracra-nial vascular malformation. In children and youngadults re-growth after complete obliteration of

    AVMs have been described. AVMs seem to have adifferent pattern of angiogenesis in children thanin adults, with a higher potential for new abnor-mal vessels to form [37]. Similarly, cavernous an-giomas can recur after complete resection, espe-

    cially if they are associated with a developmentalanomaly of the venous drainage [38]. Intracranialaneurysms can grow and re-bleed, if they are in-completely excluded. The higher recurrence rateof coiled aneurysms than for clipped ones, is ofimportance when treating children [39]. In theabsence of sufcient data in aneurysm treatmentin children, we favour surgical clipping due to itsbetter durability. The review of this paediatric se-ries allows us to emphasise some differences inthe management of spontaneous intracranialhaemorrhages between the paediatric and adult

    population at our institutions. To start let us recallthat in the paediatric population AVMs are themost frequent cause of spontaneous haemor-rhage. Emergent work-up is mandatory and CT-scan with multislice CT-angiography is the pre-ferred imaging study [40]. In most situations itallows to diagnose the aetiology in the emergencysetting and safer life-saving surgery when needed.

    MRI and MRAngiography have their role in thefollow-up as well as in the diagnosis of unclearaetiology. However, in an emergency setting, theyhave little place. Diagnostic angiography necessi-tates general anaesthesia in the paediatric popula-tion. For this reason we prefer to combine andplan the diagnostic angiography and the thera-peutic endovascular treatment in one session.

    This mandates excellent collaboration betweenthe neurosurgeon, the interventional radiologistand the paediatric neurointensivist. Finally, thefollow-up of the paediatric population after treat-

    ment of an intracranial vascular malformationneeds to be more aggressive, with repeated imag-ing studies, as the risk of recurrence and de novoformation of vascular malformations is higherthan in adults. Our preferred imaging for follow-up is MRI, followed by multislice CT-angiogra-phy [41]. Intraarterial angiography is only re-commended for detailed treatment planning.

    Although there are no evidence-based recom-mendations in the literature, we recommend im-aging at least once at the beginning of adulthood.

    68A 10-year experience in paediatric spontaneous cerebral haemorrhage

    Conclusion

    Headaches are frequent also in the paediatricpopulation and are of benign origin in the vastmajority. However, emergency neurological

    work-up is mandatory if the headache is sudden,unusual or intense. Emergency admission ismandatory if those headaches are associated withneurological signs or symptoms. Urgent admis-sion should be considered for every headache

    characterised asrstandworst.Work-up includes an emergency CT-scan

    without and with contrast. If this shows a haemor-rhage, then a multislice CT-angiography shouldbe added. The choice of the additional investiga-tions depends on the suspected diagnosis; for ex-ample an intraarterial angiography would be usedfor arteriovenous malformations and an MRI forcavernous angiomas.

    Intracranial vascular malformations that bledshould be treated when ever possible because thenatural history carries a high cumulative risk of

    re-bleeding, particularly in the paediatric popula-tion due to the long life expectancy.The follow-up is important in the paediatric

    population and should include imaging studies,because there is a risk of recurrence even aftercomplete occlusion of the malformation.

    The long-term result for children after spon-taneous intracranial haemorrhage is not dismaland emphasises the importance of emergencytransfer to a referral centre. The outcome is grimfor children presenting in coma with xed dilatedpupils.

    In conclusion, the most important factor isnot to delay diagnosis and emergency transfer.

    Whereas an emergency CT scan may be per-formed in a general hospital setting, we stronglybelieve that the rest of the management has to beconducted in a specialised referral centre, wherethe child can benet from the expertise of aspecialised neurovascular team including neuro-surgeons, interventional neuroradiologists andpaediatric neurointensivists.

    Correspondence:

    Luca RegliService of NeurosurgeryCentre Hospitalier Universitaire Vaudois(CHUV)CH1011 Lausanne

    E-Mail : [email protected]

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