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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).


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


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.


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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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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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.


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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