emergency management in comatose children

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758 REPORTS OF INVESTIGATION

CAN J ANESTH 2000 / 47: 8 / pp 758766

Purpose: To assess the impact of emergency management on mortality and morbidity of acute rupture of cere-bral arteriovenous malformations resulting in deep coma in children, and the factors predicting outcome.Methods: Retrospective chart review of 20 children with a Glasgow Coma Scale # 8 with acute hemorrhagicstroke from a cerebral arteriovenous malformation rupture was conducted. Protocol included: early resuscitationwith tracheal intubation and ventilation after induction of anesthesia with sufentanil, and benzodiazepine, and man-nitol 20% or hypertonic saline 7.5% infusion for life-threatening brain herniation. Radiological exploration was lim-ited to contrast-enhanced CT scan preceding immediate surgical decompression. Postoperatively, children weredeeply sedated and intracranial pressure monitoring allowed titration with osmotherapy , vasopressors, hyperven-tilation or barbiturate coma to control cerebral perfusion pressure. Analysis used stratification of the type of hem-orrhage (supra or infra tentorial), location (intraparenchymal and subarachnoid, intraparenchymal andintraventricular or intraventricular alone) and relationship between presentation, evolution with resuscitation, typeof cerebral lesion, and outcome.Results: Patients had a severe initial presentation (median Glasgow Coma Scale five), eight had unilateral and eightbilateral third nerve palsy. Compressive hematoma in supratentorial localisation represented 75% of the cases. Globalmortality was 40%. Persistence of mydriasis after resuscitation increased mortality to 75%. Massive intraventricularflooding was associated with increased mortality. Good functional outcome was achieved in survivors.Conclusion: Acute rupture of an AVM can result in rapidly progressing coma. Emergency management with earlyresuscitation, minimal radiological exploration before rapid surgical decompression results in a mortality rate of40%, but a good functional outcome can be expected in the survivors.

Objectif : valuer l'effet et le pronostic d'une intervention d'urgence sur la mortalit et la morbidit d'une ruptureimprvisible de malformations artrioveineuses crbrales qui ont conduit un coma profond chez des enfants.Mthode : Un examen rtrospectif des dossiers de 20 enfants, cots # 8 l'chelle de Glasgow, qui ont subi unaccident hmorragique aigu caus par la rupture de malformations artrioveineuses crbrales, a t ralis. Leprotocole comportait : une ranimation prcoce, une intubation endotrachale et une ventilation aprs l'inductionde l'anesthsie avec du sufentanil, du mannitol 20 % ou une perfusion sale hypertonique 7,5 % pour traiterl'hernie crbrale grave. L'exploration radiologique s'est limite la scanographie de prise de contraste juste avantla dcompression chirurgicale. Aprs l'opration, les enfants ont reu une forte sdation. Le monitorage de la pres-sion intracrnienne a permis le titrage de l'osmothrapie, des vasopresseurs, de l'hyperventilation ou du coma bar-biturique pour contrler la pression de perfusion. L'analyse a port sur la stratification du type d'hmorragie(sus-tentorielle ou sous-tentorielle), la localisation (intraparenchymateuse et sous-arachnodienne, intraparenchy-mateuse et intraventriculaire ou intraventriculaire seulement) et la relation entre la condition initiale, l'volution dela ranimation, le type de lsion crbrale et les rsultats.Rsultats: Les patients prsentaient une condition initiale svre (cinq l'chelle de Glasgow), huit avaient uneparalysie unilatrale du troisime nerf et huit, bilatrale. L'hmatome compressif sus-tentoriel reprsentait 75 %

des cas. La mortalit globale a t de 40 %. La persistance de mydriase aprs la ranimation a fait augmenter lamortalit 75 %. L'panchement intraventriculaire massif a t associ un accroissement de la mortalit. Unebonne volution fonctionnelle a t possible chez les survivants.Conclusion : La rupture aigu de MAV peut rapidement voluer vers le coma. Une intervention d'urgence parune ranimation prcoce et une exploration radiologique minimale avant la dcompression chirurgicale rapide ont

Emergency managementof deeply comatose chil-dren with acute ruptureof cerebral arteriovenousmalformations

Philippe G. Meyer MD,*Gilles A. Orliaguet MD,*

Michel Zerah MD,Brigitte Charron MD,*Marie-Madeleine Jarreau MD,*Francis Brunelle MD,Anne Laurent-Vannier MD,Pierre A. Carli MD*

From the Department of Paediatric Anaesthesia,* Paediatric Neurosurgery, Paediatric Radiology, Assistance Publique-Hopitaux de Paris-Universit Paris V, Centre Hospitalier Universitaire Necker-Enfants Malades, Paris, and Department of Paediatric NeurologicalRehabilitation, Hopital National de Saint Maurice, Saint Maurice, France.

Address correspondence to: Dr. Philippe-Gabriel Meyer, Assistance Publique-Hopitaux de Paris, Centre Hospitalier Universitaire Necker-Enfants Malades, Dpartement dAnesthsie-Ranimation, 149 rue de Svres, 75015 Paris, France. Phone: 33-1-44-49-41-83;Fax: 33-1-44-49-41-70; E-mail: philippe.meyer@ nck.ap-hop-paris.fr

Accepted for publication April 30, 2000.


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Meyer et al.: AVMS RUPTURE 759

EREBRAL arteriovenous malformationsare diagnosed during childhood in lessthan 20% of the cases reported in the liter-ature.1 The first manifestation, in 60 to

80% of these pediatric cases, is an abrupt rupture

resulting in intracranial hemorrhage.2 4 Althoughmost series reporting AVMs in children include somecases of acute rupture resulting in compressivehematoma and massive intraventricular flooding withdeep coma,5 this particular entity and its specific emer-gency management have not yet been individualised.The aim of this study is to report our experience ofacute management of AVM rupture resulting in deepcoma. The results on mortality and morbidity of atherapeutic protocol including emergent aggressivecritical care, minimal radiological exploration andearly surgical decompression were analysed.

Patients and methodsPatients inclusionThis study was approved by the review board of ourdepartment who stated that informed consent for thischart review study was not required. Over 18 months,the records of 40 children admitted to our institutionwith the diagnosis of acute rupture of a cerebral AVMwere analysed. Only those who had a Glasgow comascore (GCS) of eight or less at the time of the actualbleeding were included in this study. The review con-sisted in an analysis of the recent medical historyincluding headaches, seizures, nausea and vomiting,

or the abrupt occurrence of a focal neurologicaldeficit. The clinical condition at the moment of theinitial medical evaluation and the progression of theneurological status were noted.

Initial managementA specific management protocol has been designed forthese particular neuroemergencies. It was initiatedeither outside the hospital by physicians of mobileintensive care units (SAMU) or by our team in chil-dren who deteriorated during their hospital course. Itincluded emergency tracheal intubation (ETI) andmoderate hyperventilation after intravenous induction

of general anesthesia in every comatose child.Immediately before emergency CT scan exploration,catheters for continuous arterial and central venouspressure monitoring were rapidly inserted.Osmotherapy with mannitol 20% in 0.5 gkg1 bolusor rapid infusion of 3 mlkg 1 hypertonic saline 7.5%solution were used when evidence of brain herniationwas present. The target range for plasma osmolaritywas 300-310 mosmolkg.

Radiological evaluationEmergency exploration was limited to a contrast-enhanced spiral CT-scan examination within the firsttwo hours following the episode of acute deteriora-tion. Cerebral angiography was not undertaken before

emergency surgical decompression in these veryseverely ill children. On this basis, suspected rupturedAVMs were classified into three groups with referenceto the extension of the hemorrhage. Group A includ-ed children with parenchymal hematoma and ruptureinto the subarachnoidal space, group B children witha hematoma ruptured into the ventricle, and group Cchildren presenting with isolated intraventricular hem-orrhage. Diagnosis of the anatomic type of AVM wasmade either upon operative findings or upon theresults of delayed cerebral angiography on those chil-dren who survived.

Surgical managementEmergency surgical operations were performed what-ever the clinical status after CT scan. Simple externalventricular drainage was performed when ventricularhemorrhage was isolated. It was associated with a sur-gical resection of the intraparenchymal hematoma andcautious micro-coagulation when a compressivehematoma resulting in acute midline shift was present.Only those AVMs that were superficial enough to becompletely exposed after brain decompression wereresected microsurgically at the first operation. In oth-ers, no attempt was made at this stage for complete

resection of the AVM. At the end of the operation,decompressive craniotomy and duralplasty with apatch were performed when direct dural closure wasnot possible.

Postoperative managementAll patients were maintained under general anesthesiawith a continuous infusion of sufentanil (0.2-0.5 gkg -1hr-1) and flunitrazepam (0.01-0.03 mgkg-1hr-1).Normothermia was maintained and proparacetamol(150 mgkg- 1day-1 iv ) was used systematically inorder to avoid hyperthermia. Controlled ventilationwas adjusted to maintain normoxia and normocarbia.

Intracranial pressure (ICP) was monitored by meansof an intraparenchymal electronic transducer(Codman Neurotrend ICP monitor). When needed,a continuous infusion of dopamine was used toimprove mean arterial blood pressure and to preservecerebral perfusion pressure (CPP) > 60 mmHg. In thecase of a persistent raised ICP, a retrograde jugularbulb fibreoptic catheter was used to monitor jugularbulb oxygen saturation (SvJO

2) continuously before

therapeutic hyperventilation could be instituted. This

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kind of monitoring allowed titration of hyperventila-tion according to cerebral hemodynamic conditions.As a last resort, pentobarbital was used in 5 mgkg 1

bolus followed by a continuous infusion of 3 to 5mgkg-1hr-1when all other therapeutic maneuvers had

failed to control ICP. Pentobarbital was then titratedto obtain burst suppression on EEG. All survivors hada cerebral angiography when their neurological statushad improved. When an AVM was still present at thistime, further management consisted of endovasculartreatment with embolization whenever possible. Inchildren with residual AVM, a delayed surgical resec-tion was scheduled when the residual AVM was acces-sible to surgery. In other cases, a radiosurgicaltreatment was proposed.

Final outcome was assessed at the end of the acutephase and at least six months after the initiation ofneurological rehabilitation in a specialised centre.Analysis of focal neurological deficit, residual epilepsy,

and Glasgow Outcome Score (GOS) to assess globalfunctional outcome were used.6 This score includesfive categories: a good functional result referred togood recovery or moderate persistent disability andpoor results to permanent severe disability, vegetative

state, or death.Analysis of factors possibly affecting mortality,

immediate outcome, and outcome at six months usedMann Whitney U-test and chi2 analysis as appropriate.Statistical significance was considered with P< 0.05.

ResultsThe charts of 40 children hospitalised between March1996 and December 1997 with the diagnosis of rup-tured AVM were reviewed. Among them, 20 had aGCS # 8 and were selected for study. Age at presenta-tion was 9.7 3.3 yr (median 9.5, range 2-15). Therewas no child under one year of age, and no Gallen veinmalformations. There were eight females and 12males. The previous recent medical history of the chil-dren is presented in Table I. Only one child had a pre-viously diagnosed AVM treated with partia lembolization and experienced a new bleeding episodeone year later.

Clinical presentation at the initial medical evalua-tion and evolution of the symptoms is listed in TableII. At the first medical evaluation, the median GCSwas nine (range 3-14), a focal neurological deficit was

760 CANADIAN JOURNAL OF ANESTHESIA

TABLE II Characteristics of the 20 children upon medical evaluation and evolution of the neurological presentation

Patient GCS 1 Motor response 1 3rd nerve Time of Prehospital Evolution GCS 2 Motor response 2 3rd palsy onset management nerve

palsy

1 Ple. 4 Deposturing Left Abrupt ETI+VA+IVA Deterioration 4 Decerebrate Bilateral

2 Pet. 1 0 Right hemiparesia None Abrupt none Deterioration 4 Decerebrate Bilateral

3 Zie. 5 Deposturing None 3 hr ETI+VA+IVA Deterioration 4 Decerebrate Bilateral

4 Mit. 1 2 Left hemiparesia Left Abrupt none Deterioration 7 Localize Left

5 Neg. 1 2 Normal None Day 1 none In hospital 8 Withdraw Left

6 Bou. 1 3 Left hemiparesia None Day 1 none In hospital 7 Localize Left

7 Ped. 8 Right hemiparesia None Abrupt ETI+VA+IVA Deterioration 5 Deposturate None

8 Rah. 1 2 Left hemiparesia None Week none Deterioration 4 Decerebrate Bilateral

9 Des. 1 4 Normal None Day 2 none In hospital 4 Decerebrate Left

10 Khe. 3 None None Abrupt ETI+VA+IVA Improvement 6 Localize None

11 San. 9 Localize None Day 1 none In hospital 8 Localize Right12 Dos. 6 Deposturing Right Abrupt ETI+VA+IVA In hospital 4 Decerebrate Bilateral

13 Bar. 5 Deposturing Right Day 1 ETI+VA+IVA In hospital 4 Decerebrate Bilateral

14 Lar. 1 4 Normal None Day 3 none Post embolization 8 Left hemiparesia None

15 Cal. 4 Decerebrate Left Day 1 ETI+VA+IVA Deterioration 3 None Bilateral

16 Dom. 8 Normal None Abrupt ETI+VA+IVA Deterioration 3 None Bilateral

17 Ber. 1 2 Normal None Week none In hospital 7 Withdraw Left

18 Mer. 6 Left hemiparesia None Day 1 ETI+VA+IVA In hospital 5 Deposturate None

19 Mon. 8 Left hemiparesia None Abrupt ETI+VA+IVA Deterioration 5 Deposturate Left

20 Les. 8 Normal None Day 1 ETI+VA+IVA Deterioration 5 Deposturate Right

ETI: Emergency tracheal Intubation; AV: Assisted Ventilation; IVA: Intravenous Anesthesia; In hospital: Deterioration in the hospital

TABLE I Recent medical history before acute stroke

Symptoms N %

Headache 13 65

Nausea and vomiting 6 30Seizures 1 5Abrupt neurological deficit 2 10

None 5 25


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present in seven children, four children had ipsilateralthird nerve palsy and none had bilateral fixed dilatedpupils. Fifteen children experienced an acute onsetoutside the hospital, 11 had a GCS # 8 at initial pre-

sentation, were intubated at the scene, and rapidlytransported to our centre. Another subset of fourpatients who were not comatose at the first on-sceneevaluation deteriorated acutely and became comatoseduring transportation. None of the 15 patients whobecame comatose before hospital admission died dur-ing transportation, but neurological deterioration wasnoted in all but one patient (median GCS: 5, range 3-6 upon admission). Five children deteriorated afterthey had been initially admitted to our critical careunit in less dramatic medical condition with a diagno-sis of acute rupture of AVM. One of these five childrendid so immediately after embolization of a thalamic

AVM. At the moment of the in-hospital emergent crit-ical care management, eight children had bilateralfixed pupils and eight had ipsilateral third nerve palsy,seven patients decerebrated and five had evidence ofdecortication. Initial resuscitation maneuvres are sum-marised in Table III. They resulted in at least transientstabilisation of the neurological status in all the chil-dren and regression of pupillary dilatation beforeoperation in 10 out of the 16 children (62%) present-ing with pupillary abnormalities.

All the children had a contrast-enhanced CT scanthat demonstrated an intracranial hemorrhage. Theresults of the neuroradiological explorations are sum-marised in Table IV. In spite of contrast-enhancedexamination and 3-D reconstruction, the preoperativeemergency explorations did not evidence the existingAVM in any case. Immediately after CT-scan evalua-tion, emergency surgical intervention consisted in asimple external ventricular drainage as the first opera-tion in 10 children, with evacuation of the hematoma

as the second operation in seven, evacuation of thehematoma and concomitant partial resection of asuperficial AVM during the same session in five, andsimple evacuation of the hematoma during the firstsession in five children. Dural plasty was performed infive children and decompressive craniotomy was need-ed in three. Twelve children experienced objectiveperoperative arterial spasm and were started on con-tinuous nimodipine infusion. Three children (15%)died during or immediately after surgery.


TABLE III Initial resuscitation maneuvres in the hospital beforesurgical decompression

Resuscitation maneuvres n (%)

Medical treatment 20 (100)

- Assisted ventilation 20 ( 100)- ivsedation 19 (95)- Hypertonic saline infusion 7 (35)- Mannitol 20% 13 (65)- Dopamine infusion 12 (60)

Invasive monitoring 20 (100)Ventricular drainage 2 (10)

TAB LE IV Emergency CT-scan findings

Type of hemorrhage Type of hematoma n (%) n (%)

Group A: 8 (40) None: 2 (10)Group B: 10 (50) Temporo-parietal: 6 (30)

Group C: 2 (10) Posterior fossa: 5 (25)Deep: 5 (25)Other:* 2 (10)

* One frontal, one occipital

TABLE V Angiographic explorations and timing of realisation

Patient Angiographic findings Embolization Timing ofangiography

2 Anterior choroidal Yes Day 103 PICA Yes Day 104 Normal No Day 5

6 Right internal temporal Delayed Day 1 & 67 Normal No Day 59 Right internal temporal No Day 6

10 Left PICA and PSCA No Day 112 Normal No Day 514 Right PICA Yes Day 1

15 Left MCA Yes Day 616 Right PICA and PSCA No Day 1518 Left choroidal pedicles No Day 1

19 Left calloso marginal No Day 120 Normal No Day 5

PICA: Posterior and inferior cerebellar artery; MCA: Middle cere-bral artery; PSCA: Posterior and superior cerebellar artery.

TABLE VI Final outcome

GOS at GOS 6 mo GOS 12 modischargen (%) n (%) n (%)

Bad outcome 15 (75) 13 (65) 9 (45)- Death (5) 8 (40) 8 (40) 8 (40)

- vegetative state (4) 0 0 0- Severe disability (3) 7 (35) 5 (25) 1 (5)

Good outcome 5 (25) 7 (35) 11 (55)

- Moderate disability (2) 5 (25) 4 (20) 6 (30)- Good recovery (1) 0 3 (15) 5 (25)


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The survivors were maintained under general anes-thesia and mechanically ventilated at least for the firsttwo postoperative days. The mean duration ofmechanical ventilation and ICU stay were 7 7 days(range: 2-29) and 11 6 days. The initial mean value

of ICP was 15 13 mmHg (range: 9-50) and themean maximal value was 34 20 mmHg (range: 9-80). Plasma osmolarity was carefully maintained with-in the range of 300 to 310 mosmolkg -1 during thefirst 48 hr after surgery. An infusion of mannitol orhypertonic saline solution was required at some timein the postoperative period to control ICP in all thechildren. Hemodynamic support with a continuousinfusion of dopamine was added in 12 children.Recombinant tissue plasminogen activator (rTpa) wasinjected in the ventricular drainage to maintain itspatency in two patients. Transcranial Doppler exami-nation was performed systematically in all the childrenwithin six after completion of surgery. In the twelvechildren which experienced objective peroperativevasospasm, it depicted slightly increased mean bloodflow velocities with an increased middle cerebral tocarotid artery gradient evidencing possible vasospasm.Postoperative infusion of nimodipine was used inthese twelve patients. In five children with untractableraised ICP, a retrograde fibreoptic jugular veincatheter was added. It demonstrated in all of them acerebral hyperemia commanding severe hyperventila-tion to control cerebral perfusion pressure, and onepatient required barbiturate coma.

Cerebral angiography was performed in five con-scious hospitalised children before neurological dete-rioration had occurred. Only one child had a partialembolization of a thalamic AVM in the same sessionbut deteriorated and became comatose immediatelyafter. A delayed postoperative cerebral angiographywas performed in nine of the patients whose neuro-logical status improved. The results and timing ofangiographic examinations are presented in Table V.Endovascular treatment of the remaining AVM wasperformed in five children, two children had a singlesession for embolization, and three required multiplesessions. A secondary radio-surgical treatment was

performed in one child with a complex posterior fossaAVM after partial surgical excision and subsequentembolization.

The overall mortality was 40% of the cases includinga 15% perioperative mortality. There was no increasedmortality in younger children. The incidence of deathwas higher in those children who presented immediate-ly before surgical intervention with ipsilateral thirdnerve palsy and bilateral fixed pupils in spite of aggres-sive resuscitative management (33% and 75% mortality

vs0% in children with normal pupils, P< .04). Therewas also a trend (P= .05) toward an increased mortali-ty in children experiencing massive intraventricularhemorrhage (20% mortality in group A, 50% in groupB and 100% in group C). Neither the GCS just before

operation, its motor component, nor the precise loca-tion of the AVM correlated with mortality.Interestingly, there was no survivor in a persistent veg-etative state upon discharge, but seven children hadsevere disability at that time. After six months of inten-sive neurological rehabilitation, the Glasgow OutcomeScore improved slightly and 12 mo after discharge, fivechildren had no serious disability and six had moderatedisability mainly represented by an ipsilateral hemipare-sia (Table VI). There was no residual epilepsy requiringlong-term treatment nor persistent hydrocephalusrequiring permanent CSF shunting.

DiscussionIn this series, deeply comatose children represented50% of the patients presenting with an acute rupture ofa cerebral AVM. This large proportion could beexplained by the fact that children with clinical evidenceof acute non traumatic neurological accidents were sys-tematically managed outside the hospital by a criticalcare medical team insuring their immediate survival anddispatched directly to a single regional centre. Criticalcare management including tracheal intubation (ETI)and initiation of controlled ventilation were performedeither outside or upon arrival to the hospital. Basic crit-

ical care management gained the time sufficient for per-forming minimal radiological explorations beforeimmediate surgical decompression. In patients present-ing with pupillary abnormalities upon admission, thisresuscitation resulted in regression of pupillary abnor-malities in 62% of the cases. The immediate efficiency ofcritical care management upon neurological symptomswas determinant for final survival, since 75% of the chil-dren who had persistent bilateral mydriasis after resusci-tation died. Immediate surgical decompressionperformed in patients with brain herniation, or brain-stem compression resulted in a 15% peroperative mor-tality. In the early postoperative period, control of CPP

needed intervention in most children. Brain swellingwas noted in five out of 17 survivors. Deep hyperventi-lation was effective in reducing cerebral blood flow andin adapting it to cerebral metabolism in four of the chil-dren. Vasospasm was another concern since 12 patientsexperienced peroperative spasm that was still present,despite continuous nimodipine infusion, at postopera-tive transcranial Doppler examination. A global 40%mortality was noted. A good outcome was noted 12 moafter the initial accident in 11 of the 12 survivors.



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Among these patients, six had a persistent moderatedisability and five had an independent life. There wasneither residual epilepsy requiring long term treatmentnor secondary hydrocephalus in our patients.

The abrupt rupture of a cerebral AVM is infrequent

in childhood. In most series, children represent lessthan 20% of the population.1 Except in infancy whereGallen vein malformations and large pial AVMs result-ing in congestive heart failure are predominant, hem-orrhagic stroke is the primary manifestation of AVMsin 50 to 85% of the cases.7 9 Some cases have beenreported after a trivial head trauma,1 0 but, most of thetime, no predisposing events could be found. In 15%to 30% of the cases, seizures are the first clinical man-ifestations.11,12A relationship between the type of ini-tial presentation and the size of the AVM has beendescribed, the small AVMs manifesting themselves bystrokes and the large ones by seizure.1 Deeplycomatose children could represent 50% of the cases inthe particular entity of cerebellar hemorrhages.1 3 Therelative incidence in other locations could be estimat-ed from 10% to 38% of the cases. 2,5,7,14 It can be sus-pected that this incidence could be underestimatedsince undiagnosed or inadequately emergently treatedacute hemorrhagic strokes could be a cause of out-of-hospital sudden deaths in previously healthy children.

Tracheal intubation and mechanical ventilation arethe first interventions in comatose children. Moderatehypocapnia (PaCO

2: 30-35 mmHg) can efficiently

reduce raised ICP, but the risks of dramatically reducing

the cerebral blood flow in ischemic areas with moreprofound hyperventilation has to be kept in mind.15 Inthe presence of life-threatening brain herniation, rapidinfusion of mannitol 20% is effective in lowering raisedICP.1 6The risk of increasing the volume of the intracra-nial hematoma, by decreasing the volume of the sur-rounding undamaged brain, is more theoretical thanclinically relevant. When evidence of brain herniation ispresent, mannitol could be used as a life-saving therapybefore craniotomy. Hypertonic saline solutions have theadvantage of lowering raised ICP in the same range asmannitol with an associated effect of low volume resus-citation that can be mostly useful when hemodynamic

instability is present.17,18 Direct ventricular puncture isanother means of decreasing raised intracranial pressurethat could be performed rapidly at the bedside.However, acute drainage resulting in ventricular col-lapse could result in a rapidly growing intraparenchymalhemorrhage and brain herniation.

In life-threatening situations, contrast-enhanced CTscan is the most easy and quickest examination to per-form. It allows detection of intraparenchymalhematoma and intraventricular hemorrhage and

processes the degree of brain herniation. Supratentorialhematoma represent 70% to 80% of the cases5,8 andamong them, 66% are hemispheric essentially in theparietal area. Deep-seated lesions develop in the basalganglia, thalamus and corpus callosum. When the AVM

is superficial, its rupture results in a parenchymalhematoma associated with subarachnoid hemorrhage.In deeply located lesions, massive intraventricular bleed-ing is more frequent and is an important factor in theincreased mortality. Cerebellar hemorrhages aredescribed as devastating conditions resulting in dramat-ic presentation with acute brainstem compression in50% of the cases.1 3We did not find a worse evolution ininfratentorial localisation. If CT scan is sufficient toguide surgical decompression, it is insufficient to relatea hemorrhagic stroke to the rupture of an AVM.Obviously, it cannot allow a complete scheduled surgi-cal resection without more precise preoperative identi-fication of all the feeding arteries. MRI with threedimensional reconstruction and fast sequences is a verysensitive examination for the diagnosis of AVM, espe-cially in angiographycally occult AVM (AOAVM) thatcould be responsible for 10% of the hemorrhagicstrokes so-called of unknown origin.5 The limited avail-ability, the length of the examination, and the difficul-ties encountered in the management of unstablechildren in the MRI environment limit the use of MRIexplorations in emergency situations. Cerebral angiog-raphy is the standard for exploring AVM. It could befalsely negative in as much as 10% of cases.5 Emergency

angiography in children with intracranial hematomacarries a high risk of neurological and cardiovascularcomplications and of immediate rebleeding.1 4

Emergency endovascular treatment is not advisable inthese cases, because it will not remove the brain com-pression resulting from the hematoma, which is themain life-threatening problem. Moreover, bleedinginduces modification of the angioarchitecture of theAVM and reduces cerebral blood flow within the mal-formation resulting in difficult selective catheterization.As others, we decided to exclude preoperative angiog-raphy from the protocol of examinations that could beperformed in deeply comatose children with evidence

of brain herniation.5,19 Angiography can be proposedon a delayed emergency basis, and endovascular treat-ment could be applied to residual AVM. If a completecure is obtained with embolization alone in less than10% of the cases, a staged embolization is certainly use-ful associated with surgical resection for managing largeAVM.20,21 This kind of management was successfullyused in five of the children in this series.

The need for prompt evacuation of the hematomaand/or drainage of massive intraventricular thrombus



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is not questionable.5,8,10,11 The same surgical manage-ment has been proposed in adults with profound neu-rological deterioration resulting from hemorrhagicstroke with mass effect.1 9 Such high-risk procedureshave unpredictable blood loss and potential risks of

intractable brain herniation through the dural inci-sion. However, our 15% surgical mortality comparesfavourably, although the severity of the initial presen-tation was higher, with the 48% in children treatedconservatively.1 2 There is controversy concerning theneed for complete excision of the AVM at the firstoperation. On one hand, complete excision, whenev-er possible, will prevent the risk of early rebleedingand result in neurologically normal children in 53% ofthe cases.5 On the other hand, it carries a high risk ofincreased blood loss and difficulty in controlling feed-ing pedicles that have not been clearly identified by

precise preoperative neuroradiological evaluation. Onthe top of that, it also carries a higher risk of perma-nent neurological deficit when the hematoma lies in afunctionally eloquent area. The rules that can be pro-posed for emergency management are to attempt exci-sion of the AVM only when the hematoma issuperficial and situated far away from an eloquentarea. This is particularly indicated when the preopera-tive contrast enhanced CT scan showed the AVM. Inall the other cases, a simple excision of the hematomamust be performed associated with the insertion of anexternal ventricular drainage when a ventricular hem-orrhage is present.1 9

In the postoperative period, continuous measure-ment of ICP and CPP is of critical importance since themain risks in the postoperative period are the develop-ment of cerebral ischemia or, on the contrary, of mas-sive cerebral swelling after brain decompression. Deepsedation prevents acute raised ICP related to stimula-tion, decreases cerebral metabolism,19,22 but precludesprecise clinical examination. Instead of being based ona uniform protocol, critical care management should beadapted to the dynamic requirements of each patient.2 3

The critical threshold for cerebral perfusion pressurebelow which hypoxia occurs is about 50 mmHg. Thegoal of a minimal CPP can be achieved by adequate vol-

ume expansion under central venous pressure and plas-ma osmolarity control, and liberal use of vasoactivedrugs such as dopamine.22,24 Massive intraventricularthrombosis could result in abrupt external drainageocclusion and acutely raised ICP. When classical mea-sures have failed, direct intraventricular thrombolysiswith recombinant tissue plasminogen activator is a safeand life saving method to restore shunt patency. It hasthe associated advantage of acting against cerebralvasospasm related to subarachnoidal hemorrhage.25 In

the case of raised ICP related to postoperative brainedema, osmotherapy with mannitol 20% or hypertonicsaline infusions are effective if the goal of a moderatelyincreased plasma osmolality in the range of 300 to 310mosmoll-1 can be achieved.2 6 Rapid development of

massive brain swelling after surgical decompressionresults in cerebral vasodilatation and acutely raisedICP.2 1 In the case of intractable raised ICP, severehyperventilation should not be used until cerebralischemia has been ruled out. Continuous jugular bulboximetry is useful to separate global cerebral ischemiafrom hyperemia related to cerebral swelling.2 7

Symptomatic cerebral vasospasm is a well-knowncomplication of subarachnoidal hemorrhage that mayoccur in 46% of cases after aneurysmal subarachnoidalhemorrhage.2 8 The incidence of vasospasm after pedi-atric AVM rupture is unknown. In the postoperativeperiod, transcranial Doppler sonography measuringmiddle cerebral artery blood flow velocity can be per-formed easily. It allows diagnosis of persistent arterialspasm especially when concomitant measurement ofthe internal carotid artery flow velocity can be per-formed.29 Nimodipine has proved its efficiency in pre-venting cerebral vasospasm related to subarachnoidalhemorrhage provided that normal circulating bloodvolume could be preserved.3 0With global ischemiaunrelated to documented vasospasm, high-dose barbi-turate coma has been used liberally by some authors.3 3

The side effects, hemodynamic instability andincreased rate of pulmonary complications, and the

risk of increasing cerebral ischemia with vasocerebralvasoconstriction have to be kept in mind.3 1 It shouldbe used as the last resort when other therapy has failedto control ICP.3 2

Despite aggressive medical and surgical emergencymanagement, the mortality remains high, but ourmortality rate compares favourably with the 83% pre-viously reported in children with Botterell V gradehemorrhage.5 This difference may be explained by ashorter delay between abrupt neurological deteriora-tion and surgical decompression in our patients. Morethan the severity of the initial presentation or the pre-cise location of the hematoma, the absence of

response to initial critical care and the presence of amassive intraventricular hemorrhage seem to be fac-tors responsible for the increased mortality.4 The trendtoward increased mortality in cerebellar hemorrhageas compared to hemispheric hematoma5 was notnoted in the present series. In survivors the reportedfunctional outcome is good with minimal neurologicalsequels contrasting with the severity of the initial pre-sentation.5 These good functional results are certainlyan important argument for providing prompt and



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aggressive critical care management whatever the ini-tial presentation is.

It can be concluded that acute rupture of AVMresulting in deep coma still carries a high mortality.Prompt recognition of the diagnosis, early resuscita-

tion, and adequate triage insure immediate survival.Even in moribund children, aggressive medical thera-py could be efficient. There is no place, in this imme-diately life-threatening situation, for preoperativeangiography that will not treat brain herniation. CTscan is the minimal radiological exploration beforeemergency surgical brain decompression. In survivors,aggressive emergency management and precise post-operative control of cerebral perfusion pressure, mayresult in a good functional outcome. Delayed angiog-raphy with graded embolization whenever possibleand scheduled surgical complete excision or radio-surgery will complete this emergency treatment.

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