Diagnosis and treatment of vein of Galen aneurysmal malformations

Childs Nerv Syst DOI 10.1007/s00381-009-1063-8

ORIGINAL PAPER

Diagnosis and treatment of vein of Galen aneurysmal malformations Gregory G. Heuer & Brandon Gabel & Lauren A. Beslow & Michael F. Stiefel & Erin S. Schwartz & Phillip B. Storm & Rebecca N. Ichord & Robert W. Hurst

Received: 7 November 2009 / Accepted: 19 November 2009 # Springer-Verlag 2009

Abstract Introduction Vein of Galen aneurysmal malformations (VGAM) are rare but clinically significant intracranial arteriovenous shunt lesions that most often present in neonates and infants. Methods Retrospective clinical data were collected for patients evaluated with a diagnosis of VGAM from 1994 to 2007. G. G. Heuer : B. Gabel : M. F. Stiefel : P. B. Storm : R. W. Hurst Department of Neurosurgery, University of Pennsylvania Medical Center, Philadelphia, PA, USA G. G. Heuer e-mail: [email protected] M. F. Stiefel : R. W. Hurst Division of Interventional Neuroradiology, University of Pennsylvania Medical Center, Philadelphia, PA, USA G. G. Heuer : P. B. Storm Division of Neurosurgery, Children’s Hospital of Philadelphia, Philadelphia, PA, USA L. A. Beslow : R. N. Ichord Department of Neurology, The Children’s Hospital of Philadelphia, Philadelphia, PA, USA E. S. Schwartz Department of Radiology, Division of Neuroradiology, The Children’s Hospital of Philadelphia, Philadelphia, PA, USA R. W. Hurst (*) Department of Radiology, Division of Neuroradiology, Hospital of the University of Pennsylvania, 3400 Spruce Street, Philadelphia, PA 19104, USA e-mail: [email protected]

Results Thirteen patients with VGAM were evaluated from 1994 to 2007. Seven patients presented emergently with medically intractable cardiac failure, and six were treated in the first 2 weeks of life. Five children treated after this period (1.5–31 months of age) manifested enlarging head circumference, abnormal development, or subarachnoid hemorrhage. Eleven patients were managed endovascularly. Four disease or procedure-related complications occurred. Two complications were associated with poor outcome, both of which occurred in patients treated at less than 2 weeks of age. Two other patients experienced transient neurological deficits with no evidence of permanent sequelae. Outcome in the six patients treated emergently in the first 2 weeks of life included two patients who developed normally, one with mild to moderate neurological deficits, one with severe neurological deficits, and two deaths. Outcome in the five older patients (treated between 1.5 and 31 months) was considerably better than in the group treated early and included three with normal outcome and two with mild neurological deficits. Conclusions Contemporary endovascular techniques remain the preferred treatment for VGAM in all age groups. Early diagnosis and multimodality treatment are essential for the best management and treatment of the complex constellation of clinical problems often arising from this disorder. Keywords Vein of Galen aneurysmal malformations . Endovascular . In utero . Neonates . Heart failure

Introduction Vein of Galen aneurysmal malformations (VGAM) are rare intracranial arteriovenous shunts that present almost exclusively in the pediatric population. While VGAM make up only about 1% of all intracranial vascular lesions, they are

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disproportionately represented in the pediatric population where they constitute up to 30% of intracranial vascular abnormalities [10, 13, 22]. Children with VGAM present with an age-dependent constellation of symptoms which most often includes lifethreatening medically intractable heart failure presenting in the first weeks of life. Older patients typically present with enlarging head circumference, hydrocephalus, and developmental delay [14, 21]. In addition to differing clinical presentations, nearly all studies have revealed differences in angioarchitectural anatomy, physiology, and outcomes between children presenting early in life with cardiac failure and those presenting later in infancy and childhood. The universally poor natural history of untreated VGAM at all ages and limited benefits of surgical treatment mean that current treatment relies primarily on endovascular approaches. Nevertheless, optimal management requires adjunctive intensive care and pediatric neurology input to ensure the best outcome [9, 23, 24]. Several studies have reported that approximately 60% of patients of all ages treated endovascularly had minimal to no developmental delay at follow-up [9, 14, 21, 23, 24]. However, prognosis differs by age. Patients who present early in life with cardiac failure are particularly difficult to treat [18, 19, 21]. We present a recent single institutional experience with VGAM patients, most of whom presented in the neonatal period, specifically comparing those treated within the first 2 weeks of life and those treated later.

Clinical material and methods Patients Data were collected retrospectively on a consecutive series of patients that presented to the Children’s Hospital of Philadelphia from 1994 to 2007 with a diagnosis of VGAM. The project was approved by the institutional review board. The patients were evaluated and treated by a multidisciplinary team including interventional neuroradiology, pediatric cardiology, pediatric neurosurgery, pediatric neurology, and pediatric intensive care. Patients were evaluated in utero with fetal ultrasound and/ or fetal magnetic resonance (MR) scans. After birth, patients were evaluated with postnatal MR imaging, MR arteriogram (MRA), and MR venogram. Angiography was performed only in conjunction with embolization. Results of imaging were reviewed by neuroradiology and interventional neuroradiology for presence of hydrocephalus or parenchymal abnormalities, and each VGAM was classified by angioarchitectural features as choroidal or mural [18]. Endovascular treatment Endovascular procedures in 11 patients were performed via a transarterial approach as previously described [2, 14, 17–19, 21]. Femoral artery

placement of a 4-Fr sheath (Cordis Corporation, Miami Lakes, FL, USA) was followed by targeted diagnostic angiography based on MRA. A 4-Fr catheter was used for both diagnostic angiograms and as a guide catheter for microcatheter placement. In a single patient (case 6), angiography and transarterial embolization were performed via an umbilical artery catheter. Embolic agents included nbutyl cyanoacrylate and microcoils.

Results Patient characteristics and presentations From 1994 to 2007, 13 patients presented to the Children’s Hospital of Philadelphia with a diagnosis of VGAM (Table 1). Three patients were female and ten were male. A significant number of the patients, 46% (six patients), were diagnosed in utero by fetal ultrasound or fetal MR. Three patients were diagnosed within 1 week of birth based on clinical presentation with cardiac failure, and the remaining four patients were diagnosed from 1.5 to 31 months of age. The most common clinical presentation in the group was cardiac failure diagnosed within the first week of birth, which was present in seven patients. Of those patients presenting in the neonatal period (birth–60 days), all but one presented in this fashion. A single patient presenting near the end of the neonatal period demonstrated evidence of increasing head circumference and developmental delay, manifestations which characterized all but one of the patients presenting outside the neonatal period. A single patient presented with subarachnoid hemorrhage (SAH) at 31 months of age and was also found to have hydrocephalus and enlarged head circumference (>98%ile), although he was otherwise neurologically and developmentally normal before onset of SAH. A concomitant herpes simplex viral (HSV) encephalitis was present in one patient who presented with seizures, hydrocephalus, and macrocephaly at 14 months of age. Only one of the five children treated outside the first 2 weeks of life had evidence of cardiac failure, which was medically controlled, but all had head circumferences of greater than 95%ile for age and sex. Pre-embolization imaging All patients received preprocedural MRAs (Fig. 2). Patients were followed clinically and with serial MRA studies for changes in their VGAM (Fig. 1c, d). Postnatal MR scans demonstrated preembolization hemorrhage in four patients (Table 1; Fig. 2a), ischemia in four patients, and diffuse parenchymal abnormality in five patients (Table 1; Fig. 2d). Hydrocephalus was seen in five patients and ventriculomegaly in one patient.

Childs Nerv Syst Table 1 Patient demographics and preoperative magnetic resonance findings

Case Case Case Case Case Case Case Case

1 2 3 4 5 6 7 8

Case 9 Case 10 Case 11 Case 12 Case 13

Sex

Age diagnosis

GA (weeks)

Cardiac function

Seizures

Ischemia

P/L

Hemorrhage

Struc Abn

M F M F F M M M

In In 5 7 In 6 In In

FT 36 FT NA NA FT 33 29 2/7

RVD, PFO HF HF HF HF HF, RVH, RVD, TR HF, TR, PDA Mild HF

Y Y N NA NA N Y N

Y Y N NA NA N Y N

Y N N NA NA N Y Y

Y N N NA NA Y N NA

Underopercularization – Underopercularization – – – Underopercularization Underopercularization

M M M M M

14 months 45 days 31 months 6 months In utero

FT 36 FT FT FT

Normal PFO Mild LVH Normal RVH and RVD

Y Y N N N

Y N N N N

Y Y N N N

N Y Y N N

– Underopercularization – – –

utero utero days days utero days utero utero

M male, F female, GA gestational age at birth, P/L diffuse parenchymal abnormality/leukomalacia, Struc Abn structural abnormalities, FT full term (GA>37 weeks), NA not available, RVD right ventricular dilation, PFO patent foramen ovale, HF heart failure, TR tricuspid regurgitation, PDA patent ductus arteriosus, RVH right ventricular hypertrophy

Angioarchitecture Eight of the 13 VGAMs (62%) manifested a choroidal pattern (Table 2; Fig. 3a, b) while five demonstrated a mural pattern of angioarchitecture (Table 3; Fig. 4a). All VGAMs presenting early in life with cardiac Fig. 1 MRA imaging of VGAM. a Pretreatment MR reformation demonstrating the angioarchitecture of a choroidal VGAM presenting with heart failure as a neonate (case 7). b Pretreatment MR reformation demonstrating the angioarchitecture of a mural VGAM treated as an infant (case 10). c, d Serial MRA imaging of patient demonstrating enlargement of the VGAM (case 10)

failure were characterized by choroidal angioarchitecture while five of the six presenting later in life had mural angioarchitecture. The single choroidal VGAM presenting after the first 2 weeks of life did so with SAH.

Childs Nerv Syst Fig. 2 Preprocedure and postprocedural complications of VGAM. a Preprocedural head CT image demonstrating subarachnoid hemorrhage in the left frontal lobe (arrow; case 11). b Preprocedure MR image demonstrating signs of venous congestion (arrow; case 7). c Postprocedure MR demonstrating vasogenic edema (arrow; case 10). d Postprocedural CT, demonstrating intraventricular, intraparenchymal hemorrhage, and subarachnoid hemorrhage (case 6)

Endovascular treatment One patient (case 7) did not receive endovascular treatment secondary to his critical condition and the family’s choice. He died shortly after diagnosis of intractable cardiac failure despite medical management. One patient (case 13) was clinically stable and his definitive treatment has been delayed. This patient has since developed hydrocephalus at 10 months and will be evaluated for embolization. Six patients underwent endovascular treatment within 2 weeks of birth (Figs. 3c–f and 4b–d). In the treated patients, six were treated with nBCA alone, four with a combination of coils and n-BCA (three mural type, one choroidal type), and one (mural type) with coils alone. One patient underwent three endovascular procedures, four patients were treated twice, while a single treatment was performed in the other patients. Posterior circulation vessels were treated primarily in all patients while distal ACA feeders were treated in two patients. Four patients experienced periprocedural complications: two with intraparenchymal hemorrhage (IPH); one with extensive IPH, SAH, and intraventricular hemorrhage (Fig. 2c, d); and one with a transient Parinaud’s syndrome.

An additional treated patient continued to manifest heart failure which caused death. Outcome The untreated patient died. Five of the six patients treated in the first 2 weeks of life demonstrated resolution of heart failure. The single patient (case 5) in whom failure proved intractable to embolization treatment also had considerable acquired dural feeders to the VGAM. There were two deaths in the treated group, all in patients who were treated at less than 2 weeks of life (Table 2). These included the single patient in whom heart failure proved intractable to embolization and a patient who developed intracranial hemorrhage in the face of improved cardiac function. The patients were followed long term by pediatric neurologists to determine and assess their neuropsychiatric development. Outcomes in the four surviving patients who were treated within the first 2 weeks of life included two patients who developed normally, one with mild to moderate neurological deficits and one with severe neurological deficits (Table 2). The mean age of the treated

Childs Nerv Syst Table 2 VGAM presenting emergently in the first 2 weeks of life with cardiac failure Sex

Dx age

Rx age

N

Failure resolved

Type

Complications

Outcome

FU

Case 1

M

In utero

1 day

1

Y

Choroidal

Severe MR

5 years

Case 2

F

In utero

2 days

2

Y

Choroidal

Postembolization hemorrhage –

12 years

Case 3

M

5 days

14 days

2

Y

Choroidal

–

Hemiparesisc, moderate MRd, epilepsy controlled Normal no seizures

Case 4 Case 5 Case 6

F F M

7 days 1 days 6 days

10 days 1 days 7 days

1 1 3

Y N Y

Choroidal Choroidalb Choroidal

Normal no seizures Deceased Deceased

3.5 years NA NA

Case 7

M

In utero

NAa

0

NA

Choroidal

– – Postembolization SAH, IPH, IVH –

Deceased

NA

16 months

M male, F female, Dx age age at diagnosis, Rx age age at treatment, N number of treatments, NA not applicable, IPH intraparenchymal hemorrhage, SAH subarachnoid hemorrhage, IVH intraventricular hemorrhage, MR mental retardation, FU age at last follow-up a

Family decision to not pursue treatment

b

Additional acquired dural supply

c

Ambulatory

d

Independent in most self-care

patients at follow-up was 5.4 years (range 1.3–12 years). Outcome in the five patients treated after 2 years of age was considerably better than in the group treated early and included three with normal outcome and two with mild neurological deficits, one of whom had deficits of multifactorial origin (HSV encephalitis; Table 3). The mean age of the older treated patients at follow-up was 3.1 years (range 1.3–6 years). Four of the five patients with hydrocephalus required postembolization shunting. One patient had resolution of his hydrocephalus after embolization and the patient with ventriculomegaly did not require shunting.

Discussion We describe a single institutional experience encompassing 14 patients with VGAM. Numerous studies have demonstrated that VGAM patients presenting early in life with intractable cardiac failure are particularly difficult to treat, with mortality rates as high as 62% despite treatment [8, 9, 16, 18, 19, 21, 23, 24]. In contrast, the outcome for patients presenting at older ages is considerably better with up to 80% reported as normal in some series [9, 13, 16, 20, 21]. Nevertheless, experience with this rare disorder is extremely limited, and available case series are small, limiting the certainty of conclusions that may be drawn. The intracranial shunts of VGAM are believed to arise due to abnormal arteriovenous fistula formation between embryologic choroidal arteries and the median prosence-

phalic vein of Markowski which drains the choroid plexus during early embryologic development. The persistently elevated blood flow prevents normal involution of the median prosencephalic vein [25]. In keeping with the developmental events, arterial supply to VGAM arises most commonly from embryologic choroidal arteries, followed by perforators from the posterior circulation, and rarely from thalamoperforators [21]. Two angioarchitectural variants have been delineated: a choroidal type, composed of numerous feeding arteries joining the dilated midline vein around the choroidal fissure; and a mural type, composed of a single or a few arterial feeders which join the dilated vein near a single location [18]. The choroidal type is usually characterized by much higher flow and tends to present early with cardiac failure, as was the case for all patients in our series. The mural type has lower overall flow and tends to present later in life with hydrodynamic disturbances. All but one of our patients who presented after the first 2 weeks of life had a mural type VGAM. The difficulty of attaining good outcomes in patients presenting with early cardiac failure dictates that medical evaluation and management of cardiac failure should be considered as first-line management. In cases where medical management is likely to be successful, it may sometimes be possible to delay endovascular treatment until the patient is older because treatment is technically easier and better tolerated in the older children. However, children in whom embolization is delayed must be followed closely for progression of heart failure as well as for hydrocephalus. Consequently, as was the case in our patients, when evidence of severe cardiac disease or other organ dysfunc-

Childs Nerv Syst Fig. 3 Representative angiograms from patient with a choroidal VGAM (patient 4). Pretreatment angiograms demonstrating a choroidal VGAM on lateral (a) and anterior–posterior projections (b). Microcatheter placement into the malformation (c, d). Postembolization unsubtracted views demonstrating embolization of the lesion (e, f)

tion is present, treatment may be necessary in the first weeks of life. In these cases, the goal of embolization is not always complete obliteration of the VGAM, which may be impossible without unacceptable neurological deficits, but is guided by the clinical status of the patient. Often the immediate goal of endovascular treatment is to stabilize the patient from a cardiac standpoint until the child is older and better able to tolerate additional procedures [8, 21]. In our series, three of the seven patients treated in the first 2 weeks

of life received multiple-staged procedures in an effort to resolve cardiac failure. Two of the five patients treated later in life received multiple-staged procedures. In utero diagnosis is becoming more common [6, 11, 15] due to improved fetal ultrasound and fetal MR. Early diagnosis, particularly in utero diagnosis, can be important in the management of VGAM. In our series, six of the 13 patients were diagnosed in utero. Fetal diagnosis allows for the effective stabilization and the anticipation of the

Childs Nerv Syst Table 3 VGAM presenting for treatment after the first 2 weeks of life Dx age

Rx age

N

Case 8 Case 9

M M

In utero 14 months

16.8 months 16 months

1 1

Case 10

M

45 days

48 days

2

Case 11 Case 12 Case 13

M M M

31 months 6 months In utero

31 months 9 months NA

2 1 0

Residual shunting

N

Type

Complications

Outcome

Follow-up

Mural Mural

– Transient Parinaud’s syndrome Medullary vein thrombosis, thalamic hemorrhage – – –

Normal, no seizures Mild hemiparesis, autistic, epilepsy in remissiona Mild motor delay, compensated hydrocephalus, no seizures Normal, no seizures Normal, no seizures Delayed treatment due to stable clinical condition

17months 32 months

Mural

Y N NA

Choroidal Mural Mural

15 months

4 years 6 years 10 months

M male, F female, Dx age age at diagnosis, Rx age age at treatment, N number of treatments, NA not applicable, FU age at last follow-up a

Neurological improvement from pretreatment preexisting HSV infection

postnatal needs of the child, particularly their cardiac management. Early diagnosis, including fetal MR, cannot only be used to detect these lesions but also can be useful in identifying other structural abnormalities and can potential-

Fig. 4 Representative angiograms from patient with a mural VGAM (patient 10). a Pretreatment angiograms demonstrating a mural VGAM. b Microcatheter placement into the malformation. Postembolization views demonstrating complete embolization of the lesion (c, d)

ly be used to predict concomitant parenchymal damage that affects neurological prognosis [1, 3, 4, 12, 26, 29]. Various case series have shown that neonatal patients with cardiac failure as a result of VGAM have a particularly

Childs Nerv Syst

poor outcome even with treatment [5, 7–9, 16, 18, 19, 21, 23, 24, 27, 28]. In utero signs of progressive cardiac dysfunction which can be determined by a fetal cardiologist are associated with a poor prognosis and are thought to indicate the presence of a high flow lesion that may not respond to therapy [29]. Lasjaunias and Swanstrom et al. have reported that 22% of neonatal patients commonly have extensive parenchymal damage and may not be candidates for treatment [20, 28]. It is not clear whether any treatment or management strategies can reverse or prevent this damage. Additional structural abnormalities of the brain might also guide decisions to treat a particular patient. Despite early diagnosis and aggressive treatment, the neonatal patients in our series that presented in heart failure requiring treatment in the first 2 weeks of life had a poor outcome. Most patients survived but had neurological sequelae such as epilepsy, hydrocephalus, and moderate to severe developmental delays. In contrast, patients presenting after the first weeks of life without cardiac failure have a much better prognosis. In these patients, no deaths occured and four of the five treated patients functioned normally or with minor motor abnormalities.

Conclusions Contemporary endovascular techniques can effectively be used to treat neonatal and infant patients with VGAM. Despite early diagnosis and treatment, the overall outcome of patients presenting in the first weeks of life with medically intractable cardiac failure remains poor. In contrast, those presenting later in life with minimal cardiac dysfunction have a much better prognosis. In all cases, patients with VGAM are best treated by a multidisciplinary team that can manage and treat the complex group of health problems with which young VGAM patients present. Acknowledgements Dr. Beslow is supported by grants from the NIH (T32-NS007413) and from the L. Morton Morley Funds of The Philadelphia Foundation.

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