Hydranencephaly: US appearance during in utero evolution.

Greene, M F; Benacerraf, B; Crawford, Jacqui

doi:10.1148/radiology.156.3.4023242

Cited by 35 publications

(16 citation statements)

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“…During the destructive phase, unusual ''masses'' of hemorrhage and soft tissue may be seen (4). The brain destruction is complete or almost complete in a bilateral internal carotid artery distribution, with the cerebral hemispheres replaced by fluid covered with leptomeninges and dura.…”

Section: Discussionmentioning

confidence: 99%

Case 7: Hydranencephaly

Kurtz¹,

Johnson²

1999

Radiology

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Section: Discussionmentioning

confidence: 99%

Case 7: Hydranencephaly

Kurtz¹,

Johnson²

1999

Radiology

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“…4,5,7 Of the proposed etiologies of hydranencephaly listed previously, the first is regarded by many to be the most likely, whereas animal studies have reproduced hydranencephaly in utero by carotid occlusion. 3,8,9 All imaging modalities, including US, computed tomography, and magnetic resonance, can be used to identify the features of hydranencephaly. In all cases, the imaging findings are essentially the same.…”

Section: Discussionmentioning

confidence: 99%

Hydranencephaly

Gentry

Connell

2013

Ultrasound Quarterly

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“…7) or be the result of a severe and diffuse hypoxic-ischemic brain necrosis [34,35]. The only case of hydranen cephaly resulting from posthemorrhagic hy drocephalus has been reported in a singleton case [25]. In fact, a large spectrum of brain destruction has been described under this term which should be preferred to that of 'malformation' [16].…”

Section: Hydranencephalymentioning

confidence: 99%

“…On fetal sonogram [25] it may be difficult to differentiate hydranencephaly from se vere hydrocephalus. Recognition of paired thalami and preserved ventral part of the frontal, temporal and occipital lobes elimi nate the diagnosis of holoprosencephaly.…”

Section: Hydranencephalymentioning

confidence: 99%

Brain Damage in Monozygous Twins

Droullé²,

et al. 1990

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A series of 15 monochorionic twins with a great variety of cerebral lesions is reported. Seven cases illustrate the classical situation: the recipient twin was affected and his co-twin, the donor was macerated. In 5 cases, the lesions were described in the donor twin as well and once, as early as 22 weeks. The lesions were usually hypoxic-ischemic, in 2 they were hemorrhagic. In 1 case there was a malformation. Fetal US were performed in 11 cases and the diagnosis of either IUGR, death of a fetus and/or brain lesions in the survivor could be made in 10 cases and once as early as 21 weeks. In fetuses born alive, transfontanellar US or CT scan have confirmed the diagnosis made on fetal US. The pathogenesis of the lesions is not fully understood. Lesions in the recipient twin may result from emboli or thromboplastic material originating from the macerated co-twin. We suggest that blood pressure instability or episodes of severe hypotension might as well lead to brain and/or visceral lesions in the recipient twin. In the donor, the lesions result from hypotension and/or anemia. With improvement and generalization of imaging techniques, the vitality of the fetuses as well as biometric parameters and anatomical structures will be better controlled. However, in case of a fetal death, occurrence of lesions in the survivor is unpredictable and no uniform policy has been proposed yet. Studies with Doppler and continuous monitoring of funicular circulation should improve our knowledge on feto-fetal transfusion and permit to detect hemodynamic fluctuation or impairment.

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Hydranencephaly: US appearance during in utero evolution.

Abstract: Massive intracranial hemorrhage was diagnosed in utero in a 27-week-old fetus. The subsequent development of hydranencephaly was monitored by ultrasound until term.

Cited by 35 publications

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Case 7: Hydranencephaly

Case 7: Hydranencephaly

Hydranencephaly

Brain Damage in Monozygous Twins

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