SUBARACHNOID HAEMATOMA - keywords
subarachnoid haematoma
references to subarachnoid haematoma
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Assis Z, Kirton A, Pauranik A, Sherriff M, Wei XC. Idiopathic Neonatal Subpial Hemorrhage with Underlying Cerebral Infarct: Imaging Features and Clinical Outcome. AJNR Am J Neuroradiol. 2021 Jan;42(1):185-193. Barson, A.J. (1990) 'A postmortem study of infection in the newborn from 1976 to 1988.’ In De Louvois, J., Harvey, D. (Eds) Perinatal practice, volume 6. Infection in the newborn. Chichester : John Wiley and Sons.
Boulton M, Young A, Hay J, Armstrong D, Flessner M, Schwartz M, Johnston M (1996) Drainage of cerebrospinal fluid through lymphatic pathways and arachnoid villi in sheep: measurement of 125 Ialbumin clearance. Neuropathol Appl Neurobiol 22:325-333.
Cain DW, Dingman AL, Armstrong J, Stence NV, Jensen AM, Mirsky DM. Subpial Hemorrhage of the Neonate. Stroke. 2020 Jan;51(1):315-318.
Chessells, J.M., Wigglesworth, J.S. (1970)'Secondary haemorrhagic disease of the newborn.' Archives of Disease in Childhood, 45, 539-543.
Cross JH, Harrison CJ, Preston PR, Rushton DI, Newell SJ, Morgan MEI, Durbin GM (1992) Postnatal encephaloclastic porencephaly—a new lesion? Arch Dis Child 67:307–311.
Dabrowski AK, Carrasco M, Gatti JR, Barreto ARF, Parkinson C, Robinson S, Tekes A, Sun LR. Neonatal Subpial Hemorrhage: Clinical Factors, Neuroimaging, and Outcomes in a Quaternary Care Children's Center. Pediatr Neurol. 2021; 120:52-58.
Dische MR, Gooch WM 3rd. Congenital toxoplasmosis. Perspect Pediatr Pathol. 1981;6:83-113.
Govaert, P., Leroy, J., Caemaert, J., Wood, B. (1992) 'Extensive neonatal subarachnoid hematoma.’ American Journal of Diseases of Children, 146, 635-636.
Govaert, P. (1993) Cranial haemorrhage in the term newborn infant
Clinics in Developmental Medicine nr. 129, London : Mac Keith Press, ISBN 0 901260 98 3
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Govaert P, Bridger J, Wigglesworth J (1995) Nature of the brain lesion in fetal allo-immune thrombocytopenia. Dev Med Child Neurol 37:485-95.
Govaert, P., De Vries, L. (2010) An atlas of neonatal brain sonography, second edition
McKeith Press, Wiley, UK as Clinics in Developmental Medicine, nrs 182-183., ISBN 978-1-898683-56-8.
Hayashi N, Endo S, Oka N, Takeda S, Takaku A (1994) Intracranial hemorrhage due to rupture of an arteriovenous malformation in a full-term neonate. Child’s Nerv Syst 10:344-6.
Hong L, McLaughlin L, Lai M, Guandalini M. Subpial haemorrhage in a well-term neonate. J Paediatr Child Health. 2023 May;59(5):766-768.
Impieri C, Ancona C, Bortolatto B, Laghetto I, Galzignato S, Nosadini M, Toldo I, D'Errico I, Sartori S, Calignano G, Cavicchiolo ME, Cavaliere E. Neonatal subpial hemorrhage: Padua experience and systematic review. Eur J Pediatr. 2025 Mar 24;184(4):265.
Jessen NA, Munk ASF, Lundgaard I, Nedergaard M (2015) The glymphatic system A beginner’s guide. Neurochem Res 40(12); 2583-2599.
Knight DB (2003) Neonatal shaken baby syndrome--lessons to be learned. Arch Dis Child Fetal Neonatal Ed 88:F161; author reply F161-2.Larroche, J.-Cl. (1977)'Developmental pathology of the neonate.'North-Holland : Elsevier.
Levene M, de Vries LS (1995) Intracranial haemorrhage. In: Levene, M., Punt, J. (Eds.) Fetal and Neonatal Neurology and Neurosurgery. Edinburgh: Churchill Livingstone, pp. 335–366.
Martinez-Correa S, Rafful P, Ramirez-Suarez K, Viaene AN, Beslow LA, Agarwal S, Whitehead MT, Vossough A, Teixeira SR. Imaging Patterns of Neonatal Subpial Hemorrhage: Provisional Statements on Neurologic Outcomes. AJNR Am J Neuroradiol. 2025 Aug 1;46(8):1702-1708.
McLellan NJ, Prasad R, Punt J (1986) Spontaneous subhyaloid and retinal haemorrhages in an infant. Arch Dis Child 61:1130-1132.
McLone DG, Bondareff W (1975) Developmental morphology of the subarachnoid space and contiguous structures in the mouse. Am J Anat. 142:273-293.
Morgan MEI, Hensey OJ, Cooke RWI (1983) Convexity cerebral haemorrhage in the neonate: in vivo ultrasound diagnosis. Arch Dis Child 58:814–818.
Mortazavi MM, Quadri SA, Khan MA, Gustin A, Suriya SS, Hassanzadeh T, Fahimdanesh KM, Adl FH, Fard SA, Taqi MA, Armstrong I,Martin BA, Tubbs RS (2018) Subarachnoid Trabeculae: A Comprehensive Review of Their Embryology, Histology, Morphology, and Surgical Significance. World Neurosurg.111:279-290.
Pinto C, Cunha B, Pinto MM, Conceição C. Subpial Hemorrhage : A Distinctive Neonatal Stroke Pattern. Clin Neuroradiol. 2022 Dec;32(4):1057-1065.
Raper D, Louveau A, Kipnis J (2016) How Do Meningeal Lymphatic Vessels Drain the CNS ? Trends in Neurosciences, September Vol. 39, No. 9.Rushton DI (2003) Neonatal shaken baby syndrome--historical inexactitudes. Arch Dis Child Fetal Neonatal Ed 88:F161; author reply F161-2.
Server A, Latysheva A, Nedregaard B, Rønnestad AE, Marthinsen PB. Neonatal subpial hemorrhage: clinical presentation, neuroimaging findings and outcome. Neuroradiology. 2025 Apr;67(4):1071-1080.
Tan MP, McConachie NS, Vloeberghs M (1998) Ruptured fusiform cerebral aneurysm in a neonate. Child’s Nerv Syst 14:467-9.
Valverde E, Ybarra M, Bravo MC, Dudink J, Govaert P, Horsch S, Steggerda S, Pellicer A; EurUS.Brain Group. State-of-the-art cranial ultrasound in clinical scenarios for infants born at term and near-term. Dev Med Child Neurol. 2025 Mar;67(3):322-347.
Williams AN, Sunderland R (2002) Neonatal shaken baby syndrome: an aetiological view from Down Under. Arch Dis Child Fetal Neonatal Ed 87:F29-30; discussion F30.
Yoffe, G., Buchanan, G.R. (1988) 'Intracranial hemorrhage in newborn and young infants with hemophilia.’ Journal of Pediatrics, 113, 333-336.
Zhuang X, Jin K, Li J, Yin Y, He S. Subpial hemorrhages in neonates: imaging features, clinical factors and outcomes. Sci Rep. 2023 Feb 28;13(1):3408.
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neuropathology and mechanisms
typical temporal lobe subarachnoid haematoma in an infant with septicaemia (courtesy JS Wigglesworth, Hammersmith Hospital)
arachnoid spaces and cisterns
typical images
subarachnoid haematoma
the shaken newborn
imaging findings
Some perinates develop large extravasations of blood within the pial-arachnoid membranes usually restricted to one side of the cerebrum (Larroche 1977, Chessells and Wigglesworth 1970). The term 'haematoma’ (with the eponym subpial or subarachnoid) is preferred when the volume of the collection is large, sometimes up to a few centimeters in thickness and because of its firmness due to proper clotting. Blood may dissect along the subjacent sulci and fissures thus penetrating deep into the parenchyma. The inner margin (toward the parenchyma) is linear in epidural and subdural haematoma, but irregular (festooned) in subarachnoid haematoma. It is not surprising to observe subsequent necrosis of the related cerebral (sub)cortex, possibly also due to associated uncal herniation and systemic vascular changes. Predilection of the basis of the temporal lobe and temporoparietal convexity is peculiar.
Chessells and Wigglesworth recorded five neonates dying with the particular lesion and autopsied in one centre during an eight month period (Chessells and Wigglesworth 1970). Larroche gathered 60 instances out of 2000 perinatal autopsies (3 per cent) (Larroche 1977). The high potential of this lesion to cause neonatal death explains these early postmortem findings (Govaert 1993 and Govaert and de Vries 2010). The clinical context is often that of a seriously ill neonate with anaemia, profuse bleeding tendency, intracranial hypertension and seizures.
A peculiar variant of postnatal onset subarachnoid haematoma has been reported due to shaking by physiotherapists (Cross et al. 1992, Williams and Sutherland 2002).
It remains important to document what are the consequences for survivors of any such lesion, often causing total cystic regression of for instance a temporal lobe.
allo-immune TP
multiple
DIC, asphyxia
subarachnoid haematoma: typical examples
gram (-) septicaemia
——>
ECMO related
thrombocytopenia, IUGR
subarachnoid haematoma: mechanisms
The event is most likely of venous or capillary origin, as its distribution is not related to arterial regions (Larroche 1977). The most solid hypothetical cause is failure of haemostasis (Chessells and Wigglesworth 1970). The intermediary mechanism is disseminated intravascular consumption of platelets and coagulation factors. This type of 'secondary haemorrhagic disease' can be related to (i) profound hypothermia in slightly preterm infants, (ii) asphyxia and (iii) severe rhesus iso-immunization, but (iv) the usual underlying disease is bacterial sepsis or a haemostatic problem in our experience.
An apparent asociation with exchange transfusion may well be due to the 'ritual' agonal attempt of treating DIC.
Against this background it is not surprising to find disseminated fibrin thrombi within several visceral micro-vessels (Chessells and Wigglesworth 1970). Barson reviewed perinatal infections extracted from postmortem material and listed subarachnoid haematoma as an indirect indicator of septicaemia, together with disseminated abscess formation, purulent vasculitis, the presence of intravascular bacteria and evidence of fibrin formation within small vessels (Barson 1990). He registered 27 instances (22.3 per cent) in 42 necropsies with evidence of disseminated intravascular coagulation from a series of 121 bacteraemic perinates with positive postmortem heart blood culture. This has to be compared with 17 instances (2.2 per cent) in 32 necropsies with evidence of disseminated intravascular coagulation from a series of 781 culture-negative dead perinates. His findings confirm the non-specific link between bacteraemia, intravascular consumption of coagulation factors and subarachnoid haematoma. Typical subarachnoid haematoma has also been reported in association with hereditary clotting disturbance, e.g. haemophilia (Yoffe and Buchanan 1988). A similar lesion has also been reported in association with congenital toxoplasmosis and calcifying brain damage (Dische and Gooch 1981).
1. thrombocytopenia: iso-immune, auto-immune
2. thrombocytopathy: congenital (von Willebrand disease), by salicylates or non-steroidal anti-inflammatory drugs
3. shortage of coagulation factors: congenital (V, VII, VIII, X), due to cumarins, diffuse intravascular coagulation
4. shortage of anticoagulants: protein C deficiency, FV Leiden, FII mutation
5. fetal liver failure: on account of acetaminophen, in perinatal haemochromatosis
One of two prenatal cases observed at Hammersmith hospital was associated with chronic fetal anaemia and non-immune hydrops ending in subacute multi-organ failure, the other one had alloimmune thrombocytopenia due to PlA1-incompatibility as underlying disorder (Govaert et al. 1995). Association in the latter with minor subpial bleeds and the finding with reticulin staining of a limiting membrane and some remnant molecular layer on the surface of the suspected subarachnoid haematoma suggest that differentiation between subarachnoid and pial haematoma cannot be made with the naked eye and may even require special histological techniques. This could help to explain why, in spite of the association with DIC, most of the haematomas are solid, indicating major consumption of factors as well as local assistance in the proces of clotting possibly by cerebral thromboplastic material. It accounts for the obvious hyperechoic change at the haematoma on CUS.
Although put forward as an alternative, there is little evidence for trauma, for instance to the large anastomosing vein of Labbé, as an alternative mechanism (Larroche 1977, Valverde et al. 2025).
More nodular but extensive subarachnoid bleeding has been observed in neonates with ruptured intracranial vascular anomalies such as arterio-venous angioma, aneurysm of the great vein of Galen and arterial 'berry' aneurysm (McLellan et al. 1986, Hayashi et al. 1994, Tan et al. 1998).
immediate postmortem scans of ELBW at 24w GA
The lesion occurs anywhere, most often in the temporo-parietal area. Ultrasound may suggest the diagnosis based on a hyperechogenicity against the (temporoparietal) bones, the borders of which irregularly penetrate the parenchyma (Larroche 1992). This represents sulci and fissures filled with clotted blood and tissue debris. Subdural haemorrhage will displace rather than penetrate the adjacent parenchyma. The midline may be shifted and the ipsilateral ventricle closed under pressure. Associated haemorrhage may be noticed in germinal matrix. Some neonates have multiple, both cerebral and cerebellar subarachnoid haematomas, inherent to a haemostatic problem and systemic circulatory changes.
Rarely, sonographic differentiation from a lobar parieto-temporal haematoma is possible after identification on coronal sections of a border of parenchyma embracing a lobar but not a subarachnoid haematoma. Haemorrhagic conversion of an infarct in the region of the MCA and subdural haemorrhage may also produce similar sonograms. Near a sinus thrombosis there may be limited subpial haematoma around involved draining veins.
Some subdural haematomas after trauma may present with lobar temporal lesions similar to subarachnoid haematoma, not always sparing the underlying tissue because areas drained by a lacerated vein may become necrotic and haemorrhagic, similar to primary subarachnoid haematoma.
A malignant astrocytoma, exceedingly rare, may present images that look like subacute subarachnoid haematoma, but with a clinical context that is often clearly different (normal haemostasis, no infection, no asphyxia, …).
Secondary subarachnoid haemorrhage, around the cerebellar cortex, is associated with IVH. Before fibrination, liquid blood follows CSF along the ventricles and the foramen of Magendi into the cisterna magna, from where it moves around the cerebellum to coagulate there.
subarachnoid haematoma: imaging
Differentiation from subdural bleeding is not difficult by the use of MRI.Recently radiologists attempted type classifications (Cain et al. 2020, Dabrowski et al. 2021, Assis et al. 2021, Pinto et al. 2022; Hong et al. 2023, Zhuang et al. 2023, Impieri et al. 2025, Server et al. 2025, Martinez-Correa et al. 2025). The conclusion is identical to the early postmortem reports: the lesions can remain subpial (ellipsoid or spherical), but can also be associated with cortical ischaemia and/or haemorrhage due to compression of the parenchyma. This leads to apparent involvement (primary or secondary) of medullary veins near the haematoma, often with parenchymal bleeding. The mixture of changes has been referred to as yin-yang or sandwich signs. These just describe the old finding that injury invests in the sulci and parenchyma, unlike sub- or epidural haematomas.
subarachnoid haematoma: neonatal shaking
Subarachnoid haemorrhage was one of the components of a strange pattern of haemorrhagic necrosis in both fronto-parietal lobes of extremely preterm infants (Cross et al. 1992). The lesions cavitated in the parenchyma and eventually turned out to be fatal. Reappearance of the pattern in another hospital led to the recognition of vigorous chest physiotherapy as the causal mechanism. The lesion is thereafter discussed as shaken newborn syndrome (Williams and Sunderland 2002, Rushton et al. 2003). It thus seems forceful rotation of the unsupported head may not only cause axonal injury and interhemispheric subdural bleeding, but also parietal (coup and contre-coup) subarachnoid haematoma.
Cross et al. 1992
A: haemorrhage and necrosis from the surface
B germinal matrix haemorrhage
sulci invested by haemorrhagic necrosis
near SSS
cisterns
maturation
glymphatics
after Mortazavi et al. 2018
McLone and Bondareff 1975, Boulton et al. 1996, Jessen et al. 2015, Raper et al. 2016, Mortazavi et al. 2018.
Brain is suspended in CSF-filled subarachnoid space by subarachnoid trabeculae, which are collagen-reinforced columns stretching between the arachnoid and pia mater. The trabeculae provide mechanical support to nearby neurovascular structures through cell-to-cell interconnections and specific junctions between the pia and arachnoid maters. Arachnoid spaces develop before and initially independent of CSF circulation, when the fourth ventricle outlet foramina are still closed. The membranes are complex near vascular structures and form recognizable constructs called cisterns. A substantial fraction of brain fluid is not formed by choroid plexus, but is derived from the brain itself (astrocytic aquaporin channels). This fluid finds the arachnoid space and may leave the brain along perforator arteries toward the cisterns and lymphatic connections from the base of the skull into the nasal mucosa.
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