SUBDURAL HAEMATOMA

SUBDURAL HAEMATOMA - keywords
subdural haematoma references to subdural haematoma r e f e r e n c e s n a v i g a t o r < Castillo M, Fordham LA (1995) MR of neurologically symptomatic newborns after vacuum extraction delivery. Am J Neuroradiol 16:816-8. Choy CM, Tam WH, Ng PC (2001) Skull fracture and contralateral cerebral infarction after ventouse extraction. BJOG 108(12):1298-9. de Vries LS, Eken P, Beek E, Groenendaal F, Meiners FC (1996) The posterior fontanelle: a neglected acoustic window. Neuropediatrics 27:101–104. Govaert P, Vanhaesebrouck P, de Praeter C (1992) Traumatic neonatal intracranial bleeding and stroke. Arch Dis Child 67:840-5. 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. Grant EG, Borts F, Schellinger D, McCullough DC, Smith Y (1981) Cerebral intraparenchymal hemorrhage in neonates: sonographic appearance. Am J Neuroradiol 2:129-32. Grzybowski DM, Herderick EE, Kapoor KG et al (2007) Human arachnoid granulations part I: a technique for quantifying area and distribution on the superior surface of the cerebral cortex. Cerebrospinal Fluid Res 4:6 Hamida N, Hakim A, Fourati H, Ben Thabet A, Walha L, Bouraoui A, Mnif Z, Gargouri A. Dissection artérielle cervicale néonatale secondaire à un traumatisme obstétrical [Neonatal cervical artery dissection secondary to birth trauma]. Arch Pediatr. 2014 Feb;21(2):201-5. Hanigan WC, Olivero WC, Miller TC (1993) Traumatic neonatal intracranial bleeding and stroke. Arch Dis Child 68(3 Spec No):339-40 Hannah JA (1936) The aetiology of subdural hematoma: an anatomical and pathological study. J Nerve Ment Dis 84:169–186 Huang AH, Robertson RL (2004) Spontaneous superficial parenchymal and leptomeningeal hemorrhage in term neonates. Am J Neuroradiol 25:469-75. Jhawar BS, Ranger A, Steven D, Del Maestro RF, Cohen AR, McComb JG, Humphreys RP, Hill A (2003) Risk factors for intracranial hemorrhage among full-term infants: A case-control study. Neurosurgery 52(3), 581–590. Kehrli P (1999) Le sinus sagittal supérieur. Etude embryologique, histologique et anatomique, vol 1. Thèse de Doctorat de l’Université Louis Pasteur. Key A, Retzius G (1875–1876) Studien in der Anatomie des Nervensystems und des Bindegewebes. Samson and Waller, Stockholm, Sweden Kumar M, Avdic S, Paes B (2004) Contralateral cerebral infarction following vacuum extraction. Am J Perinatol 21:15-7 Le Gros Clark WE (1920) On the Pacchionian bodies. J Anat 55 (Pt 1):40–48 Lequin MH, Peeters EA, Holscher HC, de Krijger R, Govaert P (2004) Arterial infarction caused by carotid artery dissection in the neonate. Eur J Paediatr Neurol 8:155-60 Looney CB, Smith JK, Merck LH, Wolfe HM, Chescheir NC, Hamer RM, Gilmore JH (2007) Intracranial hemorrhage in asymptomatic neonates: Prevalence on MR images and relationship to obstetric and neonatal risk factors. Radiolog, 242(2), 535–541. Pollina J, Dias MS, Li V, Kachurek D, Arbesman, M (2001) Cranial birth injuries in term newborn infants. Pediatr Neurosurg 35:113-9. Mack J, Squier W, Eastman JT (2009) Anatomy and development of the meninges: implications for subdural collections and CSF circulation. Pediatr Radiol (2009) 39:200–210 Maertens P (1989) Imaging through the posterior fontanelle. J Child Neurol 4 Suppl:S62-7. Nikam RM, Kandula VV, Yue X, Krishnan V, Kumbhar SS, Averill LW, Paudyal B, Choudhary AK (2021) Birth-related subdural hemorrhage: prevalence and imaging morphology. Pediatric Radiology 51(6), 939–946. Rooks VJ, Eaton JP, Ruess L, Petermann GW, Keck-Wherley J, Pedersen RC (2008) Prevalence and evolution of intracranial hemorrhage in asymptomatic term infants. American Journal of Neuroradiology 29(6),1082–1089. Schwartz P : Geburtsschaden bei Neugeborenen, Gustav Fisher Verlag, Jena, 1964).Steinbok P, Haw CS, Cochrane DD, Kestle JR (1995) Acute subdural hematoma associated with cerebral infarction in the full-term neonate. Pediatr Neurosurg 23(4):206-15 Whitby EH, Griffiths PD, Rutter S, Smith MF, Sprigg A, Ohadike P, Davies NP, Rigby AS, Paley PMN (2004) Frequency and natural history of subdural haemorrhages in babies and relation to obstetric factors. Lancet 363(9412), 846–851. Winkler P (1998) Advances in paediatric CNS ultrasound. Eur J Radiol 26:109-20. typical examples veins and haemorrhage pial veins imaging aspects Compression of the skull, in itself resulting from different types of pressure, leads to moulding with displacement of bones and attached structures, to increased intracranial pressure and to venous distension. The pubic site is most affected by pressure. Pressure effects are more relevant during the second stage of labour. ICP builds up gradually following rise of amniotic pressure (in about a minute) and ICP may be higher than amniotic pressure. Any pressure rise depends on: duration of external pressure, magnitude of pressure, area size and site (vertex less affected than equatorial plane). Skull fractures merit special attention to exclude evolution to growing skull fracture. Mechanisms between dystocia (unusual development of forces on the cranium during delivery) and stroke (haemorrhagic and/or not) are a.o.: embolism from a burdened umbilical vascular system, traction on neck arteries (Lequin et al. 2004, Hamida et al. 2014), thrombus formation in ductus venosus or the heart, and skull compression (Govaert et al. 1992, Hanigan et al. 1993, Steinbok et al. 1995, Choy et al. 2001, Kumar et al. 2004). The clinical presentation is often not specific and without clinical seizures: apnoea, fever, irritability. development of the superior sagittal sinus historical account > subdural haematoma in infancy tentorial tears Subdural haemorrhage (SDH) is the most frequent ICH (intracranial haemorrhage) in term infants, due to rupture of abnormal, lacerated, congested or thrombosed veins. This has been one of the most studied topics in perinatal pathology (see historical account). Although haemorrhage may occur from rupture of an artery, most follow abnormal distension, laceration or thrombosis of veins. This means that normal venous anatomy has to be studied in extenso before understanding subdural or other haemorrhages. Population studies of asymptomatic newborns have established an incidence of limited SDH of 26-46% (Looney et al. 2007, Rooks et al. 2008, Nikam et al. 2021). Asymptomatic SDHs are usually small (< 3 mm) and resolve in 3-4 weeks (Whitby et al. 2004, Rooks et al. 2008). In some term infants congestion only can be retained as an explanation for choroid plexus haematoma, IVH and bleeding in and round the temporal lobe. In the absence of traumatic labour and with normal haemostatic tests, vascular dysplasia is a rare cause of haemorrhage. Risk factors associated to a delivery followed by symptomatic ICH include coagulation disorders, vaginal delivery, assisted delivery with forceps/vacuum extraction and/or prolonged second stage of labor (Jhawar et al. 2003, Rooks et al. 2008, Nikam et al. 2021). location types of SDH dural histology subdural haematoma s u m m a r y trauma algorithm for haemorrhage subdural haematoma: summary A graphic symmary of types of subdural haematoma using cranial ultrasound. subdural haematoma location types contusion near fontanel vitamin K deficiency convexity subdural haematoma chronic hygroma basal subdural haematoma uncus herniation and stroke von Willebrand disease “minor" left tentorial tear centrotentorial subdural haematoma major left tentorial tear "minor" left tentorial tear with early hygroma of clot posterior subdural haematoma mastoid and posterior grunting only From early on in the nineteenth century a multitude of authors were interested in birth trauma. This topic became a 'fil rouge' throughout perinatal medical science up to the twentieth century's sixties. Boosters of interest have recently been given by modern imaging techniques. Therefore, in this chapter, we shall attempt summarizing genuine milestones in our knowledge of at or near term intracranial bleeding. Until recently, this discussion was inevitably linked to birth trauma in the mechanical sense of the word. Up to about 1960 most references are found via Naujok's detailed monography on "Geburtsverletzungen' from 1934 and via Schwartz's minute description of the related literature in his monography from 1964 (for some of the old references we relied on Schwartz P : Geburtsschaden bei Neugeborenen, Gustav Fisher Verlag, Jena, 1964). For the sake of clarity the reference to the related journal is added to the paragraph immediately behind the author's name. 1. Cruveilhier (1831): this anatomist designed a famous atlas on brain and other pathology, containing an excellent picture of intracranial bleedings in the chart 'apoplexie des enfants nouveau-nés'; he recognized intraventricular, subarachnoid and subdural haemorrhage in the perinate. 2. Weber (1851-1854): moulded overlapping cranial bones can lacerate falx and/or tentorium, leading to dilatation and possible thrombosis of the superior sagittal sinus. 3. Ruge (1875): falx bleedings can be caused by spontaneous vaginal deliveries. 4. Kundrat, Ballantyne (1890): interparietal bone displacement during precipitate delivery can influence the superior sagittal sinus and/or its bridging veins to the extent that the latter may rupture and cause bleeding over the convexity of the cerebral hemisphere near the midline; venous infarction of the underlying brain may be associated; these lesions tend to occur more in skulls with limited (at term) or weak (in the preterm) interstitial membranes (= interosseous suture tissue). 5. Seitz (1907): intracranial bleeding is caused by congestion of the great cerebral vein and its afferent smaller vessels; this congestion follows pressure differences between presenting part and uterus; supratentorial haemorrhages differ clinically from the ones in the posterior fossa (crying, restlesness, tense fontanelle versus apathy, opisthotonus, clonic seizures, apnoea). 6. Beneke (1910) (Muenchener Medizinische Wochenschrift 1910; 4 : 2125-2127): bitemporal skull compression elevates the calvarium and stretches the tentorium retained by the occipital lobes; consequently the medial superior tentorial fibers are prone to damage (Tentorium-strahlung der Falx) associated with peritentorial bleeding and congestion of the great cerebral vein; cerebellar coning can be another sequence of events; tentorial damage outnumbers convexity subdural haemorrhage; both difficult and easy (Sturzgeburt) delivery can be responsible. 7. Ylppo (1919) (Z Kinderheilk 1919; 20 : 212-431): preterm infants tend to have intradural and pial bleeds more readily than actual dural tears. 8. Holland (1920-1937) (Am J Obstetr Gynecol 1937; 33 : 1-18): this author reports on 81 tentorial tears in 167 fresh stillbirths (48%), 46/81 delivered head first (25 by forceps extration) and 35/81 from the breech (more deaths in breech delivery due to suboccipitofrontal skull compression than to cord prolapse). Intracranial lesions are of 4 varieties : a) overstretching and tearing of dural septa by anteroposterior shortening of the calvarium because of suboccipito-bregmatic compression resulting in rostral and superior displacement of the falco-tentorial junction; parallel oval falx tears and laceration of the anterior vertical tentorial margin are characteristic; most tears, in themselves, are not fatal; b) vessel injury, either traumatic laceration resulting in subdural haemorrhage, or venous engorgement and ulterior vessel rupture; a mechanistically logical weak point is the entrance of the great cerebral vein of Galen into the straight sinus; the former becomes kinked and obstructed by the tentorial lift; sites of bleeding are torn pontine or cerebellar bridging veins or genuine sinus lesions, especially of the straight sinus; c) intraparenchymal haemorrhage within the territory of the great cerebral vein or within the pons; d) brain and meningeal congestion with intracranial hypertension. 9. Siegmund (1923) : subdural haemorrhage can cause external hydrocephalus. 10. Dollinger (1927) : some infants have an intracranial bleed not eliciting seizures and not altering consiousness; they present with the 'small picture' of symptoms such as weakness, nutritional problems, respiratory difficulty. 11. Rydberg (1932) : characteristic presentation with intracranial haemorrhage is with a free interval, lasting hours to days, preceding poor nursing, apathy, high cry and then progressing into seizures, irregular respiration, rigidity...; uncharacteristic features are cyanosis and respiratory problems. 12. Naujoks (up to 1934) (Die geburtsverletzungen des Kindes, Ferdinand Enke Verlag, Stuttgart, 1934) : apnoea in the absence of shock or asphyxia either points to intracranial haemorrhage and/or brainstem damage. 13. Hemsath (1933) (Am J Obstetr Gynecol 1934; 27 : 194-203): the heel of Achilles of the newborn skull is the 'occipital hinge' between squamous and lateral parts of the occipital bone; osteodiastasis between these parts can follow difficult birth of the aftercoming head in breech delivery, high forceps extraction with the occiput pushed against the maternal symphysis or difficult shoulder delivery with one hand grasping the occiput; the subsequent lesions in and even above the posterior fossa are outlined in the chapter on occipital osteodiastasis. 14. Craig (1938) (Arch Dis Childh 1938; 13 : 89-124) : in his clinical description of 126 autopsied newborns with intracranial haemorrhage, started from a subdivision into 42 tentorial tears associated with subdural haemorrhage, 20 isolated subdural bleedings, 36 subarachnoid haemorrhages, 22 intraventricular and 6 parenchymal bleeds. Nulliparity was a risk factor for subdural haemorrhage, prematurity for intraventricular haemorrhage, forceps delivery for tentorial injury and breech extraction for subdural bleeding with intact tentorium. Craig recognized the danger of rotation of the descending fetal head, either manually or with an instrument. A mere 4 cases presented with haemorrhagic diathesis and three died of recurrent bleeding due to 'ill-considered' handling. Some of Craig's clinical descriptions are timeless neurological markers : agitated eye movements, unnatural alertness and anxiety of facial expression, darting adder-like protrusion of the tongue, sponginess of the fontanelle, cerebral cry. Peculiar to subdural haemorrhage were phase changes from depressed to irritative states, reflex irritability and generalized hypertonia. If within the posterior fossa subdural bleeding could present with nuchal rigidity and head retraction, deep cyanosis and athetoid movements and tremors. Subarachnoid haemorrhage was difficult to recognize on a clinical basis. Intraventricular bleeding differed because of its dramatic acuteness and rapidly lethal course with painful crises, an agonal facial expression and terminal pyrexia. Intracerebral haemorrhage, diagnosed in large term infants alone, manifested with a prolonged course, hypothermia, flaccid inactivity and extreme physical weakness contrasting with continuous mental restlesness and an expression of fear on the face. 15. Meier (1938) (Zschr Kinderheilk 1938; 59 : 556-558): described impression of the prae-interparietal ossicle as a cause of thrombosis of the superior sagittal sinus in a large preterm infant without birth asphyxia. 16. Kehrer (1939) (Die intrakraniellen Blutungen bei Neugenorenen, Ferdinand Enke Verlag, Stuttgart, 1939): his thesis on intracranial haemorrhage in the newborn focussed mainly on etiology. Some descriptions of prenatal brain trauma are given. For neonatal bleedings the causal scheme is as follows : 1) asphyxial congestion of pial-arachnoid veins; 2) 'saugwirkung' with venous congestion limited to the structures in the presenting part; 3) bone displacement resulting in dural membrane injury and laceration of major sinuses. This displacement is due to either excessive moulding, breech delivery or mechanical manoeuvres. Bilateral tentorial injury is common in occipito-posterior presentation and high forceps extraction whereas unilateral injury characterizes prolonged delivery from occipito-anterior position and midpelvic forceps traction, the latter probably due to contralateral parietal impression against the pubic bone. Kehrer gave adequate descriptions of massive interhemispheric subdural haematoma and cerebellar coning. He documented the possibility of fatal cranial birth trauma due to fundal pressure or during caesarean section. 17. Clifford (1941): chronic infantile subdural haematoma is a possible corolary to birth trauma. Twilight sleep, used for the reduction of maternal discomfort, increases the use of instruments during delivery (this observation was recently done over for epidural analgaesia and vacuum extraction). 18. Saunders (1948) (J Obstetr Gynaecol 1948; 55-61): direct traction on the scalp from a point near the large fontanelle, results in tightening of the falx and subsequent tentorial lift, the whole mechanism referred to as 'galea-forceps'. Tentorial trauma is either due to anteroposterior skull pressure, laterolateral pressure, direct scalp traction or traction on the whole body in breech delivery. 19. Kendall (1952) (J Pediatr 1952; 41 : 125-132): cephalhaematoma has an incidence of 3.06 % following forceps versus 0.18 % following spontaneous vaginal delivery. Occipital cephalhaematoma usually relates to breech delivery. 20. Sulamaa (1953) (Acta Obstetr Gynaecol Scand 1952; 31 : 400-412) : presented numerical data on birth trauma from one University Hospital in Helsinki, between 1925 and 1941, with 815 (2.1 %) neonatal deaths in 38826 full-term deliveries. There were 120 peripartal subdural bleedings in 602 autopsies (50 stillbirths, 70 neonatal deaths), 11 tentorial and 26 falx tears. The incidence of dural tears was 0.18/1000 spontaneous deliveries and 4.88/1000 forceps extractions. Subdural bleeding was even more common after forceps (1.6 %) than breech (1.3 %) delivery. 21. Grontoft (1953): in a similar gigantic study reported on 72 tentorial tears in 120 perinates with intracranial haemorrhage. He distinguished between tentorial tear with severe bleeding (38/72), with minor haemorrhage (25/72) and post-mortem tentorial injury (9/72). An additional 12 pial haemorrhages were documented despite intact dural membranes. Convexity subdural haemorrhage was not observed at all, according to the author because of systematic prophylaxis with vitamin K at birth. Unilateral tentorial stress was found in 14/27 stillbirths and in 6/36 neonatal deaths, suggesting that this pattern of lesion is common after fetal death. These post-mortem tears can still be associated with bleeding from patent valveless sinuses. Severe tentorial laceration (38/72) was increasingly more frequent with rising birth weight, reaching 66 % in a subgroup of perinatal deaths at or above 4500 grams. Bleeding was almost invariably bilateral, the brunt of haematoma formation being in the middle cranial fossa and never in the posterior fossa alone. Both forceps (15/38) and breech (11/38) delivery were the main causes. Mechanical trauma increased with gestational age, the reverse being true for birth asphyxia. Male preponderance was excessive in the subgroup with mild peritentorial haemorrhage (23/25), where most deliveries had been spontaneous vaginal (13/25). Pial bleeding over cerebrum and/or cerebellum affected preterm infants (9/12) with asphyxial background (12/12) or haemorrhagic tendency (3/12). 22. Schipke (1954): acute neonatal subdural haematoma and infantile convexity subdural haematoma are different degrees of the same disorder, caused by rupture of cerebral bridging veins or of the great cerebral vein of Galen and its tributaries. Subdural puncture can be life-saving even in the neonatal setting. 23. Lebensohn (1956): neck rotation with forceps can cause ischaemia in the region of the basilar artery with subsequent failure of upward gaze from mesencephalic injury. 24. Schreiber (1957): reports one of the first intentional distinctions between convexity subdural bleeding of the infant and neonatal supratentorial subdural haemorrhage following tears of lateral tentorial veins. Although in the latter disorder, most blood was located under and lateral to the temporal lobe, subdural puncture was positive in 13/17. Craniotomy was recurred to in 15/17, mainly because of uncal herniation with ipsilateral mydriasis (13/17). Two died, 9 had a normal or fair outcome, 4 were severely handicapped. 25. Saint-Anne Dargassies (1957): reports craniotomy on day 20 for an epidural haematoma, caused by forceps extraction. The child presented with seizures, contralateral hemiparalysis, parietal bone fracture and oscillating intracranial hypertension. Subsequent neuromotor development was normal at 13 months. 26. Fulst (1960): in a report destined to defend vacuum extraction as an instumental delivery method, 4 % of cephalhaematomas and a 'few' subgaleal bleedings were reported in 300 extractions. The lack of danger of ventouse application over the anterior fontanelle is claimed, rephraising Malmstroms idea that vacuum does not effect intracranial structures directly. Two of the neonates with subgaleal haemorrhage died on the first day of life. 27. Boon (1961): vacuum delivery can cause erosion of parietal bones, subgaleal bleeding and intracranial accumulation of air. 28. Lauridsen (1962): vacuum extraction is dangerous if prolonged (more than 30 minutes). Some adverse effects in 69 vacuum deliveries from at or below the mid-pelvic plane : failed extraction 5/69, skin abrasion 15/69, cephalhaematoma 6/69, severe jaundice 2/69, residual skin changes on follow-up 4/69. 29. Wylie (1962): elective forceps delivery with axis-tractionometry permits subgrouping into easy (< 10 kg), average and difficult (> 20 kg) 'maximum pull'. Potentially traumatic deliveries occur at all stations. Small as well as large infants may pose difficult problems. Difficult traction is necessary in 42 % of nulliparous, versus 16 % of nulliparous women. Over 2 % of nulliparous women can only be delivered with tractional forces of > 30 kg. Between 20 and 30 kg the operator can know the force exerted and abandon further efforts to deliver vaginally. 30. Aguero (1962): in 100 consecutive vacuum extractions, all by resident staff, he recorded 10 deep cutting skin marks, 3 skin avulsions, 15 phlyctenes, 12 ulcers, 8 intracranial bleedings, 5 fatal tentorial tears, 4 survivors with neonatal seizures. 31. Lehman (1963): two fatal vacuum extractions on record in 6000 live births at Gothenburg, both with subgaleal bleeding, one due to rupture of the interparietal synchondrosis and underlying superior sagittal sinus. Traumatic delivery can be fatal in the absence of tentorial damage. 32. Awon (1964): in a post-mortem human experimental setting vacuum traction causes parietal tenting. 33. Issel (1967): found mechanical cranial birth trauma in +- 20 % of perinatal autopsies. Perinatal mortality rates were 0.08 % in spontaneous multiparous delivery, 0.8 % in nulliparous delivery with at least 24 hours of labour, 1-2 % in spontaneous breech delivery, 2.4 % in nulliparous forceps delivery, 9 % in nulliparous delivery with high forceps extraction and between 10 and 20 % in difficult breech extraction. 34. Emmanouilides (1967): demonstrated in vivo diagnosis of neonatal convexity subdural haematoma by transumbilical aortography. 35. Schenker (1967): major intracranial haemorrhage detected in 0.6 % of vacuum versus 1.3 % of forceps extractions. 36. Robinson (1968): delayed onset (more than 6 hours after birth) of neonatal subgaleal bleeding can be explained by vitamin K deficiency. This author also calculated that for each cm of postnatal increase of the head circumference about 40 ml of blood is lost in the virtual subgaleal space. 37. Ahuja (1969): described 13 subgaleal bleedings in 310 consecutive vacuum deliveries, versus 0 in 12000 spontaneous vaginal births. Three of them were associated with neonatal death, one with a torn cerebellar tentorium. He pointed out the importance of a low (< 10 %) Thrombotest, but suggested that adequate prophylaxis would need fresh frozen plasma in addition to IV vitamin K. 38. Thorn (1969): reviewed the clinical presentation of neonatal intracranial haemorrhage. 39. Towbin (1970): perinatal intracranial damage can be schematically presented in 4 varieties. I : Subdural haemorrhage : a) central tentorial tear with basal cerebral and posterior fossa haemorrhage (if the vein of Galen or straight sinus are involved); b) falx tear with interhemispheric subdural haemorrhage; c) vein of Galen tear; d) circumferential dural sinus injury due to fracture, moulding or osteosiastasis and usually rapidly fatal; e) stretch-tears of cerebral bridging veins due to overlapping parietal bones with (fronto-parietal) convexity subdural haematoma, usually at full term and well tolerated. II : Lesions of cord and brainstem, found in 10-33 % of perinatal autopsies : a) cord lesions : laceration, oedema and congestion, acute neuronal damage, focal malacia or haemorrhage; b) brainstem lesions : laceration of the cerebellar peduncles by stretch, erosion of cerebellum and stem by pressure, focal haemorrhage; c) spinal and cranial nerve root avulsion or perineural haemorrhage; d) spinal dural tear, epidural (preterm, cervical) - intradural and subdural haematoma, arachnoideal congestion and haemorrhage; e) paramedullar damage to vertebral arteries, perivertebral muscles. All these lesions are usually due to elongation and torsion of the fetal body, or to excessive vertebral flexion. III : Periventricular haemorrhage of the preterm infant (venous haemorrhagic infarction). IV : Cortical infarction in term infants. 40. Gilles (1970): acute hydrocephaly in posterior fossa subdural haemorrhage can be due to subtentorial bleeding with downward anterior displacement of the cerebellum against the fourth ventricle, to occipital osteodiastasis (with upward anterior displacement of the cerebellum and obliteration of the basal cisterns) or to angulation of the aquaeduct. 41. Fedrick and Butler (1971) (1958 British Perinatal Mortality Survey): by definition mechanical birth trauma in this study consisted of subdural haemorrhage associated with laceration of falx, tentorium or great cerebral vein. The reported overall incidence was 3.5/1000 births, 1.5/1000 being neonatal deaths. Six % of full-term infants had a birthweight of at least 2 standard deviations above the mean. The delivery method in the neonatal death group was by secondary caesarean in 2.8 %, by primary caesarean in 3.7 %, by forceps extraction in 17.0 %, breech vaginal in 30.2 % and spontaneous vaginal in 38.2 %. Labour exceeded 24 hours in 17.0 % of the neonatal deaths with birth trauma. Nulliparity was a risk factor (48.5 %). Some incidences were calculated for birth trauma in relation to the delivery mode : 1.5/1000 live births, 5.6/1000 forceps deliveries, 21.8/1000 breech deliveries, 7.8/1000 deliveries with labour lasting more than 48 hours, 3.1/1000 deliveries of unmarried women, 2.1/1000 firstborns, 5.3/1000 deliveries of mothers below 20 years of age and 4.3/1000 deliveries of mothers above 40 years of age. The lowest incidence (0.8/1000) was registered in the group with spontaneous vaginal delivery from occipito-anterior presentation. 42. Tank (1971): documented 3 torn tentoria and 1 epidural haematoma in 900 consecutive breech deliveries. 43. Ponte (1971): detailed the clinical history, angiographical diagnosis and surgical treatment of a basal convexity subdural haematoma presenting with dry subdural tap, uncal herniation and contralateral seizures following spontaneous vaginal delivery. 44. Pryse-Davies (1973): gave a comprehensive description of brain swelling in 183 perinatal necropsies (30 abortions, 64 stillbirths, 89 neonatal deaths). Gyral flattening was present in 63 % of the post-mortems on infants with gestational age above 32 weeks, and was much less common in small preterm children. The greatest incidence was on record following intrapartum asphyxia : gyral flattening 28/39, uncal grooving 15/39, cerebellar coning 9/39 (the latter being the severe end of the brain swelling spectrum). Uncal herniation was observed in 41 % of perinatal deaths following instrumental delivery, 25 % of the oxytocin augmented spontaneous labours, 11 % of spontaneous vaginal deliveries, 9 % of spontaneous breech deliveries and 57 % of the breech deliveries ended with instrumental application to the stuck aftercoming fetal head. Brain swelling was not due to water but to vascular engorgement. Growth retardation increased the risk of perinatal brain swelling. Moulding alone seemed unlikely to cause uncal herniation or cerebellar coning. Cerebellar coning has three major causes : brain swelling, spinal cord traction in breech delivery, posterior fossa subdural haematoma. 45. Natelson (1973): published one of the first follow-up studies of cranial birth trauma. His material consisted of 6 neonatal deaths and 36 neonates discharged alive from one neonatal unit in a 5 year period. Amongst the survivors there were 18 fractures and 24 haematomas. Depressed fractures were related to difficult delivery in 14/15, were asymptomatic in 12/15 and carried an excellent prognosis with normal development in 13/15. Two infants with linear fracture were severly traumatized; one basal skull fracture presented as haemotympanum and ipsilateral facial paralysis. Acute subdural haematoma (10/42) caused early demise in 5; 4 were diagnosed in life by subdural puncture and then operated upon (2 burr holes, 2 membranectomies), three of them surviving with severe sequelae. One of the subdurals was associated with a large falx haematoma. Intracerebral haematoma with uncal herniation was recognized in one neonate during emergency craniotomy. Chronic convexity subdural haematoma was diagnosed in 13 infants, 4 with gross preceding birth trauma. Global assessment : neonatal death 6/42, normal development 19/42. 46. Simmons (1974): hypernatraemia associates with neonatal intracranial bleeding. 47. Deonna (1974): commented on the in vivo diagnosis of convexity subdural haematoma by subdural puncture, brain scan and angiography. 48. Pape (1976), Grunnet (1976), Martin (1977) and Donat (1979): in preterm infants cerebellar haemorrhage is part of a supratentorial intraventricular bleeding in half; the rest is caused by occipital bone impression as in occipital osteodiastasis or due to face-mask ventilation, by diffuse intravascular coagulation or by arterio-venous aneurysm. 49. Bleyer (1976): maternal anticonvulsants can contribute to fetal haemorrhagic diathesis in concert with birth trauma, causing intracranial and visceral bleeding. Prophylaxis should be by IV administration of vitamin K at birth and plasma if the cord coagulation prophile is abnormal. 50. Abroms (1977): from two personal observations of convexity subdural haemorrhage following breech delivery, the authors propose the following indications for caesarean section in breech presentation : hyperextension of the fetal head, dysfunctional labour, cephalopelvic disproportion. 51. Deonna (1977): low CSF glucose (< 40 mg/dL) is a predictor of posthaemorrhagic hydrocephalus, not of cerebral palsy, in case of meningeal bleeding. 52. French (1977): the first CT diagnosis of posterior fossa subdural haematoma, confirmed at craniotomy. 53. Easa (1978) : localised visceral e.g. intracranial bleeding can generate disseminated intravascular coagulation, which in its rebound phase (after 1 to 4 days) presents with thrombocytopaenia, normal or elevated serum fibrinogen, elevated f VIII, reduced or normal PTT. 54. Cohen (1978) : neonatal subgaleal bleeding can be the presenting feature of haemophilia. 55. Dolinskas (1978) : the falx density on CT scan indicates subarachnoid haemorrhage in paediatric skull trauma. 56. Donat (1978): full-term intraventricular haemorrhage almost invariably originates in the chorioid plexus of neonates with respiratory difficulties. 57. Zimmerman (1978): in battered child syndrome, a specific parieto-occipital interhemispheric subdural haematoma is recognized in 17/28 infants. It is associated with retinal bleeding (76 %) and is caused by vigorous shaking, with a low reported incidence of direct skull trauma (12 % with skull fracture). Its origin probably resides in ruptured posterior cerebral bridging veins. Residual posterior cerebral artery infarction is recorded in half of them. For details on pathogenesis and CT diagnosis of interhemispheric subdural haematoma, see Kasdon (1979). 58. Plauche (1979): vacuum extraction causes major intracranial haemorrhage in 3-7/1000 manoeuvres, with fatal outcome in 0.5-1/1000. 59. Chiswick (1979): studied 86 Kielland forceps deliveries in comparison with 86 matched spontaneous vaginal deliveries. The indication for forceps application was long second stage in 49/86 and fetal asphyxia in 32/86. Forceps N = 86 Item Spontaneous vaginal N = 86 4 neonatal death 0 3 tentorial tear 0 15 delayed respiration 3 20 abnormal neuro-behaviour 2 37 fetal asphyxia 14 In the absence of fetal asphyxia abnormal neurological behaviour was still recorded in 7/49 forceps versus 1/72 spontaneous vaginal deliveries. Rotational forceps carries a neonatal mortality rate thrice that of forceps from occipito-anterior position. 60. Cooper (1979): epidural haematoma can be the presenting feature of delayed haemorrhagic disease due to isolated breastfeeding without vitamin K supplement at birth. In this report atrophy within the ipsilateral middle and posterior cerebral artery zone was documented. 61. 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Zonana, J., Adornato, B.T., Glass, S.T., Webb, M.J. (1986) 'Familial porencephaly and congenital hemiplegia.' Journal of Pediatrics, 109, 671-674. Zorzi, C., Angonese, I., Zaramella, P., Benini, F., Dalla Barba, B., Cavedagni, M., Melli, R., De Carolis, G. (1988) 'Periventricular intraparenchymal cystic lesions : critical determinant of neurodevelopmental outcome in preterm infants.' Helvetica paediatrica Acta, 43, 195-202. mitochondrial disorder historical account of subdural haematoma: references from Govaert 1993 traumatic mechanisms of perinatal brain damage The complex fusion of primitive vessels in the midline leaves intraluminal septae, also called Willis’ cords. Kehrli in 1999 described two different functionally related layers—one to the vault, the other to the cerebral leptomeninges and the cortex; the epidural space is an interface between the cranial vault and the underlying cortex covered with leptomeninges. The SSS is a delicate venous confluence area. The first 6 weeks of life numerous epidural vascular plexus form. At this stage, most neural tube drainage has a ventro-lateral direction. As the meninx primitiva differentiates into contiguous but distinct layers, venous drainage also differentiates into discrete systems. Separation of the drainage of the brain from the dural venous drainage gives rise to the specific anatomy of the bridging veins. Initially, there is a primitive endothelial plexus of venous connections between dural and pial layers. However, early in the first trimester, the continuous net of primitive endothelial channels draining the brain and those draining the dura undergo a venous cleavage, such that most of the numerous primary venous anastomoses between the pia and dura resorb. It is around the 8th week that the superior sagittal sinus becomes easily recognisable and enlarges in the craniocaudal region. At the beginning of the fetal period, the torcular region has a perisinusal space within the epidural space that is occupied by an extremely rich vascular plexus. Initially, it will drain the bony portion of the region (squamous portion of the occipital bone) before later becoming the torcular that is so developed in neonates. meningeal layers and the superior sagittal sinus The few remaining venous anastomoses enlarge and become the definitive bridging veins. The veins draining the majority of the dorsal convexity of each cerebral hemisphere collect into the superior cerebral veins. These superficial veins coalesce to form between 10 and 18 large bridging veins that eventually penetrate the dura–arachnoid interface layer and travel for a variable distance within the dura before entering the superior sagittal sinus. meningeal layers Le Gros Clark in 1920 emphasized that lateral lacunae are part of a dense parasagittal “meshwork of veins.” Although the function of this venous plexus is not fully understood, it likely plays a role in the movement of CSF from the subarachnoid into the venous and lymphatic system. While they may play a dominant role in the adult, arachnoid granulations are not fully formed in the infant. Le Gros Clark 1920: “At birth they are imperceptible even on examination with a hand lens. At the age of six months they are still invisible, but by 18 months they are quite obvious on close inspection. They appear in the first instance in the regions where the parietooccipital and central veins open into the sagittal sinus. From there they spread forwards and backwards along the superior margin of the cerebral hemispheres, and at the age of three they are disseminated over a considerable area.” Arachnoid granulations occur with greatest frequency in the parasagittal venous plexus (Grzybowski et al. 2007). The arachnoid villi are interdigitated between the trabeculae of the dura at the site of the intradural venous plexus. The bridging veins independently enter the sinus beneath the parasagittal venous plexus. The intimate relationship between the parasagittal venous plexus and arachnoid villi might bear relevance to the known association of SDH to states of both increased (benign extracerebral collections of infancy) and decreased CSF volume (spontaneous intracranial hypotension). Intrinsic brain and dural veins separate early in development (Mack et al. 2009). Most primary venous anastomoses between pia and dura resorb. Remaining anastomoses develop into bridging veins, between 10 and 18 large veins that eventually penetrate the dura–arachnoid interface layer and travel for a variable distance within the dura before entering the superior sagittal sinus. These veins are not fragile and only rupture under considerable force, making them improbable sources of subdural haematoma without trauma. Vascularity of the dura in infancy is very strong. Key and Retzius in 1875 noted the presence of a fine capillary network located along the inner portion of the dura. Hannah in 1936 speculated that the inner dural capillary layer is the origin of subdural haematoma. Penetrating branches of the meningeal arteries leave the superficial dural surface and extend to within 5 to 15 μm of the dural border cell layer, to end in a rich capillary network. The dural venules of this network are permeable and innervated by branches of the trigeminal nerve. These “leaky” vessels near the dura–arachnoid interface are candidates for the source of subdural bleeding. subarachnoid space For convexity subdural haematoma it is not difficult with cranial ultrasound to locate the haemorrhage between the dura mater of the sinus sagittalis superior and the arachnoid membrane that floats over clear arachnoid fluid. To precisely indicate the source of bleeding either at the dural veins draining into a trabecula or at a bridging vein is not possible. subdural space infantile subdural haematoma SSS Developmental anatomy of the pial cerebral veins The cortical veins of the cerebrum have been examined by upward injection of the internal jugular vein in five fetuses, whose ages ranged from six months to term [O’Connell 1934]. The surface veins are separated into three layers: a superficial, which forms the superficial vessels of the head; an intermediate, which forms the dural sinuses ; and a deep portion which intimately covers the nervous tissue and later forms the cerebral veins. Continuity between the superficial and middle venous strata persists only in the emissary veins. The cerebral veins have important connections with the dural system, firstly in the region where both sets of vessels drain into the primary head vein, and secondly, on the dorsal aspect of the cerebrum close to the midline. In this midline region there is an anastomosis between the vessels of opposite sides which is called the sagittal plexus, and from this the superior and inferior sagittal sinuses and the straight sinus develop. As expected the deepest stratum of the anterior plexus sends some of its anterior branches radiating from the insula to the margin of the hemisphere. This arrangement persists in late fetal and adult life, the superficial middle cerebral vein sends tributaries radiating across the surface of the hemisphere towards its margin. The radiation of the cortical veins from the region of the insula is very well marked in the fetus and persists in adult life. The superior members of this group of vessels approach the margin of the hemisphere at right angles to the frontal side, but their terminal portions, in most cases, change direction before entering the sinus. From observations on the changes in their direction, which occur between the later months of fetal life and adult life, it is considered that all these vessels originally entered the sinus approximately at right angles to its long axis, but especially posterior (parietal and occipital) veins turn anterior before entering the SS, so that their outgoing flow is against streaming in the SSS. The size of these vessels is inversely proportional to their numbers. In both adult and fetus eight veins were the commonest number present on each side (range 5 to 13). The veins enter the dural wall of the sinus for a short distance posterior to the final entry into the inner sinus wall. With the growth of the cerebral hemisphere, there is a tendency towards separation of these vessels into (a) a superficial middle cerebral system and (b) a system of veins around the margin of the hemisphere—the superior and inferior cortical veins. In many the continuity of the original channel is not interrupted, and hence the superior anastomotic veins (at least three in number) and the inferior anastomotic veins (usually two in number) persist as evidence of the original arrangement. The direction of the cortical veins of the cerebrum is determined by the growth of the cerebral hemisphere. As a result of the growth anteriorly of the frontal lobe and posteriorly of the main mass of the hemisphere, the direction of the terminal portions of the superior vessels is altered, the anterior veins being directed posteriorly and the posterior veins coursing obliquely anteriorly as they pass to the superior sagittal sinus. The posterior inclination of the inferior veins, as they pass to the transverse sinus, has a similar explanation. One of the members of the superior cortical series of veins is found in each of the precentral (referred to as vein of Trolard), central and postcentral sulci, and similarly a tributary of the superficial middle cerebral vein is found in each of the sulci which separate the opercula of the insula. The middle cerebral veins drain into cavernous sinus or sphenoparietal sinus. Of tributaries of the superficial middle cerebral vein, some pass anteriorly in the direction of the frontal pole; others pass superiorly, with varying degrees of obliquity, to supero-medial margin of the hemisphere ; while the remainder pass postero-inferiorly to the temporo-occipital region. Of the larger veins radiating from the stem of the lateral fissure the majority, if not all, terminate by passing from the surface of the cerebrum into one of the large venous sinuses—either superior sagittal or transverse. There are many variations in the number and size of cerebral convexity veins. Most often a large precentral bridging vein (Trolard) connects to the SSS and a large post-insular vein (Labbé) drains into the transverse sinus. These veins are connected in different ways to the superficial and hence deep middle cerebral veins. At birth the lacunae laterales are absent, and later appear and they grow pari passu with the arachnoid granulations after term birth. In adults past middle age the lacunae laterales are two in number—one being placed on each side of the superior sagittal sinus. The "chords of Willis " found in the superior sagittal sinus persist as evidence of its original plexiform character. The lacunae laterales serve as lateral extensions of the lumen of the superior sagittal sinus over the supero-medial margin of the cerebral hemisphere in the posterior frontal, parietal and sometimes also the anterior occipital regions, where the majority of the arachnoid granulations are found. The floor of each lacuna is everywhere carpeted by a layer of these granulations. Cerebral venous thrombosis commonly occurs in the SSS, particularly in its parietal segment. Several anatomical factors have been contributed to this prevalence. One of them is that the BVs drain into the SSS against the blood flow in the sinus, thus causing turbulence in the blood stream. This study found that nearly all the BVs (97%, 561/581) entered the parietal segment of the SSS at an angle opposed to the direction of blood flow in the sinus, with an average angle of 35°. Most importantly, the entrances of these BVs were angled in a three-dimensional way, not simply along the sagittal axis, and before entering the SSS, the veins always adhered or ran parallel to the sinus. Therefore, a shift of the brain in any direction with traction on the BVs may deform the venous wall, inducing thrombosis. Le gros Clark, WE (1920) On the Pacchionian Bodies. Journ. Anat. 55, 40. 0'Connell JEA (1934) Some observations on the cerebral veins. Brain 57:484-503. Sargent P (1911) Some Points on the Anatomy of the Intracranial Sinuses. Journ. Anat. and Physiol. 46, 69. Schwartz P : Geburtsschaden bei Neugeborenen, Gustav Fisher Verlag, Jena, 1964 Streeter L (1918) The Development of the Venous Sinuses of the Dura Mater in the Human Embryo. Amer. Journ. Anat 18, 145-178. T cerebral pial veins bridging to the SSS posterior basal veins and haematomas central tentorial convexity brain haemorrhage MRI became crucial to diagnose these lesions. All types of haemorrhage may be identified with CUS but this is difficult due to their eccentric location, under bone and on the edge of the sector. A basal subdural haematoma may look like a lobar temporal haemorrhage and it may be confused with a subarachnoid haematoma. High frequency scanning can reveal a subdural clot under the superior sagittal sinus. Quite often there is subarachnoid CSF retention under a subdural haematoma producing a neat picture of the arachnoid membrane between collections of different echogenicity. Fresh subdural haemorrhage may initially remain hypodense before fibrin formation (as during heparinization for extracorporeal membrane oxygenation). It is impossible to differentiate with US between minor subdural bleeding and contusion of parenchyma under bony margins moved during excessive moulding, unless one insonates directly on the lesion from a lateral fonticulus. For posterior fossa haematoma scanning is most informative over the mastoid fontanel; for occipital subudral haematoma over the posterior fontanel. It may still be indicated to document overlying bone lesions with CT scan when trauma is supected. subdural haematoma: general aspects in imaging coronal CT scan with pericerebellar haematoma due to tentorial tear (vacuum extraction) A subdural haemorrhage above the tentorium may be associated with a central tentorial tear, even though the epicentre of bleeding will in reality be situated in the ambient and quadrigeminal cisterns and above and around the cerebellum. Genuine convexity subdural haematoma starts from a torn bridging vein near the superior sagittal sinus or from an anastomosing vein along the parietal hemispheric convexity: in this case the bulk of clot is located above the insula, often centred around the superior sagittal sinus. A tear in the non-central part of the tentorium or a rupture of an anchor vein of the transverse sinus will produce accumulation of blood under and along the temporal lobe, often with posterior interhemispheric extension: this is called basal subdural haematoma, the location of which is beneath the insula. Such subdural haemorrhage is nearly always the consequence of birth trauma, although vascular anomalies and coagulation disturbances must be excluded. Subdural haemorrhage may also follow rupture of an anchor vein for instance following abundant drainage for treatment of hydrocephalus. axial CT: subgaleal haematoma, subdural haematoma along the falx (arrowheads), fissured bones (arrow)(difficult vacuum extraction with rupture of the superior sagittal sinus) central tentorial tear with peri- and subtentorial subdural haematoma (T1 MR) limited basal subdural and temporal haematoma (vacuum extraction)(T1 MR) red surfaces link to examples navigator for examples of subdural haematoma Central tentorial damage (from Govaert 1993) Synonyms : tentorial laceration or tear, falco-tentorial injury. Anatomical description : This chapter covers traumatic lesions associated with overstretching and tearing of the central tentorial fibers, mainly the 'vertical stress band' as described by Holland in 1937, sometimes associated with falx injury in the vicinity of the inferior sagittal sinus. The tentorium can be torn across its full thickness, when the free anterior margin is almost invariably involved, or have partial superficial tears (fraying) (Pape and Wigglesworth 1979). If (i) the line of injury crosses a major vein, such as the straight sinus, vein of Galen or in rare cases the transverse sinus or if (ii) even in the absence of a true tentorial laceration, a persistent tentorial sinus (or one of its tributaries) is damaged, acute and massive peritentorial bleeding will often lead to early death both from hypovolaemic shock and hypertension within the posterior fossa (Craig 1938, Pape and Wigglesworth 1979). The site of blood collection is within the middle cranial fossa (BaSDH) (Gröntoft 1953), between the bases of the cerebral hemispheres (BaIHSDH) and high up in the posterior fossa (SuPFSDH). If only minor vessels (bridging veins to cerebellum and brainstem or small tentorial veins) are involved, haemorrhage can be minimal and not fatal, with symptoms not starting before the second half of the first day (subacute presentation). Full thickness tears sometimes lack haemorrhage, suggesting that rupturing of bridging veins in the neighbourhood must cary more clinical weight, although the injured tentorium serves as one of the hallmarks of mechanical trauma. Onset of hydrocephaly beyond the first week following posterior fossa or peritentorial haematoma constitutes the chronic presentation, sometimes delayed into the second month of life (French and Dublin 1979). The alledged possibility of tentorial arterial damage is not documented in neonates (Welch and Strand 1986). Unilateral tears are more common if they come about after intrauterine death (Gröntoft 1953), but may also relate to oblique distortion of the skull as for instance by improper application of forceps blades (Pape and Wigglesworth 1979). The collected work of Schwartz has demonstrated particular vulnerability of the transition zone between straight sinus and great cerebral vein to displacement of the falco-tentorial junction, leaving the vein of Galen kinked, distended, often thrombosed and sometimes ruptured (Schwartz 1964). Rarity of the latter findings in present perinatal autopsies is partially explained by reduction of the duration of labour in the past decades. The association between occipital osteodiastasis and tentorial changes is detailed elsewhere. Incidence : There is doubt whether the incidence of severe tentorial damage has fallen in the latter part of this century. Already in the interwar period Sulamaa and Vara 1952 reported only 11 tentorial tears discovered at necropsy in 602 autopsies from 38,826 term deliveries (0.3 per thousand), with a 25-fold increase in forceps extracted deceased infants. The incidence of cranial birth trauma, most of it probably involving tentorial damage, was 3.1 per thousand births in the British Perinatal Mortality survey of 1958 (Butler and Bonham 1963). The lowest rate was recorded in term early neonatal death (about one per thousand) and the highest ones were found in preterm perinatal death (about 10 per thousand) and early neonatal death of children with gestational ages above 43 weeks (40 per thousand). Barson, describing the period 1976-1981 in an English population, recorded 0.96 tentorial tears in 1000 deliveries of all gestational ages (Barson 1983). He documented as much as 10 per cent of tentorial trauma in perinatal deaths with gestational age below 29 weeks. At Gent University Hospital we estimated an incidence of in vivo recognized tentorial damage in 0.8 per thousand liveborn infants weighing at least 1000 grams at birth. Most of these data can in fact not really be compared because the reporting centres differ in selection of referred cases, because the incidence of tentorial damage in survivors was never recorded before the advent of modern imaging and even with it some lesions will go unnoticed In addition most authors refer to tentorial damage as a percentage of their perinatal autopsy material which is useless for comparison between different centres. Personal observations over the last few years suggest that for one tentorial injury discovered at post-mortem examination, there are at least two survivors with in vivo suspected tentorial injury. That would hint to an incidence of between two and three major tentorial lesions per thousand live births, possibly increasing up to one per cent in instrumental deliveries. These data should of course be confirmed by prospective study. In a recent prospective magnetic resonance study of neonatal intracranial pathology no attempt was made to deduce the actual incidence of tentorial damage (Keeney et al. 1991). Pathogenesis : Most pathophysiological considerations, if not all, have been founded on postmortem experience. In summary, several authors around the turn of the century, like Beneke in 1910 and Holland later on, popularized the concept of tentorial stress during delivery. Holland pointed out the vulnerability of the vertical central tentorial fibers (Beneke's Tentorium-strahlung der falx). Overstretching of these dural structures is inherent to (i) excessive calvarial moulding, be it because of bitemporal (Beneke) or occipito-frontal (Holland) compression, with subsequent rostral lift of the falco-tentorial junction or (ii) due to impression of the occipital bone as in difficult breech delivery or improper application of forceps blades (Wigglesworth and Husemeyer 1977). As pointed out by many authors, the obstetrical context is either that of a stormy or prolonged spontaneous vaginal delivery (Beneke 1910), of a difficult midpelvic or high cavity instrumental (Holland 1937, Craig 1938, Kehrer 1939, Sulamaa and Vara 1956, Chiswick and James 1979) or of an assisted breech delivery (Hemsath 1934, Holland 1937, Tank et al. 1971), the latter especially if associated with forceps extraction of the trapped aftercoming head. Caesarean section before the onset of labour can complete this list as an exceptional circumstance leading to tentorial injury. The general idea is that excessive skull traction results in proportionately excessive skull compression (see chapter on calvarial bone displacement). In a review of in vivo diagnosed or suspected tentorial damage we definitely recorded vacuum extraction as a possible cause of tentorial damage in those countries where this method of delivery is popular (Japan, Russia, Belgium, Scandinavian countries...) (Govaert et al. 1990). The alledged originality of a contemporary report (Hanigan et al. 1990), stating that vacuum delivery causes tentorial damage by direct traction on the falx, is misplaced in two ways : it does not substantiate the concept of direct ventouse influence on deeper cranial structures and omits references to several necropsy studies where the relation between vacuum delivery and tentorial injury had already been clearly established (Aguero and Alvarez 1962). At least one report we could trace, by Saunders in 1948, superficially seems to support this idea of direct stress because galeal traction over the anterior fontanelle in deceased neonates was clearly shown to lift and stretch the falco-tentorial junction in the direction of the traction applied ('galea forceps'); it cannot be excluded that galeal traction increased the general skull compression and thus produced this sequence of events. Clinical setting : The presenting signs and symptoms of 15 personal observations and 63 in vivo suspected central tentorial tears gathered from the literature, have been reviewed in an attempt to propose management guidelines (Govaert et al. 1990). The features described are essentially those of posterior fossa subdural haemorrhage. Two recent reports increase to 90 the total number of clinically detailed peritentorial bleedings we evaluated (Hanigan et al. 1962, Huang and Shen 1991). As described in the definition, the arbitrary cut-off between acute and subacute presentation lies at 12 hours after birth. Tables I and II show the presenting neurological syndrome as well as outcome in relation to mode of presentation and undertaking or not of suboccipital craniotomy. Comparison between presentation and outcome illustrates the somewhat artificial nature of this separation between acute and subacute presentations. The obstetric history preceding each type is similar, as are the incidences of seizures and hydrocephalus. Probable indicators of severity are intracranial hypertension with apnoea and/or abnormal breathing patterns such as sighing and gasping, resulting in a higher need of endotracheal support. Cranial nerve palsies, of facial and eye musculature, seem to be more common in acutely presenting tentorial damage (Dubose Ravenel 1979, Baleriaux et al. 1980, Serfontein et al. 1980, Hernansanz et al. 1984). Lumbar puncture theoretically endangers the newborn by enhancing the risk of cerebellar coning in cases of outspoken hypertension within the posterior fossa (Dubose Ravenel 1979). We conclude that, apart from opisthotonus and Battle's sign (Young and Zalneraitis 1980), fixed bradycardia and sighing might be somewhat indicative of severe posterior fossa haemorrhage. Neither seizures nor intracranial hypertension are obligatory. Pulmonary haemorrhage was recorded as an agonal event in lethal tentorial injury (Blank et al. 1978). Radiological assessment : Several recent reports corrected the lack of in vivo descriptions of tentorial damage by means of ultrasound, CT scan and NMR imaging (Scotti et al. 1981, Govaert et al. 1990, Keeney et al. 1991, Huang and Shen 1991). Skull X-rays may show occipital osteodiastasis, suture diastasis around the occipital bone (see chapter on moulding) or bone fractures. Ultrasound is a very reliable screening method for detection of severe falco-tentorial bleeding (Bejar et al. 1985), but lacks precision in delineating lesions in the posterior fossa and interhemispheric fissure. Axial incidence and scanning through the posterior fontanelle can add up the diagnostic yield (Govaert et al. 1992). The lesion to be sought for is an additional density riding on the superior part of the cerebellar vermis behind the brainstem and filling the cisterna ambiens. Very few reports link CT findings with postmortem observations (Govaert et al. 1990, Blank et al. 1978, Menezes et al. 1983). Our personal review and the one by Huang independently came up with remarkably similar conclusions. On CT scan tentorial damage is very likely in the presence of : (i) a pericerebellar and sometimes parenchymal haemorrhagic density; (ii) marked haemorrhages on sections through the tentorial apex, around the straight sinus and behind the third ventricle, coalescing to form a somewhat triangular density with its basis against the occipital bone; (iii) a bleeding in between the posterior cerebral hemispheres (BaIHSDH). Coronal images, either direct or by reconstruction, are most helpful to understand the regional distribution of blood (Serfontein et al. 1980, Scotti et al. 1981, Rolland et al. 1982, Menezes et al. 1983, Koch et al. 1985, Coker et al. 1987, Govaert et al. 1990). NMR scan, it is suggested, is even superior in delineating the precise anatomical locations of haemorrhage, in demonstrating associated parenchymal damage due to asphyxia or vascular lesions and in documenting superior sagittal sinus thrombosis (Hanigan et al. 1990, Keeney et al. 1991). Especially minor bleedings that will otherwise be missed are likely to be diagnosed by magnetic resonance imaging, even up to several weeks after the acute event. Our personal experience is limited because the latter method either requires adequate sedation of the infant with its accompanying problems, or the availibility of skilled staff with plenty of time just to sooth a restless newborn. Although the result is clearly superior and the radiation danger absent, it needs further study to show how much will be missed by careful US scanning and one early (in the first three days of life) CT scan. Management and prognosis : controversy has dominated the literature on this aspect, encouraging us to sort out the actual state of the art having had recent experience with succesful surgical and conservative treatment (Govaert et al. 1990). 1) Neurosurgical intervention has an invaluable place in some patients because it can correct intracranial hypertension instantly (Gilles and Shillito 1970, Carter and Pittman 1971, Menezes et al. 1983). The only obvious indication is either acute hydrocephalus because of obliteration of the CSF pathways in the posterior fossa or life-threatening brainstem compression with apnoea and/or fixed bradycardia and/or systemic hypertension and/or lost oculocephalic reflexes. If indeed one prefers a neurosurgical approach the only safe way is to perform suboccipital craniotomy before ventricular drainage, because primary shunting of the supratentorial ventricles may result in acute upward herniation of the cerebellum and brainstem. Care must be taken not to injure the transverse sinus in the process of removing the postcerebellar clots and not to cause additional damage to the cerebellar hemispheres (Tanaka et al. 1988). The goal seems to be correction of intracranial hypertension and not removal of all posterior fossa coagula. After a couple of days the collection, its volume ranging from 10 to 75 ml, is partially liquefied to become a genuine hygroma in the chronic stage. 2) Both conservative and neurosurgical treatment permit neurologically intact survival in about 50 per cent of the infants, most with comparable bleeding size (Fishman et al. 1981, Gouyon et al. 1981). 3) Craniotomy does not prevent late-onset 'resorptive' hydrocephalus (Govaert et al. 1990). As outlined by Tanaka, there is a biphasic ventricular dilatation after severe posterior fossa haemorrhage with an acute phase due to obstruction of CSF pathways by compression and a chronic phase due to deficient absorption or circulation of CSF. The latter is related to the amount of associated subarachnoid haemorrhage or caused by recurrent bleeding into an hygromatous collection (French and Dublin 1971, Tanaka et al. 1988). Even in late-onset hydrocephalus at the age of six months, after demonstration of the communicating nature of the ventricular dilatation e.g. by isotope cisternography, conservative treatment with serial lumbar punctures and drugs that inhibit CSF production can be succesful (Koch et al. 1985, Von Gontard et al. 1988, Govaert et al. 1990). Immediate postsurgical problems to meet with can be a CSF fistula or a pseudomeningocoele (Dubose Ravenel 1979), both necessitating reintervention in some infants. On follow-up, in addition to post-haemorrhagic hydrocephalus, one should be looking for the development of cysts in and around the cerebellum (Koch et al. 1985, Huang and Shen 1991), posterior fossa subdural hygroma (French and Dublin 1971, Govaert et al. 1990, Huang and Shen 1991) (Figure 8) and cystic dilatation of the retrocerebellar subarachnoid space (Adam and Greenberg 1978, Dorsic et al. 1983, Govaert et al. 1990). The relevance of these findings is poorly understood. Even following huge peritentorial haemorrhage, the only sequels can be delayed gross motor development in infancy or residual nystagmus, with intact mental and ulterior motor development as illustrated by two personal observations, details of which were published elsewhere. These concentrated versions highlight the power both of 'expectatio armata' and emergency neurosurgical intervention. Table I Neurological signs in 90 neonatal posterior fossa subdural bleedings (percentages between brackets) General Focalizing tense fontanelle 53 (59) apnoea 28 (31) hypotonia 32 (36) irregular breathing 27 (30) seizures 32 (36) (gasping, sighing) lethargy, depressed opisthotonus 12 (13) archaic reflexes 29 (32) skew eye deviation 11 (12) vomiting 15 (17) facial palsy 10 (11) irritability 13 (14) abducens palsy 4 ( 4) weak cry 11 (12) anisocoria 4 ( 4) high cry 11 (12) Battle's sign 3 ( 3) hypertonia 9 (10) oculomotor palsy 1 ( 1) Table II Neonatal posterior fossa subdural bleeding outcome versus presentation and management Craniotomy (N = 44) No Craniotomy (N = 46) Presentation Acute Subacute Acute Subacute (N = 15) (N = 29) (N = 19) (N = 27) Birth asphyxia 0 2 7 3 Symptoms . apnoea 5 6 11 6 . tense fontanelle 14 18 13 8 . seizures 4 7 10 11 . irregular breathing 8 7 6 5 . fixed bradycardia 4 3 3 4 . skew eye deviation 5 1 2 2 . cranial nerve palsy 5 4 5 1 Hydrocephalus . requiring shunt 5 9 3 2 . treated conservatively * 0 0 0 3 Fatal outcome 0 3 9 6 Normal survival 10 12 8 13 * with serial lumbar punctures and acetazolamide < tentorial tears Hydrocephalus due to tentorial injury At least two stages of hydrocephalus are known following severe tentorial trauma. In the first days after birth clots may obstruct CSF flow: the obstructive stage, often clearly seen under the transverse sinus in mastoid sections. Due to a mass effect of the haemorrhage in the posterior cranial fossa, compression of the aqueduct or fourth ventricle may also occur. Later, after an interval of weeks or even months, hydrocephalus may occur due to disturbed resorption, leading to a two-staged event with a neonatal peak of ventricular dilatation and another in infancy. Mechanisms here are residual obstruction of the CSF circulation in the peritentorial arachnoid spaces and occlusion of the villi in the arachnoid granulations. During recovery some babies go through a temporary stage of hygroma in the posterior fossa. The pericerebellar spaces are so dilated that the vermis ‘floats’ in CSF with possible clot remnants in the cisterna magna. This may later lead to arachnoid cyst formation in the posterior fossa or quadrigeminal cistern. Two clinical and echographic entities exist with posterior fossa subdural haematoma duie to birth trauma. The most frequent and well-known entity is traumatic birth with sufficient compression of the cranium to cause a partial or complete tear of the free tentorial margin. The site of least resistance is located next to the insertion of the straight sinus and its transition towards the great cerebral vein. Haemorrhage around the laceration will extend from the quadrigeminal cistern to the interhemispheric fissure above and behind the corpus callosum, in the transverse fissure under the corpus callosum, in the space above the cerebellar vermis and above the tentorium itself, and under and between the occipital lobes. In our experience those lesions are almost always related to difficult instrumental traction or breech delivery. Alternatively, excessive pressure on the base of the occipital bone, whether manual or instrumental, may displace it inwards towards the posterior fossa, at the fibrous junction between its squamous and lateral portions, a phenomenon called occipital osteodiastasis. Ultrasound aspectsThe centrotentorial tear cannot be directly identified echographically. However, a perilesional haemorrhage of sufficient size will show up in coronal section as a density between the echoic strips of choroid plexus. Sagittal sections in particular allow diagnosis of a tentorial tear if, after ‘difficult’ birth, a density is found behind the usual retrotectal white echo-line of the quadrigeminal cistern. The latter forms a bridge between vermal reflections and the tela choroidea of the third ventricle. The centrotentorial clot rests on the cerebellar vermis and appears to penetrate into cerebellar substance. The clot may have irregular margins because it penetrates into cisterns and fissures. Axial sections through a sphenoidal fontanelle may confirm this assumption provided dense reflections are found behind the cerebral peduncles and subdural blood is seen in the vicinity of the transverse sinus. Even partial tears with limited perilesional haemorrhage (fraying) may be identified echographically as an asymmetric linear peritentorial echodensity on coronal sections. Mastoid views can show the presence of extra-parenchymal material (clot in different stages of organisation) around the cerebellum near the transverse and sigmoid sinus. Mac OS X 2ÖATTRÜ,Ücom.apple.TextEncodingëcom.apple.provenanceöcom.apple.quarantineutf-8;134217984Â.Im0ÖWq/0081;00000000;;

Cerebrus