:Acta . lXTeuroch rurgica

Acta Neurochir (Wien) (1990) 106:52-64

9 by Springer-Verlag1990

On the Management of Neonatal Tentorial Damage. Eight Case Reports and a Review of the Literature P. Govaert*, L. Calliauw**, P. Vanhaesebrouek*, F. Martens**, and A. Barrilari*** * Department of Paediatrics, Neonatal Intensive Care Unit, ** Department of Neurosurgery, Ghent University Hospital, and *** Department of Paediatrics, AZ Maria Middelares, Ghent, Belgium

Summary

cations or of the great cerebral vein of G a l e n 8. Both

From the history of 15 personal patients-8 reported here in extenso- and from 63 patients in the literature with the diagnosis of posterior fossa subdural haemorrhage during life, we discuss the possibility of detecting tentorial damage on computed tomography (CT) and ultrasound (US) scan. The association of a (peri)cerebellar haemorrhage with peritentorial bleeding around the straight sinus and a subdural haemorrhage between both occipital cerebral lobes is suggestive of tentorial laceration(s). Both coronal CT scan and sagittal US scan are very helpful in locating these haemorrhages near the falco-tentorial junction. The conservative management of one of our infants with very extensive but asymmetric posterior fossa haemorrhage, leading to resorptive hydrocephalus, is compared with both surgical and conservative treatment of patients from the literature. Two reasons that warrant neurosurgical intervention are: life-threatening brain-stem compression- as in one of our own patients - and acute obstructive hydrocephalus. Craniotomy of the posterior fossa within the neonatal period does not prevent later-onset resorptive hydrocephalus. The communicating nature of this latter process is adequately demonstrated by lumbar isotope cisternography. Finally, neonatal posterior fossa subdural haemorrhage is one of the many causes of cyst-likestructures behind the cerebellum.

types present acutely, within a few hours o f birth. Subacute p r e s e n t a t i o n o f P F S D H after the first 12 hours of life, the third type, is typical for injuries of cerebellar

Keywords: Tentorium; newborn; subdural haemorrhage; hydrocephalus; vacuum extraction.

bridging veins or of the tentorial leaflets, w i t h o u t damage to m a j o r vessels 4. I f u n r e c o g n i z e d or a s y m p t o m a t i c , the latter m a y present in the late n e o n a t a l or infantile period as h y d r o c e p h a l u s due to retrocerebellar h y g r o m a 2, 12 It is the p u r p o s e of this report to describe 4 n e w b o r n s with a u t o p s y - c o n f i r m e d tentorial lesions where C T a n d / o r US scan of the b r a i n were available. F r o m these a n d some data from the literature we will try to propose guidelines for in vivo diagnosis o f n e o n a t a l tentorial damage, as m a d e clear with the example of four surviving infants. F r o m our o w n experience with two of the survivors (patients 5 a n d 8) a n d a review of 63 patients from the literature, we c o m m e n t o n ,,how to manage" neonatal PFSDH.

Case Reports Patient 1 (L. T., inborn) (83/2112) (Figs. 1 and 2)

Introduction T e n t o r i a l d a m a g e is often associated with primary

neonatal

posterior

fossa

subdural

haemorrhage

( P F S D H ) , a rare v a r i a n t of n e w b o r n i n t r a c r a n i a l bleeding, the m a j o r cause of which r e m a i n s a difficult deliveryl0, 17, 18, 22, 30, 31. Three m a i n types o f P F S D H exist. The first, occipital osteodiastasis, is due to disp l a c e m e n t o f the occipital s q u a m a towards the brainstem as a c o n s e q u e n c e of difficult d e v e l o p m e n t of the aftercoming head in breech delivery 16. The second is due to r u p t u r e o f a m a j o r sinus within d u r a l redupli-

This girl, third child in her family, is delivered at term. The first stage of delivery takes 10 hours. After 40 minutes the second stage is ended with 10 difficult vacuum extractions starting at 2 cm above Hodge's interspinal plane. Three cup detachments and an abraded skin at the vertex confirm the difficulty of the extraction. She weighs 3,510g, her length and head circumferenceat birth are 52 and 36cm respectively. The Apgar scores are 3 and 5 at 1 and 5 minutes. Her umbilical artery pH is 7.24. After a short bag and mask resuscitation she is admitted to the intensive care unit. Hypotonia, somnolence, grunting, paleness and a tense fontanelle are the main signs and symptoms initially. Two hours later she is resuscitated after a cardiorespiratory arrest. In the followinghour she deteriorates and dies in shock, metabolic acidosis and bilateral mydriasis. Immediate J(-

P. Govaert et al.: On the Management of Neonatal Tentorial Damage

Fig. 1. (Patient 1): uncontrasted CT scan in patient 1 (immediatel 5 after death, day 1): subdural bleeding around both cerebellar hemispheres, diastatic lambdoid suture on the left, severe extraosseous bleeding

rays o f the skull reveal elevated parietal bones with fragmentation of the medial margins. A post-mortem C T scan confirms the clinical diagnosis of extensive intracranial bleeding (Fig. 1). Post-mortem findings include: subgaleal bleeding, bilateral tentorial tear (Fig. 2), posterior fossa subdural bleeding, supratentorial subarachnoid haemorrhage and rupture of the great vein of Galen. Conclusion: Bilateral tentorial damage and subgaleal Needing due to difficult vacuum extraction; acute PFSDH because of a ruptured vein of Galen.

Patient 2 (F. H.-J., outborn) (85/2540) (Fig. 3)

This boy, second child, is delivered at 31 weeks of gestation. An urgent vacuum extraction is undertaken because of abruptio pla-

53

Fig. 3. (Patient 2): uncontrasted CT scan in patient 2 (day 2): convexity subdural bleeding on the right, bilateral bleeding along the tentorium behind the cerebral peduncles

centae. His presentation is occiput posterior and the extraction starts at 1 cm above Hodge's interspinal plane. The second stage takes 45 minutes. He weighs 1,960 g, his length and head circumference at birth are 42 and 31 cm respectively. He is resuscitated with bag and mask because of Apgar scores of 3 and 4 at 1 and 5 minutes. Two hours later he is found to be apnoeic, atonic and hypothermic. After endotracheal resuscitation he is transferred to our neonatal intensive care unit. Meanwhile generalized tonic seizures and a tense fontanelle have complicated the clinical picture. Upon admission he is not reactive to pain. Even when adequately ventilated he suffers from bouts of bradycardia. Nystagmoid eye movements are present. The US scan of the brain reveals bilateral intraventricular haemorrhages. C T scan on the second day of life (Fig. 3) further demonstrates severe subdural bleedings both above and underneath the

Fig. 2. (Patient 2): right tentorial leaflet is torn from incisura to adhesion on the occipital bone (arrow), several haemorrhages within the falx cerebri

54

P. Govaert et al. : On the Management of Neonatal Tentorial Damage

Fig. 4. (Patient 3): US scan (7,5 MHz) in patient 3 (day 1): a) Sagittal plane: dense reflections above the superior cerebellar vermis in the vicinity of the great cerebral vein. (CC corpus callosum, P V 3 plexus ventriculi tertii, V4 ventriculus quartus, VC vermis cerebelli), b) Coronal plane (posterior fontanelle): circumscribed densities behind the mesencephalon. (MES mensecephalon, GL V glomus of the lateral ventricle)

tentorium as well as mild dilatation of the lateral and third ventricles. These findings and the background of severe asphyxia before referral lead to discontinue intensive care. Post-mortem findings include: a bleeding tentorial tear on the left and a haemorrhage within the unruptured right tentorium; subdural bleeding along the right cerebral convexity, at the base of both cerebrum and cerebellum; extensive intraventricular haemorrhages. Conclusion: acute PFSDH and convexity subdural haemorrhage due to tentorial damage after urgent vacuum extraction of a preterm infant.

Patient 3 (S. P., inborn) (88/5156) (Fig. 4) This boy is the second of male twins born to a nulliparous mother after a pregnancy of 28 weeks. Premature rupture of the membranes and tocolytic failure are the compounding features. The second stage of his delivery takes 13 minutes. He presents in full breech and is delivered with the Mauriceau-manceuvre and forceps extraction of the aftercoming head. At birth, face and members are extensively ecchymotic. Despite an umbilical artery pH of 7.35, he is resuscitated with endotracheal ventilation from birth because of Apgar scores of

P. Govaert et al.: On the Management of Neonatal Tentorial Damage

55

Fig. 6. (Patient 4): uncontrasted CT scan in patient 4 (day 2) (coronal plane): thickened tentorial leaflets near the junction with the falx; pericerebellar haemorrhage Fig. 5. (Patient 4): X-ray of the skull in patient 4 (day 1): anterior displacement of the occipital squama towards the brain-stem

2 and 5 at 1 and 5 minutes. His birth weight is 1,220 g, length and head circumference are 41 and 27 cm respectively. A tense fontanelle, hepatomegaly, tonic seizures and hypovolaemic shock are apparent in the delivery room. He is hypotonic and lethargic. Within a few hours he becomes bradycardic even under adequate ventilation and dies in shock soon thereafter. US scan of the brain before death is suggestive ofa haemorrhage in the triangle between tentorium, brainstem and pineal region (Fig. 4 a, b). Post-mortem examination confirms the suspected tentorial tear near the falco-tentorial junction and demonstrates a large subdural haemorrhage in the posterior fossa and a tear in the inferior sagittal sinus. Conclusion: acute PFSDH in a very preterm boy with tentorial damage at the falco-tentorial junction after difficult forceps extraction of the aftereoming head in a breech delivery.

Patient 4 (D. G. D., outborn) (90/559) (Figs. 5 and 6) This boy, second child, is delivered at 37 weeks of gestation with difficult breech extraction. Spontaneous passage of the breech itself is uncomplicated but then the cervical opening closes down around the neck. Attempts to deliver the aftercoming head with forceps and fundal pressure fail several times. Ultimately the cervix unlocks spontaneously. His Apgar scores are 1 at 1 and 5 minutes. Birthweight is 2,700 g, head circumference 33 cm. After endotracheal resuscitation he remains ventilated because of associated pulmonary hypertension. When hypotension and oliguria complicate the picture he is transferred to our department at the age of 18 hours. He is hypotonic and acidotic. Spontaneous motor activity is absent. The fontanelle is not tense. Pupillary reaction to light is very sluggish but present. Primitive reflexes are abolished. Pain reactions are poor except for painful grimacing upon movement of the head. The occipital bone is depressed underneath the parietal bones. Seizures are not observed. The pulse rate varies around 60 bpm. After initial stabilization with

expanders, vasopressors and hyperventilation there is an abrupt shock-phase in the beginning of the second day of life. Associated anaemia and abdominal distension suggest a haemoperitoneum. Ultrasound discloses bleeding around the liver and spleen besides a peritentorial haemorrhage on sagittal brain scan. The impossibility of stabilizing the blood pressure necessitates surgical exploration. Upon abdominal incision massive bleeding from the decapsulated right liver leads to exsanguination despite transfusion of 600 ml of blood over 45 minutes. Post-mortem X-rays of the skull document the suspected occipital osteodiastasis (Fig. 5) and a clavicular fracture on the left. CT scan immediately after death confirms a supra- and infratentorial haemorrhage with irregular thickening of both tentorial leaflets near their junction with the falx (Fig. 6). Post-mortem examination documents subdural haemorrhages around the cerebellar hemispheres, impression of the occipital bone and bilateral tentorial tears near the incisura. Apart from extensive liver damage, bilateral adrenal haemorrhages are present. Conclusion: occipital osteodiastasis, acute PFSDH and fatal liver damage during difficult delivery of the aftercoming head in a breech presentation.

Patient 5 (D. M. J., outborn) (89/875) (Figs. 7-9) This boy is the second child in his family after an uneventful pregnancy. Labor starts spontaneously at term. In spite of augmentation of labour with oxytocin, the second stage lasts 100 minutes and delivery is performed under epidural analgaesia with at least six difficult vacuum extractions complicated by one cup detachment, Apgar scores are 2 and 5 at 1 and 5 minutes. Birth weight is 3,700 grams, length 54cm. Resuscitation with bag and mask permits a satisfactory recovery. The next morning, 16 hours after birth, he is found to have multifocal clonic seizures and appears to be very pale, hypotonic and feverish (38,3 °C). Lumbar CSF is bloody and does not coagulate. Ultrasound scan of the brain demonstrates ventricular dilatation. After the administration of packed cells and anticonvulsants (phenobarbital and diazepam) he is referred to our department,

56

P. Govaert et al.: On the Management of Neonatal Tentorial Damage

Fig. 7. (Patient 5): uncontrasted CT scan in patient 5 (day 2): a) Subdural bleeding around the cerebellum, especially on the right, b) Massive haemorrhage covering the right tentorial leaflet and a smaller one on the left, moderately enlarged supratentorial ventricles with anteriorly displaced occipital horns, c) Broad subdural bleeding in the posterior interhemispheric fissure behind the third ventricle along the straight sinus, d) Reconstructed coronal image: massive bleeding above the right cerebellum from falco-tentorial junction to occipital bone

mostly because his muscle tone does not recover and apnoeas complicate the picture. Upon admission 18 hours after birth, his head circumference is 37,5 cm. He is atonic and minimal withdrawal reactions follow painful stimuli. Apart from sporadic bicycling movements, there is no spontaneous motor activity. A large caput succedaneum covers the left occipital and parietal region. The fontanelle is soft. His face is without mimicry but oculocephalic reflexes are present. From their near mydriatic position at rest the pupils react to light. On day three a transient anisocoria is noted. Corneal reflexes are absent. Occasionally the eyes deviate in an erratic manner. Both primitive (archaic) and tendon reflexes are absent. In the first hours after admission a few central apnoeic attacks are noted. Very striking are episodes of deep gasping. The pulse rate varies from 80 to 110 bpm. His blood pressure remains normal. The head circumference does not increase. Blood examinations reveal anaemia, hyponatraemia, hypocalcaemia and discrete evidence of disseminated intravascular coagulation. Both eye grounds are covered with retinal haemorrhages. Ultrasound scan of the brain suggests bleeding on the side of the cerebral peduncles and blood is clearly seen in the cistern of the great cerebral vein between the vermis cerebelli and the pineal gland, dilatation of lateral and third ventricles is present. Evident diastasis is seen on X-rays between the occipital and parietal bones. On C T scan several bleedings are recognized: extra-osseous above the occipital bone, subdural around both cerebellar hemispheres, subdural especially overlying the right tentorial leaf, subdural between the posterior parts of both cerebral hemispheres (Fig. 7). The ventricles are mildly enlarged (Evans' Index 0.29). His bradycardia is sinusal with normal PQ and QTc intervals. An EEG is disturbed

because of diffuse ,,epileptic" activities (2-3 Hz delta waves). A tentative diagnosis of supra- and infratentorial subdural haemorrhages due to tearing of at least the right tentoriaI leaflet is made. The boy remains atonic and motionless but the apnoeic attacks subside spontaneously. Some tonus reappears in aii extremities on the fourth day and a weak grasp reflex seems to come back in both hands. Gradually

Fig. 8. (Patient 5): uncontrasted CT scan in patient 5 (day 18): retrocerebellar hygroma

P. Govaert et al. : On the Management of Neonatal Tentorial Damage

Fig. 9. (Patient 5): unconstrated CT scan in patient 5 (day !40): large cyst-like hypodense fluid collection behind the vermis cerebelli

mobilization results in grunting and painful grimaces. Seizures are not seen beyond the fourth day of life. The sucking reflex is faintly present on day 5. Shivering movements of head and arms are the first spontaneous motor activities. Oral feeding is begun on day 6 and parenteral nutrition is stopped after two weeks. Meanwhile transient fullness of the anterior fontanelle, together with ventricular dilatation, is present between days 6 and 10 but regresses spontaneously. A repeat C T scan on day 18 reveals a hypodense retrocerebellar fluid collection with a thickness of 2 cm between vermis and occipital bone (Fig. 8). Before discharge on day 25 a control EEG is found to be normal as is a brain-stem-evoked-responseaudiometric evaluation. A second episode of ventricular enlargement is documented on US scan at the end of the first month, once again joined with a tense anterior and posterior fontanelle and intermittent sunsetting. Prominent occipital venous networks surround the posterior fontanelle. Once more this hydrocephalus regresses spontaneously around day 40. Head circumference follows the 90th centile, length the 75th and weight the 50th. At 3 months of age development is normal except for some head lag. After an uneventful period of combined follow-up with the referring paediatrician, a third phase of ventricular dilatation and macrocephaly becomes evident about 140 days from birth. At that moment his head circumference is 49,2 cm and the fontanelle is tense and enlarged. His eyes have the sunset sign and there is a bilateral rotatory nystagmus. Despite intracraniaI hypertension there are no feeding problems and psychomotor development is normal except for axial hypotonia. Ultrasound documents evident dilatation of the supratentorial ventricles but a small sino-cortical width (no enlargement of fronto-parietal subarachnoid spaces). C T scan merely confirms these findings and shows evident patency of the fourth ventricle; a triangular hypodense CSF collection lies behind the cerebellar vermis, with an anteroposterior width of about 5 cm (Fig. 9). Isotope cisternography with indium DTPA, after lumbar injection, documents maximal ventricle reflux and absence of normal pericerebral CSF ascent, thus confirming the patency of the pathways between the lumbar subarachnoid space and the fourth and other ventricles. Lumbar CSF contains 310 mg/dl of protein. Between day 140 and day 180 a total of 23 lumbar punctures permit the evacuation

57

Fig. 10. (Patient 6): unconstrated CT scan in patient 6 (day 3): discrete bleeding along the right cerebellar hemisphere, evident extracerebral bleeding covering the posterior tentorium especially on the left

of 450 ml of fluid. From day 140 to 174 he receives oral acetazolamide (100mg/kg daily) and furosemide (I mg/kg daily). From day 175 to 240 the acetazolamide is continued alone. A control cisternogram during the final lumbar puncture documents persistent ventricle reflux, but some pericerebral ascent is evident at 48 hours. Meanwhile US scan demonstrates a reduction of the hydrocephalus (third ventricle width on axial scans regresses from 17 to 10mm) and at the same time the sinocortical distance increases progressively from 2 to 7 ram. Despite evident ventriculomegaly persisting at the age of 280 days, the head circumference follows the curve betweent the 90th and 97th percentile and the fontanelle is sunk shortly after the onset of serial lumbar punctures. The occiput remains larger than the frontal calvarium and the nystagmus, though less impressive, is still present at the age of 1 year. The boy sits up alone from 7,5 months post-term and has a normal mental development. Conclusion: massive subacute PFSDH with asymmetrical distribution after difficult vacuum extraction; resorptive hydrocephalus of late onset.

Patient 6 (A. S., inborn) (89/5712) (Fig. 10) This boy is the third child in his family. He is delivered at 39 weeks of gestation with very difficult vacuum extraction (6 tractions) assisted by fundal pressure. His Apgar scores are 9 at 1 and 5 minutes. He weighs 3,910g, his length and head circumference are 54 and 37,5cm. During the first two days of life he is grunting and has a poor appetite. On the third day fever, bilious vomiting and abdominal distension complicate the picture. In the presence of fluid-air levels on abdominal X-rays, in the absence of spontaneous passage of stools and because of deterioration of the general condition he is operated upon after having excluded a microcolon on gastrografin enema. Following colonic derivation his general condition stabilizes and rectal biopsies confirm the suspected diagnosis of Hirschprung's disease. Neurological signs noted in the meantime are: opisthotonus, variable hypertonia, fixed bradycardia (around 110 bpm) and skew deviation of the eyes. CTscan (Fig. 10) demonstrates a small bleeding along the right cerebeliar hemisphere and a haemorrhage near the falco-tentorial junction on the right, besides subdural bleeding overlying the tentorium above the transverse sinus. In the course of his

58

P. Govaert et al. : On the Management of Neonatal Tentorial Damage

Fig. 11. (Patient 7): US scan (7,5 MHz) in patient 7 (day 4): Coronal plane (right): parenchymal densities in both occipital periventricular regions. Parasagittal scan slightly to the left of the sagittal plane (left): large density covering the anterior tentorial part

hospitalization he remains quiet, prefers a retroflexed head position and has a large posterior fontanelle. CT and US scan of the brain are suggestive of an asymmetric retrocerebellar fluid collection and a very mild ventricular enlargement. This boy has been lost to followup. Conclusion: mild subacute PFSDH after difficult vacuum extraction.

Patient 7 (D. G., outborn) (90/282) (Figs. 11 and 12) This boy, firstborn in his family, is delivered at term after an uneventful pregnancy. Labour starts spontaneously. The first stage takes 5 hours. His presentation is occiput anterior. A vacuum extraction is started after 5 minutes into the second stage because of foetal bradycardia. The liquor is scanty and not meconium stained.

There is no objective information on foetal acid-base status or position of the head in relation to the interspinal plane at the onset of extraction. He weighs 1,970 g, his length and head circumference are 46 and 32 cm. Apgar scores are 7 and 8 at 1 and 5 minutes. Simple aspiration is sufficient to resuscitate the neonate. Fourteen hours later he is found to be pale, moaning and icteric. Upon clinical examination at referral he experiences pain if the head is moved. There is a subgaleal haemorrhage somewhat confined to occipital and nuchal regions. His cry is high pitched. There are no apnoeic attacks, the pulse rate varies between 120 and 140bpm. Moro and sucking reflrexes are present. The irides are bloodstained, the selerae icteric. The eye movements remain normal. His head circumference has increased to 33,5cm. The fontanelle is not tense and seizures have not been observed. Blood examinations document anaemia and disseminated intravascular coagulation. Skull X-rays are suggestive of suture diastasis. US scan (Fig. 11) demonstrates cerebral parenchymal densities in the occipital periventricular area on both sides and a haemorrhagic iaesion in the quadrigeminal cistern and the superior part of the cerebellar vermis. The CT scan confirms the large extracerebral bleeding both beneath, around and above the tentorium; a nodular bleeding rests in the quadrigeminal and ambient cisterns before the tentorial incisura; there is no hydrocephalus. Coronal CT scan confirms the cerebral ischaemic zone and the bleeding beneath the falco-tentorial junction (Fig. 12). Further neonatal evolution is without further clinical problems. Conclusion: subacute PFSDH with presumed damage at the falcotentorial junction after an uneventful vacuum extraction.

Patient 8 (D. M. N., outborn) (90/572) (Figs. 13-15)

Fig. 12. (Patient 7): unconstrated CT scan in patient 7 (day 7) (coronal plane): haemorrhage between vermis superior and falco-tentorial junction, hypodense (ischaemic) zone in left cerebral corticosubcortical occipital region

This firstborn girl is delivered at 38 weeks of gestation in the breech position. An easy Bracht maneeuvre is the only manipulation needed. Her Apgar scores are 5 and 9 at 1 and 5 minutes. She weighs 2,300g, her length and head circumference are 47 and 33cm respectively. Only a few hours later she is found to be pale and poorly responsive during the first feeding attempt. Her fontanelle is very tense. The pulse rate varies around 90 bpm. Irregular jerky eye move-

P. Govaert et al. : On the Management of Neonatal Tentorial Damage

59

Fig. I3. (Patient 8): US scan in patient 8 (day 1) (sagittal plane): densities between vermis superior, genu corporis callosi and mesencephalon

Fig. 14. (Patient 8): uncontrasted CT scan in patient 8 (day 1): a) huge retrocerebellar haemorrhage, very pronounced on the left, b) broad-based peritentorial haemorrhage on the left

ments are noticed, almost restricted to the vertical plane. The left pupil is slightly larger than the right and does not respond to light. Before referral the local paediatrician documents anaemia (9 g/dl) and moderate metabolic acidosis, besides hyperglycaemia. She is endotrachcally ventilated and transported with a presumed diagnosis of intracranial hypertension due to cerebral bleeding. Upon admission her tone is normal. The eyes are kept open constantly. Painful stimulation results in withdrawal of the touched member, without change in mimicry. The primitive reflexes are absent. There are no epicranial birth lesions. Obvious seizures cannot be recognized clinically, although a dystonic posturing of the left arm and clenching of the left hand are striking. U S scan of the brain is suggestive of a very large bleeding in the region between the vermis superior and midbrain (Fig. 13); the supratentorial ventricles are mildly dilated (third ventricle width 2 mm); a clear asymmetry is seen in the division of the bleeding which is mainly located on the left behind the brain stem. Emergency C T scan confirms an extensive haemorrhage above, around and beneath

the tentorium; especially on the left this bleeding creates the impression of life-threatening compression of the cerebellum and brain stem (Fig. 14). Faced with impending fatal brainstem injury and acute ventricular dilatation due to posterior fossa haemorrhage an emergency eraniotomy is performed within three hours after admission. After suboccipital incision the neurosurgeon discovers and removes around 20 ml of solid clot from the retrocerebellar space. The underlying cerebellar hemisphere is not lacerated but ischaemia due to compression is evident. Careful deeper inspection reveals a left tentorial tear near the insertion against the occipital bone. The left transverse sinus is covered with blood, but an actual laceration cannot be confirmed. The occipital bone defect is replaced with a flap of dura mater. Immediately following surgery the anterior fontanelle is sunk. During the operation the pulse rate remains steady around 95 bpm, but slowly climbs to normaI in the ensuing days. Extubation follows five days later and enteral feedings can be started at the end of the first week. A complete right facial palsy is still present at the age of 2 weeks. Conclusion: acute PFSDH due to tearing of the left tentorium after uneventful breech delivery without occipital osteodiastasis; successful emergency posterior fossa craniotomy because of intracranial hypertension.

Discussion

O v e r the p a s t ten years, the d i a g n o s i s o f P F S D H was m a d e in the cases o f 15 n e o n a t e s in o u r d e p a r t m e n t , t w o o f w h o m h a v e b e e n r e p o r t e d b e f o r e s. T h e eight cases p r e s e n t e d h e r e are p a r t i c u l a r b e c a u s e o f t e n t o r i a l d a m a g e , a u t o p s y - c o n f i r m e d in p a t i e n t s 1 to 4, p r o b a b l e f r o m U S a n d / o r C T s c a n in p a t i e n t s 5 to 8, c o n f i r m e d d u r i n g n e u r o s u r g e r y in p a t i e n t 8. F r o m a r e v i e w o f the l i t e r a t u r e we c o l l e c t e d 63 i n s t a n c e s o f n e o n a t a l P F S D H

diagnosed in vivo a' 4

7, 10 15, 17, 18, 20, 21, 23, 25 32

I n f o r m a t i o n o n c o r r e l a t i o n b e t w e e n in v i v o f i n d i n g s a n d a u t o p s y - c o n f i r m e d t e n t o r i a l lesions is scarce.

P. Govaert et al.: On the Management of Neonatal Tentorial Damage

60 Blank reported a neonate where CT scan and autopsy data are available 4. Menezes described a newborn where tentorial injury was confirmed during posterior fossa craniotomy 21.

Table 1. Neurological Signs in 78 Neonates with in vivo Diagnosed

Posterior Fossa Subdural Haemorhage N

S e v e r a l a u t h o r s d o c u m e n t e d p r o b a b l e t e n t o r i a l lesions w i t h c o r o n a l 7' 21, 27, 28 o r sagitta118' 26 C T scan. Blank's patient presented four days after an uneventful vaginal delivery at term 4. The boy needed endotracheal ventilation. CT scan of the brain (day 6) documented anterior displacement of dilated supratentorial ventricles, retrocerebellar bleeding, haemorrhagic densities around the rectal sinus covering the tentorium cerebelli and an irregular posterior interhemispheric subdural haemorrhage ending in a nodular density in the cisterna ambiens. The boy died on the seventh day. Postmortem findings included an incomplete tear of the left tentorial leaflet, not involving major vessels. The haemorrhage compressed and displaced the brain stem towards the clivus, partially obliterating the fourth ventricle. Menezes' second patient was a male newborn delivered by caesarean section because of delay in the second stage of labour 21. Eight hours after birth he became lethargic and was resuscitated endotracheally because of bradycardia and recurrent apnoea. CT scan (day 2) demonstrated marked supratentorial ventricular dilatation, a large bleeding within the cerebellar vermis and a haemorrhage around tile rectal sinus with a broad basis towards the torcular Herophili. Coronal reconstructed images confirmed the localization of the bleeding between the vermis and the falco-tentorial junction. During posterior fossa craniotomy that same day a solid subdural clot was found at the tentorial incisura, covering the superior cerebellar vermis. Though not actually visualized, tentorial damage must have been very likely. This boy needed a ventriculoperitoneal shunt on day 6. He was found to be normal 16 months later. Serfontein's first patient, a girl, was delivered at term with forcipal extraction due to foetal distress 28 After endotracheal resuscitation coronal CT scan (day 5) revealed a large haemorrhage between the right tentorial part and the cerebellum. Exactly from that spot a subdural clot was removed later that day. After 9 months she was ,,appropriate" for her age and still without hydrocephalus. Another very probable in vivo diagnosis of tentorial damage was made by Coker in a boy born after repeat caesarean section 7. CT scan described a large haemorrhage around the straight sinus, evident supratentorial hydrocephalus and - upon coronal reconstruction-the major site of bleeding seemed to be within the falco-tentorial junction. Following craniotomy he reco~ vered to be ,,normal" at the age of 6 months. Scotti, in a report concentrated on the CT diagnosis of neonatal posterior fossa haemorhages, described similar images in a coronal CT scan taken on the second day of life from a term newborn with nonspecified neurological problems 27. Upon craniotomy, an infratentorial clot was removed from underneath the right tentorial Ieaflet. With a least 2 years of follow-up this child developed normally. Both Rolland and Koch reported several convincing cases of PFSDH 18, 26, in whom sagittal CT scan clearly demonstrated the peritentorial nature of a huge subdural haemorrhage in 3 of their patients. Both of Koch's patients presented subacutely with seizures about 1 day after birth. Rolland's patient was subjected to craniotomy and survived to be normal. One of Koch's patients had a residual left occipital cyst and right visual field defect. F r o m t h e s e r e p o r t s a n d o u r p a t i e n t s 1, 2, 4 a n d 8

General signs: tense fontanelle(s) decreased motor tone lethargy, depressed archaic reflexes seizures vomiting weak cry high cry hypertonia jitteriness

45 31 27 25 14 11 11 9 6

Focalizing signs: irregular breathing (gasping, sighing) apnoea fixed bradycardia skew deviation of the eyes, nystagmus opisthoto nus facial palsy abducens palsy anisocoria Battle's sign oculomotor palsy

24 24 14 11 10 10 4 4 3 1

1) a p e r i c e r e b e l l a r s u b d u r a l h a e m a t o m a a n d s o m e t i m e s i n t r a c e r e b e l l a r b l e e d i n g is p r e s e n t (Figs. 1, 10, 14),

2) on sections through the tentorial apex, around the straight sinus and behind the third ventricle, marked haemorrhages are present, coalescing to form a somewhat triangular density with its base against the occipital bone (Figs. 3, 7, 14), 3) a haemorrhage is present between the posterior cerebral hemispheres (Fig. 7). Coronal and sagittal CT reconstructions or direct images are of obvious value for better definition of the laesion around the falco-tentorial junction 7' 18, 21, 26-28 (Figs. 6, 7, 12). Sagittal and coronal US scans through the anterior fontanelle have been helpful in localizing a s u s p e c t e d h a e m o r r h a g e a r o u n d o r in t h e c e r e b e l l u m 3" 14, 24, 29 (Figs. 4, 11, 13). C o r o n a l views t h r o u g h t h e p o s t e r i o r a n d axial views t h r o u g h t h e s p h e n o i d f o n t a n e l l e m a y a d d to d i a g n o s t i c p r e c i s i o n . T h e c o m b i nation of CT and US findings together with the obstetric d a t a a n d t h e clinical p r e s e n t a t i o n , a r e v i r t u a l l y d i a g n o s t i c f o r t e n t o r i a l d a m a g e in p a t i e n t s 5 to 8. C o n s i d e r i n g the s y m p t o m s r e p o r t e d in t h e a b o v e m e n t i o n e d 63 cases o f in v i v o d i a g n o s e d P F S D H

from

with ,,verified" tentorial damage we suggest that C T

the l i t e r a t u r e a n d o b s e r v e d in 15 o f o u r o w n p a t i e n t s ,

scan is very suggestive o f tentorial involvement if:

8 o f w h o m are p r e s e n t e d here, a r e c o g n i z a b l e s y m p t o m -

P.

Govaert et al.: On the Management of Neonatal Tentorial Damage

61

Table 2. Neonatal Posterior Fossa Subdural Haemorrhage : Outcome versus Presentation and Treatment

Gestational age < 34w

Craniotomy (N = 41)

No craniotomy (N = 37)

acute N=15

acute N-18

subacute N=26

subacute N-19

0

l

2

4

3 2 2 5 2

7 7 1 8 0

2 3 6 7 0

4 3 4 6 0

0

2

7

3

5 4 8 5 5 14 4

5 3 7 i 4 16 6

11 3 5 2 5 12 9

3 4 4 2 1 3 6

5 0

7 0

3 0

2 3

0

2

9

6

i0

12

7

7

Delivery spontaneous vaginal forceps vacuum breech caesarean section Birth asphyxia Symptoms apnoea fixed bradycardia irregular breathing skew eye deviation cranial nerve palsy tense fontanelle seizures Hydrocephalus requiring shunt stabilized with serial lumbar punctures and diuretics Fatal outcome Normal survival

complex points to this kind o f bleeding (Table 1): a tense fontanelle, a decrease or absence o f m o t o r tone, lethargy and weakened or absent (primitive) reflexes, apnoea, irregular breathing, fixed bradycardia, opist h o t o n u s and skew deviation o f the eyes. A p a r t f r o m opisthotonus and Battle's sign 32, the fixed slowing o f the pulse and the sighing are somewhat specific for p a t h o l o g y in the posterior fossa. The bradycardia m a y have been absent in patients 4 and 7 due to associated anaemia. Facial palsies are not u n c o m m o n 2, 10, 17. 21, 28, 3~. Neither seizures nor a tense fontanelle are necessary for the diagnosis. O u r data confirm the occurrence o f tentorial damage after difficult v a c u u m extraction 17' 18, 3o, 3i. The m o d e o f delivery in the 78 reviewed patients was spon-

taneous vaginal in 16, with v a c u u m extraction in 13 (8 o f our own cases), with forceps extraction in 15, breech in 26 and caesarean section in 2 (mode o f delivery u n k n o w n in 6) (Table 2).

A c o m p a r i s o n between 33 patients with acute (neurological s y m p t o m s within 12 hours o f birth) and 45 with subacute presentation (Table 2) reveals no obvious differences as to the m o d e o f delivery, the presence o f seizures, the incidence o f birth asphyxia or the mortality rate (9 o f the 33 acute P F S D H patients, 8 o f the 45 subacute). The only obvious dissimilarity was the need for endotracheal ventilation: 15 out o f 33 acute versus 3 of 45 subacute presentations. Cran i o t o m y o f the posterior fossa in 15 and a ventricle shunt in 8 o f the 33 acute cases were not really different from the 26 and 9 respectively in 45 subacute presentations. PFSDH

W h e t h e r or not to resort to neurosurgery f o r P F S D H

has fervent supporters on either side. O u r first patient might have been better off with urgent surgery, but also with better paediatric care. The second one succ u m b e d due to associated asphyxia and inadequate resuscitation. Hyperacute neurological disaster pre-

62

cluded surgery in the third one. The fourth died because of associated splanchnic damage. The fifth and seventh patient's histories underscore the power of surgical abstinence even in the face of huge bleedings with obvious signs and symptoms. The immediate successful reduction of intracranial pressure in patient 8 demonstrates the invaluable place of urgent neurosurgery of the posterior fossa in some neonates. It would be unwise to proclaim the superiority of one particular treatment modality from a retrospective survey of the literature on a rare happening such as neonatal PFSDH. The comparison (Table 2) between 41 patients with and 37 without craniotomy seems to suggest that fatal outcome is almost always restricted to witholding of surgical intervention. However, prematurity and birth asphyxia contributed substantially to the worse prognosis in the conservative group. Several patients in this latter group presented with the clinical picture that led to emergency craniotomy in the operative group TM 14, 18 Both managements seem to permit neurologically intact survival in the large majority. This comparison suggests that the fatal outcome in neonatal PFSDH is not purely related to the witholding from craniotomy in infants presenting with similarly severe bleedings. Including 4 patients reported here, 17 succumbed following diagnosis. After having excluded compounding factors leading to death such as septicaemia (13, two cases), aortic rupture during catheterization 13, associated birth asphyxia 2~ (our patient 2) and very low birth weight (27, two cases) (our patient 3), one can retain four newborns where the cause of death may have been the bleeding in itself and craniotomy was not performed 4' 8. 27. Blank's patient was described above. One of the neonates reported by Scotti, born with breech delivery at term, died prior to surgery on the first day of life 27. The authors suggest that occipital osteodiastasis was the cause of death in this neonate. The seventh infant described by Koch died shortly after referral on day 8 due to massive haemorrhage with intracranial hypertension and signs of ,,irreversible brain-stem dysfunction" 18. Our own first patient was not resuscitated adequately but post-mortem findings demonstrated the probable unavoidability of death due to laceration of a major intracranial vessel. On the other hand, one girl delivered at term with low outlet forceps, presented subacutely with seizures, irregular breathing and abducens palsy but died within 24 hours after craniotomy on day 30 due to streptococcal sepsis with meningitis 13. Two other neonates experienced trauma to the transverse sinus during surgery 31. Our patient 5 is the third reported to have been

P. Govaert et al. : On the Management of Neonatal Tentorial Damage

treated conservatively both for his acute neonatal episode and the ensuing late onset hydrocephalus. Von Gontard treated his first patient with acetazolamide and furosemide without serial lumbar punctures as in ours t4. Koch achieved a complete cure in one of his newborns with major peritentorial bleeding and subsequent hydrocephalus treated conservatively 18 The preceding observations tend to prove that in the absence of impending fatal brain-stem compression and complete occlusion of the pericerebellar CSF pathways (haematoma expected to be less than 15 ml on CT scan 3l), surgical abstinence can be a safe alternative to craniotomy of the posterior fossa. Tanaka clearly demonstrated the spontaneous regression of obstructive ventriculomegaly during the acute phase 31. The incidence of ,,resorptive" hydrocephalus and need for shunt placement do not differ significantly either between acute and subacute presentation, or between operative and conservative approach (Table 2). Therefore, craniotomy cannot be performed just to prevent late onset hydrocephalus. The amount of associated subarachnoid haemorrhage may be a useful indicator of the subsequent risk for this type of hydrocephalus 31. Inversely, our patient 8 proves the power of reducing life-threatening intracranial hypertension by emergency craniotomy. If indeed one favours urgent neurosurgical intervention the only safe way to follow is: first craniotomy of the posterior fossa for the removal of as much clot as feasible; second, if necessary, ventricular drainage. Isolated ventricle shunting may lead to upward herniation of the brain-stem s. In cases of hydrocephalus due to PFSDH, lumbar isotope cisternography together with US or CT scan may document the communicating nature of the hydrocephalus as in our fourth patient. This creates the possibility of treating the ventricular enlargement with serial lumbar punctures and drugs that inhibit CSF production. The evolution of the CT pictures in patient 5 illustrate that severe neonatal PFSDH may lead to a retrocerebellar hygroma 2' 12 (Fig. 8). As far as we know demonstrated only once with CT before is the subsequent development of a cyst-like structure in the posterior fossa together with hydrocephalus 26 (Fig. 9). In the differential diagnosis of cystic structures around the cerebellum, one should include this possibility 1, 9, 19

In conclusion our data and a review of the patients from the literature suggest that: 1) tentorial damage can be suspected in vivo; 2) the only evident reasons for performing a pos-

P. Govaert et al. : On the Management of Neonatal Tentorial Damage

terior fossa craniotomy in a neonate with PFSDH are life-threatening brain-stem compression with bradycardia despite endotracheal ventilation, and complete obliteration of the pericerebellar spaces with acute early onset hydrocephalus; 3) craniotomy does not prevent resorptive hydrocephalus; 4) isotope cisternography helps documenting the communication between ventricles and lumbar space following PFSDH, and may therefore predict the possibility of successful conservative treatment with serial lumbar punctures and CSF production inhibitors; 5) neonatal PFSDH may lead to a retrocerebellar cyst-like fluid collection. Addendum After receiving the galley proofs the following publication appeared: In Pediatrics 1990; 85: 534-539, Hanigan etal. recently described three infants with probable tentorial damage due to vacuum extraction. They refined the anatomical diagnosis with MRI in 2 neonates. None of these children had posterior fossa craniotomy and none developed hydrocephalus that needed shunting. Two were severely retarded on follow-up despite absence of birth asphyxia. The authors suggest, but do not substantiate, a vertical stress of vacuum extraction on the dural membranes.

Acknowledgement Our sincere thanks go to Dr. E. van de Velde (Professor of Radiology) for the co-interpretation of the CT scans and to Mr. E. van de Velde for the photographical part of the study, as well as to the whole secretarial group.

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63 8. Craig WS (1938) Intracranial hemorrhage in the newborn. Arch Dis Child 13:89-124 9. Dorsic D, Altenburg H, Herter T (1983) Diagnosis and treatment of cystic non-tumorous lesions of the posterior fossa in children. In: Jensen H-P, Brock M, Klinger M (eds) Advances in neurosurgery, vol 11. Springer, Berlin Heidelberg New York, pp 299-303 10. Dubose Ravenel S (1979) Posterior fossa hemorrhage in the term newborn: report of two cases. Pediatrics 64:39-42 11. Fishman MA, Percy AK, Cheek WR, Speer ME (1981) Successful conservative management of cerebellar hematoma~ in term neonates. J Pediatr 98:466-468 12. French BN, Dublin AB (1971) Infantile chronic subdural hematoma of the posterior fossa diagnosed by computerized tomography. J Neurosurg 47:949-952 13. Gilles FH, Shillito J (1970) Infantile hydrocephalus: retrocerebellar subdural hematoma. J Pediatr 76:529-537 14. Gontard Avon, Arnold D, Adis B (1988) Posterior fossa hemorrhage in the newborn-diagnosis and management. Pediatr Radiology 18:347-348 15. Gouyon JB, Alison M, Nivelon J-L (1981) Conservative management of cerebellar hematoma's in neonates. J Pediatr 90: 827-828 16. Hemsath FA (1934) Birth injury of the occipital bone with a report of thirty-two cases. Am J Obstet Gynecol 27:194-203 17. Hernansanz J, Mufioz F, Rodriguez D, Soler C, Principe C (1984) Subdural hematoma's of the posterior fossa in normalweight newborns. J Neurosurg 61 : 972-974 18. Koch TK, Jahnke SE, Edwards MSB, Davis SL (1985) Posterior fossa hemorrhage in term newborns. Pediatr Neurol l : 96-99 19. Little JR, Gomez MR, MacCarty CS (1973) Infratentorial arachnoid cysts. J Neurosurg 39:380-386 20. Martin R, Roessmann U, Fanaroff A (1976) Massive intracerebellar hemorrhage in low-birth-weight infants. J Pediatr 89: 290-293 21. Menezes AH, Smith DE, Beli WE (1983) Posterior fossa hemorrhage in the term neonate. J Neurosurg 13:452-456 22. Pape KE, Wigglesworth JS (1979) Birth trauma. In: Haemorrhage, ischaemia and the perinataI brain, Chapter 5, Spastics International Medical Publications, pp 61-84 23. Pedespan JM, Dautheribes M, Galperine RI, Diard F, Demarquez JL (1989) H~matome sous-dural de la fosse post~rieure chez un nouveau-n~ fi terme. Arch Fran~ P~diatr 46:367-368 24. Peterson CM, Smith WL, Franken EA (1984) Neonatal intracerebellar hemorrhage: detection by real-time ultrasound. Radiology 150:391-392 25. Pitlyk PJ, Miller RH, Stayura LA (1967) Subdural hematoma of the posterior fossa: report of a case. Pediatrics 40:436-439 26. Rolland M, Fouch~ S, Sevely A, Manelfe C, R~gnier C, Tr~moulet M (1982) H~matomes de la fosse post6rieure chez le nouveau-n~ fi terme. Nouv Presse M6d 11:1317-1320 27. Scotti G, Flodmark O, Harwood-Nash DC, Humphries RP (1981) Posterior fossa hemorrhages in the newborn. J Comp Ass Tomogr 5:68-72 28. Serfontein GL, Rom S, Stein S (1980) Posterior fossa subdural hemorrhage in the newborn. Pediatrics 65:40-43 29. Stone JL (1985) Posterior fossa subdural hematoma in newborns. J Neurosurg 62:626

64 30. Takagi T, Fukuoka H, Wakabayashi S, Nagai H, Shibata T (1982) Posterior fossa subdural hemorrhage in the newborn as a result of birth trauma. Child's Brain 9:108-113 3 I. Tanaka Y, Sakamoto K, Kobayashi S, Kobayashi N, Muraoka S (1988) Biphasic ventricular dilatation following posterior fossa subdural hematoma in the full-term neonate. J Neurosurg 68: 211-216

P. Govaert et al. : On the Management of Neonatal Tentorial Damage 32. Young RSK, Zalneraitis EL (1980) Retroauricular cephalhematoma as a sign of posterior fossa subdural hematoma. Clin Pediatr 19:631-632 Correspondence and Reprints: Govaert P., M.D., Department of Paediatrics, Neonatal Intensive Care Unit, Ghent University Hospital, De Pintelaan 185, B-9000 Ghent, Belgium.