Posttraumatic intfaventricular haemorrhages

ACTA NEUROCHIRURGICA

Acta Neurochirurgica 55, 283--293 (1981)

9 by Springer-Verlag 1981

Departments of Neurosurgery and Neuroradiology*, University of Padua, Italy

Posttraumatic Intraventricular Haemorrhages By

M. Z u c c a r e l l o , R. I a v i c o l i * , K. P a r d a t s c h e r * , P. Cervellini, D. F i o r e * , S. M i n ~ r i n o , and M. G e r o s a With 10 Figures

Summary Of a series of 350 patients studied for blunt head trauma by CT scan 10 were found to have an intraventricular haemorrhage (IVH); in 8 cases we could find concomitant CT abnormalities as well as intracerebral contusion or haemorrhage, and in two cases no other CT abnormality was noted. CT scan represents the first reliable and non-surgical tool for identifying this process. Two possible mechanisms that govern the formation of an IVH are postulated: a) an erosion of the ventricular wall by an intracerebral haemorrhage; b) the rupture of subependymal veins deformed by the negative pressure following dilatation of the ventricular wall. The prognosis in our cases is severe.

Keywords: Head injury; computed tomography; intraventricular haemorrhage; pathogenetic mechanisms. Introduction

Computed tomography represents a great advance in the diagnosis of a wide variety of intracranial lesions, particularly those secondary to head trauma. CT scan allows not only a specific diagnosis in a minimum amount of time, but also shows some intracerebral lesions difficult or impossible to diagnose as well as intraventricular haemorrhage (IVH). To our knowledge only one study has been carried out specifically on the occurrence of I V H in blunt head trauma s0, while some other authors report sporadically cases of I V H in head trauma 2, a, 6, 8, 9 0001-6268/81/0055/0283/$ 02.20

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Materials and M e t h o d s Of a total of 4,500 CT studies of the head performed over a 15-month-period from August 1978 to November 1979, 350 were of head-lnjured patients. We used an Ohio nuclear Delta 25 scanner with 256 X 256 matrix and with images recorded on X-ray film. All the studies were performed within 24 hours of the injury. Most headinjured patients who required a CT scan were not cooperative, and required sedation with intravenous diazepam. Of the 350 patients studied for blunt head trauma 10 were found to have a clearly identified intraventricular haemorrhage: 8 were found to have concomitant CT abnormalities, contusion, or intracerebral haemorrhage, and only two showed IVH as the only finding.

Case Reports Case 1: A 81-year-old male was admitted because he was struck by a car. He was comatose, with dilated pupils and a left hemiparesis. Computed tomograpIay revealed small intracerebral haemorrhages, frontal intracerebral haematoma, right subdural haematoma, and blood in the left lateral ventricle. His condition deteriorated steadily, and he died a few days later. No autopsy was performed. Case 2: A 37-year-old female was admitted following a motor vehicle accident. She was comatose, with unequal pupils and a left hemiparesis. Computed tomography showed right hemisplaeric oedema, and blood in the right lateral, third, and fourth ventricles (Fig. i). Her clinical course improved in the first week, then she died of bron&opneumonia. No autopsy was performed. Case 3: A 20-year-old male was admitted following direct trauma in the frontal region. He was comatose, with dilated pupils, decerebrate regidity, and no localizing signs. Computed tomography demonstrated a frontal left intracerebral haemorrhage, blood in the posterior horns of both lateral ventricles, and a blood collection in the subependyma of the right lateral ventricle wall (Fig. 2). Immediately following the CT scan he experienced a cardio-respiratory arrest. Autopsy findings included left frontal skull fracture, subarachnoid, subduraI, and multiple intracerebral haemorrhages, and brain stma contusion as well as blood in all the ventricles. Case 4: A 50-year-old male alcoholic was admitted following a motor vehicle accident. He was unconscious, but responding semipurposefully to pain; a left hemiparesis was present. Computed tomography revealed a large right extradural haematoma, bilateral frontal contusions, subarachnoid haemorrhage, and blood in both lateral ventricles. He was operated on, improved, and was discharged 16 days later with only a residual left hemiparesis.. Case 5: A-50-year-old male was admitted comatose following a motor vehicle accident. Purposeful movement was elicited by painfut stimuli on the left; a right hemiplegia was present.

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Fig. 1. Case 2. Note blood in body of right lateral ventricle

Fig. 2. Case 3. A blood collection is present in the subependyma of the right lateral ventricular wall Computed tomography showed blood in the region of the basal ganglia on the left and in both lateral ventricles. An intraventricular catheter placed into the right frontal horn yielded bloody cerebrospinal fluid. Left carotid arteriography revealed no ventricular enlargement, displacement of the ventricular system, and an intracerebral mass lesion. Repeated CT scan a week later showed blood in the posterior horn of the right lateral ventricles. The size of the lateral ventricles appeared to be larger than in the previous study, with a slight reduction in size of the intracerebral haematoma (Fig. 3).

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Fig. 3. Case 5. Parenchymal haemorrhage and blood ha both occipital horns

Fig. 4. Case 6. Intracerebral haematoma and extensive IVH in both laterai ventricles, with blood density in the third ventricle His clinical course vacillated somewhat, and 40 days after the admission he died of bronchopneumonia. Autopsy findings included multiple intracerebral haemorrhages, an intracerebral haematoma in the basal ganglia, and blood in all the ventricles. Case 6: Struck by a car three hours before his admission, this 81-year-old man was comatose and variably decerebrate. Computed tomography showed an extensive intracerebral and intraventricular haemorrhage (Fig. 4). Blood was present in the Right fronto-parietal region and in the ventricular system. He died a few hours after the scan. Autopsy was not ~erformed~

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Fig. 5. Case 7. CT scan shows a parenchymal haemorrhage in both basal ganglia and blood in both lateral ventricles

Fig. 6. Case 8. Blood is seen in both lateral ventricles

Case 7: A 52-year-old man was admitted following a motor vehicle accident. He was in deep coma, and variably decerebrate. Computed tomography revealed subarachnoid and ventricular haemorrhage, and blood in both basal ganglia (Fig. 5). He died one hour after the scan. No autopsy was done. Case 8: This 18-year-old man was admitted unconscious after a motor vehicle accident. The pupils were dilated, and he was variably decerebrate. Computed tomography showed blood in all the ventricular system and in the left basal ganglia (Fig. 6).

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Figs. 7 a and 8 a. Case 9. Blood in both lateral ventricles and in the corpus callosum

Figs. 7b and 8 b. Case 9. Repeat CT scan shows a slight ventricular dilatation and disappearance of the blood

He died three days after the scan. Autopsy findings included small subarachnoid and subdural haemorrhages, blood in ali the ventricular system, multiple intracerebral haemorrhages, larger parenchymal haemorrhage in the basal ganglia, and loci of softening in the upper pons. Case 9: A 17-year-old boy was admitted following an accidental severe head injury. He was comatose. Purposeful movement was elicited by painful stimuli. A right hemiparesls was present. Computed tomography revealed a parenchymaI haematoma in. the corpus

Posttraumatic Intraventricular Haemorrhages

Fig. 9 a. Case 10. Blood is present in all the ventricular system

Fig. 9 b. Case 10. CT scan shows a pontine low-density area

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callosum and blood in the lateral ventricles (Figs. 7 a and 8 a). He improved on conservative management, and repeated CT scan eight weeks later showed no residual blood in the lateral ventricles and absorption of the haematoma; the sizes of the lateral ventricles appeared to be larger than in the original study (Figs. 7b and 8 b). A neurological examination showed a mild right hemiparesis and a slight ~ntellectual decline.

Fig. 10. Case 10. Photograph of horizontal section through the lateral ventricles as seen from above. Rupture (asterisk) of left transverse caudate vein Case 10: A 20-year-old young man was admitted unconscious following a severe motor vehicle accident. He was decerebrate, and his pupils were dilated. Computed tomography showed blood in all the ventricular system, and a pontine contusion (Figs. 9 a and b). He died six hours after the scan. Autopsy findings included blood in all the ventricular system, without cerebral hemisphere haemorrhages, but with haemorrhages in the mesencephalon and upper pons. The examination of the inner lateral ventricular walls showed rupture of the transverse caudate vein (Fig. 10).

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Discussion

Prior to the advent of CT the diagnosis of I V H could be made with good probability only in some cases with involvement of the third and fourth ventricles 1-~,la. These cases show a classical clinical picture, described by Sanders and McDonald, consisting of deep coma of acute onset, focal deficit, symptoms of mesencephalic herniation, and central regulation disorders; death ensues within 24 hours as result of respiratory paralysis. Echoencephalography and cerebral angiography could sometimes identify this type of lesion 4, 1~, is, but only by ventricular tap or autopsy could one be sure of an exact diagnosis of I V H 7, 11, 13 CT represents the first reliable nonsurgical tool for identifying this process. Merino de Villasante and Taveras found three cases of I V H in 100 patients with head trauma, two of them with concomitant intracerebral haematomas. Moseley and Zilkha found only one case of I V H associated with an extensive intracerebral haematoma. Dublin et al. found four cases of I V H in 200 patients with head trauma but not specify whether the lesion was solitary or associated. French and Dublin reported nine cases of I V H in 316 patients, seven asociated with an intracerebral haemorrhage and two with multiple cerebral contusions. Little et al., in a series of 54 patients with IVH, reported one case following head trauma; Debois found five cases in 60 patients with intraventricular haemorrhages. Oliff et al. described six cases of I V H in 200 patients who had sustained blunt head trauma. Although an accurate estimation of the true incidence of this phenomen is not yet possible, our findings nevertheless suggest that intraventricular haemorrhages are not so rare as supposed. We have found 10 cases, with an incidence of 2.6~ in accord to that found by Oliff. Another controversial aspect of this entity is its pathogenesis: in fact the pathogenetic mechanism that governs the formation of a post-traumatic I V H is not yet clear. It was been postulated and suspected that I V H following head trauma may be related to unsuspected arteriovenous malformations in the ventricular walls which rupture following trauma 4, s. But in the literature at least 20 cases of choroid plexus arteriovenous malformations have been reported, while the incidence of traumatic I V H is significantly higher; we have not found any case that can confirm such a hypothesis. It is ,our opinion that two different mechanisms should be invoked to explain this process: a) when the I V H follows or is associated with an intracerebral haematoma, it can be postulated that there is

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a dissection of blood from an intracerebral haematoma through the ependymal lining with extension of the blood into the ventricular space (Fig. 4). b) When the finding of IVH may be considered as solitary or when there is not an extension of an intracerebral haematoma into the ventricular system, another me&anism could be postulated. Unterharns&eidt and Seller in the "Head Injury Conference" in Philadelphia in 1966 hypothesized that the lesions observed in the midline structures, mainly primary haemorrhages in the subependyma of the ventricles and in the portions of the corpus callosum (Figs. 7 and 8) located near by may result from a development of negative pressure in this region. The ventricular walls and the portion of the corpus callosum adjacent to the ventricles are particularly subject to the effects of the negative pressure. When a blow is applied along the sagittal diameter of the skull the resulting deformation will consist of an increase in the minor axis and a decrease in the major axis of the ellipsoidal skull; these changes will result in an increase in total volume with a dilatation of the ventricles. The ventricular walls contain the so-called subependymal veins that lie in all parts of the ventricular system. The rupture of veins deformed by the negative pressure and following dilatation of the ventricular walls could be the origin of the solitary ventricular haemorrhage (Fig. 10, Case 10). Tlae results of CT have confirmed such a hypothesis (Fig. 2), and moreover in these cases the ventricular size was normal, because the haemorrhage was not due to the rupture of a vessel by the force of the blood pressure as is the case with a cerebral artery. With respect to the prognosis it is difficult to draw some conclusion because so few cases are reported. Merino de Villasante and Taveras stated that there is a close relationship between "the severity of clinical presentation and CT demonstration of the abnormality responsible for the clinical status". However, it is our opinion that both in the case of IVH associated with other intracranial lesions and in the case of solitary IVH the prognosis is very poor, in the first instance because of the extremely severe concomitant brain destruction, and in the second case because the acceleration trauma that produces such a deep lesion brings about two consequences: a) A brain stem contusion, not always revealed by CT scan (Fig. 9 b), but suspected by the clinical course and confirmed at autopsy. b) A development of bilateral hemispheric oedema that, if often unremarkable at the time of CT examination as reported by Merino de Villasante and Taveras and observed by us, can appear even some hours after trauma.

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References

1. Debois, V., L'h~morragie ventriculaire. CorrElation entre la symptomatologie clinique et la tomodensitom~trie. Neurochirurgie 25 (1979), 71--77. 2. Dublin, A. B., French, B. N., Rennick, J. M., Computed tomography in head trauma. Radiology 122 (1977), 365--369. 3. French, B. N., Dublin, A. B., The value of computerized tomography in the management of 1,000 consecutives head injuries. Surg. Neurol. 7 (1977), 171-183. 4. Hodge, C. J., King, R. B., Arteriovenous malformation of choroid plexus. Case report. J. Neurosurg. 42 (1975), 457--461. 5. Larsen, S. J., Love, L., Mittelpunkt, A., Unilateral intracranial hematoma without shift of the anterior cerebral artery. Amer. J. Roentgenol. 92 (1964), 786--791. 6. Little, J. R., Blomquist, G. A., Ethier, R., Intraventricular hemorrhage in adults. Surg. Neurol. 8 (1977), 143--149. 7. McDonald, J. V., Midline hematomas simulating tumors of the third ventricle. Neurology 12 (1962), 805--809. 8. Merino de Villasante, J., Taveras, J. M., Computerized tomography in acute head trauma. Amer. Roentgenol. 126 (1976), 765--778. 9. Moseley, I. F., Zilkha, E., The role of computerized tomography (EMI Scanning) in the diagnosis and management of cranio-cerebral trauma. J. Neuroradiology 3 (1976), 277--296. 10. Oliff, M., Fried, A. M., Young, A. B., Inrraventricular hemorrhage in blunt head trauma. J. Comput. Assist. Tomogr. 2 (1978), 625--629. 11. Ojemann, R. G., New, P. F. G., Spontaneous resolution of an intraventricular hematoma. J. Neurosurg. 20 (1963), 899--902. 12. Pia, H. W., The diagnosis and treatment of intraventricular hemorrhages. In: Progress in Brain Research, Vol. 30 (Luyendijk, W., ed.), pp. 463--470. Amsterdam: Elsevier Pub. Co. 1968. 13. Pia, H. W., The surgical treatment of intracerebral and intraventricular hematomas. Acta neurochir. (Wien) 27 (1972), 149--164. 14. Sanders, E., A study of primary, immediate or direct hemorrhage into the ventricle of the brain. Amer. J. Med. Sci. (N. Set.) 82 (1881), 85--128. 15. Unterharnscheidt, F., Sellier, K., Mechanics and pathomorphology of closed brain injuries. Conference: Head Injury Planning Committee, Chicago, Febr. 7-9, 1966. Chapter 26, pp. 321--341. Philadelphia: Lippincott. 1966. Author's address: M. Zuccarello, M.D., Department of Neurosurgery, Via Giustiniani 3, 1-35100 Pado~a, Italy.

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Acta Neurochlrurgica,VoI. 55, Fasc.3--4