Neuroradiologg
Neuroradiology (1985) 27:313-317
© Spfinger-Verlag 1985
CT findings in eclampsia C. Colosimo Jr 1, A. Fileni 1, M. MoschinP, and P. Guerrini 2 Institutes of 1Radiology, 2Anaesthesiology and Intensive Care Medicine, Catholic University, Rome, Italy
Summary. Cranial CT was performed in five patients with eclampsia: densitometric modifications were present in all cases. Only one patient, who later died, displayed multiple loci of cerebral haemorrhage; all others presented bilateral, symmetrical, nonenhancing hypodensities with mass effect interpreted as cerebral oedema. At CT performed 7-14 days after interruption of the pregnancy, these characteristic hypodense lesions were no longer present while neurological symptoms disappeared. Keywords: Eclampsia - C T - toxemia of pregnancy - gestosis
Eclampsia is the occurrence of one or more convulsions in a patient with toxemia of pregnancy (preeclampsia) [1]: Arteriolar vasospasm is said to be
the essential element in causing changes in the various organs and systems [2]. In particular, arteriolar vasospasm is responsible for brain damage which leads to convulsions and may, in turn, lead to maternal death [2, 3]. This is a report of characteristic cranial CT findings in five patients with eclampsia.
Patients and methods
Between January 1980 and April 1984, CT scans were carried out on five patients, four of whom had been brought to the emergency department on account of one or more episodes of convulsions associated with the typical clinical and laboratory picture of eclampsia (third trimester gestosis). One was already hospitalized at the time of the first neurological signs, due to evidence of scleroderma and preeclampsia. Data concerning previous history, obstetric,
Table 1. Synopsis of clinical data
Patients
1. CG-28 years
2. PC-17 years
3. DA-21 years
4. GC-23 years
5. DM-24 years
Past Obstetric History
Gravida Para Abortus
Gravida Para Abortus
Gravida Para Abortus
Gravida Para Abortus
Gravida Para Abortus
1 0 0
1 0 0
Concomitant disease Week of pregnancy Blood pressure
1 0 0
Duodenal ulcer 36th
35th
35th
-
1 0 0
2 0 1
Scleroderma 33th
34th
Edema
180/100 ++
165/100 ++
150/110 +
150/100 +
170/100 ++
Proteinuria
++
+
+
+
+
Neurological findings Coma (1st grade) Coma (1st grade) righ slight fight hemiparesis slight left hemiparesis, aphasia hemiparesis hemianopsia
Drowsiness no neurological deficit
Drowsiness transitory Coma (1st grade) blindness rigor nucalis, left hemiplegia, right hemiparesis
Recovery
Complete
Complete
Complete
Complete
Died from cerebral haemorrhage
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delivery of living fetuses in all cases. CT was carried out immediately after caesarian section while the patient was still under sedation. Four of the five patients (Table 1) showed a rapid improvement, following caesarian section, with no residual neurological damage. The patient with scleroderma died 4 days after CT with severe endocranial hypertension, renal and cardiorespiratory failure and autopsy findings of brain haemorrhage. The CT examination, in all cases, was performed with a Pfizer 0450, with a scanning time of 4.5 s, slice thickness of 7 mm. Contrast medium was given intravenously (150 cc of Selectografin 70% in 7 min) in three out five patients. All patients, with exception of the one that died 4 days after CT, were submitted to further CT scanning by the same technique 7-14 days after the first examination.
Results
Fig. 1 A-F. Case 1. A, B (not enhanced), C, D (enhanced). Bilateral symmetric hypodensities (arrowheads)in the posterior temporal cortex, without enhancement and mass effect, in the examination performed immediately after caesarian section. E, F Follow-up CT (10 days after) shows only slight hypodensity in the left posterior cortex (arrows)
clinical and laboratory findings (Table 1) show a prevalence of primigravidae and absence of hypertension prior to pregnancy. Upon hospitalization all patients presented the typical association of arterial hypertension, oedema with excessive weight gain, and proteinuria. Three of the patients were in first grade coma and two were drowsy. Neurological symptoms ranged from nothing to hemiplegia. Besides adjunctive medical treatment, a caesarian section was performed under general anaesthesia with
Results of CT, given in Table 2, refer to focal densitometric modifications, mass effect, ventricular size, considered as an index of state of cerebral oedema. Results of follow-up CT in four of five cases are also given. Focal densitometric modifications were observed in all patients: in four of the five patients these presented as hypodensities without enhancement, in patient 5 (Fig. 3) as hyperdensity due to multiple parenchymal haemorrhages. In patient 1 (Fig. 1) the hypodense lesions were bilateral and almost symmetrical, wedge shaped with a cortical base, in the posterior temporal regions, without enhancement and without mass effect, with normal ventricular dimensions, the overall appearance being very similar to that of localized ischaemic lesions. In the other three cases (case 2, Fig. 2 and cases 3 and 4) the hypodense areas were also bilateral with a symmetrical tendency and without enhancement but with a preference for the white matter and a marked mass effect resulting in reduction in the size of the ventricular system due to cerebral oedema. Patient 5 with scleroderma and cerebral haemorrage (Fig.3) presented a large right parieto-occipital intraparenchymal hematoma with shift of the median structures and two smaller hyperdense haemorrhagic areas in the left hemisphere (gyrus cynguli and frontal cortex); blood was also noted in the interhemispheric fissure. The cerebral oedema in this patient was marked and widespread, to the extent that the subarachnoid spaces were almost obliterated. Follow-up CT, 7-14 days after the initial CT, in the first four patients showed almost complete disappearance of densi-
315 Table 2. CT findings and follow-up
Patients
Focal lesions
1 CG (Fig. 1)
Bilateral symmetric hypodensities No m.e. in the posterior temporal cortex, No enhancement Bilateral hypodensities, almost Marked symmetric, of the parietal white m.e. matter. No enhancement Bilateral symmetric hypodensities in Slight the white matter of the frontal lobes m.e. Diffuse hypodensity of the cerebellar Marked hemispheres; bilateral hypodensities m.e. in the occipital white matter. No enhancement Large parenchymal hematoma in the Marked right parieto-occipital white matter; m.e. small haemorrhages in the left gyms cinguli and left frontal cortex. Blood in the interhemispheric fissure
2 PC (Fig.Z) 3 DA 4 GC
5 DM (Fig. 3)
Mass effect
Ventricular size
Follow-up CT
Regular
Slight hypodensity in the left posterior temporal cortex
Markedly reduced
Complete return to normal
Slightly reduced
Complete return to normal
Flattened fourth ventricle
Complete return to normal
Complete disappearance of the ventricles
No follow-up CT Autopsy: multiple cerebral haemorrhages. Severe edema.
Fig.2 A-E Case 2. A-C Unenhanced CT - immediately after caesarian section-shows bilateral hypodensities in the white matter of both posterior parietal lobes (arrows);there is marked mass effect and edema and ventricular size is reduced. E, F (Enhanced CT, 9 days after, reveals complete return to normal
nal picture o f endocranial hypertension, renal and cardiorespiratory failure, presented at autopsy cerebral d a m a g e corresponding exactly with that revealed in the CT. F u r t h e r m o r e severe cerebral oedem a was present with widespread p u n c t i f o r m haemorrhages while endarteritis was visible in the arteries o f small and m e d i u m calibre, with histologic pattern o f the sclerodermal type. The cerebellar tonsils were herniated in the f o r a m e n m a g n u m .
Discussion
tometric modifications which was parallel with the progressive regression o f the neurological s y m p t o m s following caesarian section. Only in patient 1 did the e x a m i n a t i o n on the 7th d a y reveal the persistence o f a small h y p o d e n s e area in the left t e m p o r a l cortex, nevertheless in the absence o f mass effect and enhancement. Patient5 with cerebral h a e m o r r h a g e w h o died 4 days after caesarian section with a termi-
At present the term p r e e c l a m p s i a is preferred to that o f toxemia o f p r e g n a n c y to indicate the clinical picture characterized b y excessive weight increase and oedema, arterial hypertension and proteinuria [1]. Associated with these signs, the a p p e a r a n c e of one or m o r e episodes o f convulsions m a y be considered typical of eclampsia. The p r e e c l a m p s i a - eclampsia
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Fig.3 A-C. Case 5. Large haematoma in the right posterior parietal white matter. Note also two smaller foci of haemorrhage in the left frontal cortex (arrows)and in the left girus cynguli (arrowheads)as well as blood in the interhemispheric fissure
syndrome occurs in approximately 2% of pregnancies in the western world but tends to increase in poorer countries or where diet is poor [4]. The condition, which shows a prevalence for primigravidae, is responsible for a high percentage of maternal and fetal deaths. The exact causes of the syndrome is not yet known, but it is suggested that a relative uterine ischemia may induce the release into the maternal circulation of vasoconstrictive substances responsible, in turn, for the arteriolar spasm which represents the essential pathogenetic element of the alterations in the various organs. [2]. The onset of convulsions and neurologic disorders is not directly related to the severity of the clinical picture and laboratory findings in preeclampsia. Furthermore, the neurological situation is seen to return to normal in the uncomplicated cases, with interruption of the pregnancy which is essential in the management of eclampsia [2, 5, 6]. Anatomo-pathologic findings in the brain of patients dying from eclampsia reveal the presence of haemorrhage in the parenchyma and, above all, cerebral oedema [3, 7, 8]. Even in the absence of true haematoma it is not uncommon to find diffuse petecchial haemorrhages. Indeed the pathological findings closely resemble those of sever hypertensive encephalopathy in which the haemorrhage is the result of prolonged cerebral ischemia [2, 6]. Only recently have sporadic reports appeared in the literature on cranial CT findings in eclamptic patients [5, 6, 9]. Benedetti [6] described a case in which the CT scan demonstrated only a picture of diffuse cerebral oedema with compression of the ventricular system in a patient showing complete regression of the eclamptic syndrome following interruption of the pregnancy. Gaitz [9] presented a case in a primigravida with eclampsia and tetraparesis accompanied on the CT scan, by bilateral, symmetrical hypodense lesions in the capsular region with cerebral oedema. After the
complete disappearance, in this patient, of the lesions visible on the CT scan on the 10th day there was still a mild but persistent spastic paraparesis. Finally, Beeson [5], in a case of eclampsia preceded by blindness reported the symmetrical bilateral appearance of hypodense areas in the occipital white matter. In this patient also, visual disturbance disappeared 24h after caesarian section and CT at follow-up demonstrated the disappearance of hypodensity and cerebral oedema. Our series is of five patients all of whom submitted to CT immediately after caesarian section. A typical pattern of eclampsia was present in all (Table 1), the neurological situation showing some variations; none of these women showed evidence of hypertension prior to pregnancy, not even patient 5 who had scleroderma. From results of CT studies (Table 2) it can be seen that - with the exception of patient 5 with multiple sites of haemorrhage - all others presented bilateral hypodense "lesions" with a symmetrical tendency and without enhancement. Nevertheless examination of the lesions in patient 1 (Fig. 1) reveals some differences with respect to the hypodense lesions, which involve mainly the posterior temporal cortex and have a typical triangular shape; there is no evidence of mass effect and cerebral oedema is not associated (the ventricles show no sign of compression). The pattern, therefore, is not unlike that of bilateral ischemic lesions in the watershed areas between posterior and middle cerebral artery supply. In contrast, in case 2 (Fig. 2) and in the other two patients without haemorrage - as well as in the other cases reported in the literature - hypodense lesions are always bilateral and almost symmetrical but they are found chiefly in the white matter, with mass effect and cerebral oedema demonstrated by the marked compression or even obliteration of the ventricles. The attenuation values, nevertheless, are similar
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in all lesions of all patients without haemorrhage and are very similar to those of recent ischemic lesions. However, the constant finding of neurological recovery with the disappearance of modifications at follow-up CT confirms that the densitometric alterations are induced by areas of reversible ischemic damage and not infarction. The patient that died with cerebral haemorrhage also presented lesions in both hemispheres (Fig. 3) with sever oedema. It is probable, therefore, as suggested in the literature [2, 6], that cerebral haemorrhage occurs as a result of severe prolonged hypertensive - ischemic damage and it is for more likely to occur in patients with pre-existing arterial hypertension or systemic disease giving rise to arteriolar damage (such as scleroderma).
Conclusions
In all the patients with eclampsia except one with bilateral hemorrhages, CT revealed densitometric modifications, characteristically bilateral and practically symmetrical hypodensities without enhancement and completely reversible. In most of the patients in the present series, and in those in the literature, the lesions involve mainly the white matter, they have mass effect and are associated with cerebral oedema. One of the cases in the present seties, however, showed slightly different changes in as much as there was an involvement, bilaterally and almost exclusively, of the cortex, the localization and extent of which was typical of ischemic lesions. Studies on a larger number of cases are necessary in order to offer an explanation for the different behaviour of the "eclamptic cerebral lesions" the distribution of which appears to be in relationship to symmetrical areas of vascularization. CT is indispen-
sable in the study of patients with eclampsia, not only to exclude cerebral haemorrhage but also to evaluate and monitor brain oedema and densitometric evolution of the lesions in relation to the neurological course of the disease. Aknowledgemenr We would like to thank Marian Shields for the English version of the paper and Giovanna Azzocchi for the preparation of the manuscript
References 1. Hughes EC (1972) Obstetric-gynecologic terminology prepared by the Committee on Terminology of the American College of Obstetricians and Gynecologist. Davis, Philadelphia 2. Danfort DN (1977) Obstetrics and gynecology. Harper and Row, Maryland 3. Sheehan HL, Lynch JB (1973) Cerebral lesions. In: Pathology of toxemia in pregnancy. Williams and Wilkins, Baltimore 4. Hibbard LT (1973) Maternal mortality due to acute toxemia. Obstet Gyneco142: 263-267 5. Beeson JH, Duda EE (1982). Computed axial tomography scan demonstration of cerebral edema in eclampsia preceded by blindness. Obstet Gynecol 60:529-532 6. Benedetti TJ, Quilligan EJ (1980) Cerebral edema in severe pregnancy-induced hypertension. Am J Obstet Gynecol 137: 860-862 7. Govan AD (1976) The histology of eclamptic lesions. J Clin Pathol 29:63-69 8. Jewett JF (1973) Fatal intracranial edema from eclampsia. N Engl J Med 289:276-277 9. Gaitz JP, Banford CR (1982) Unusual computed tomography scan in eclampsia. Arch Neurol 39:66 Received: 27 August 1984 Dr. C. Colosimo Jr. Istituto di Radiologia Policlinico "A. Gemelli" Largo A. Gemelli, 8 1-00168 Roma Italy