European Journal of Radiology, 11 (1990) 46-53 Elsevier 46 EURRAD 00059 Computed tomographic changes of the brain in toxaemia of pregnancy Taiyewo M. Kolawole ‘, Pravinchandra J. Patel’, Basim Yaqub2, Abdul Rhaman Al-Tahan2, Tajuddin Malabarey ’ and Abdul Aziz Al-Meshari ‘Departments of Radiology, ‘Medicine and ‘Obstetrics & Gynaecology.King Khalid University Hospital,King Saud University, Riyadh. Saudi Arabia (Received 24 August 1989; accepted after revision 2 March 1990) Key words: Computed tomography, brain; Computed tomography, haemorrhage; Toxaemia, brain; Eclampsia, complication; Brain, CT Abstract Four cases of toxaemia of pregnancy examined with computed tomography scans of the brain are reported. A review of the literature reveals 19 other cases with previously repored CT brain scans. The review shows intracerebral oedema as the main finding. Haemorrhage, massive or punctate was noted in four cases. The pathogenesis of the CT changes and the clinico-radiological correlation of the visual disturbances are discussed. Introduction Until recently, the pathophysiology of toxaemia of pregnancy was studied mainly by autopsy. In some patients the radiological contribution to the patho- physiology has been mainly through angiography. Com- puted tomography (CT), being a nearly non-invasive modality in vivo, is now used for detailed studies of internal organs, and in particular the brain, since it provides tremendous display of anatomy and pathol- ogy. However, its use has been limited in toxaemia of pregnancy. This paper reports our findings in four cases and also reviews the CT changes in toxaemia of preg- nancy in 19 others in an attempt to further elucidate the pathophysiology and correlate clinico-radiological find- ings in toxaemia in pregnancy. Case 1 A 31-year-old woman, 38 weeks pregnant, with toxaemia in pregnancy, blood pressure being 140/90 mmHg and in labour, underwent a Caesarean section Address for reprints: Prof. T.M. Kolawole, Radiology Department (No. 40), King Khalid University Hospital, P.O. Box 2925, Riyadh 11461, Saudi Arabia. due to an obstruction in the second stage of labour. On the delivery of the baby, the uterus was found to be atonic with persistent and intractable bleeding. There- fore hysterectomy was performed. During the hysterectomy there was severe blood loss. Later the patient developed cardiac arrest. Routine resuscitative measures restored circulation after three minutes. The respiratory distress caused hypoxia and hypotension. The patient regained con- sciousness 72 h after cardiac arrest, and later the blood pressure improved ranging between 130/90 and 160/100 mmHg. On the fourth postoperative day, focal seizures in- volving the left half of the face and conjugate occular deviation to the left were noted. Neurological exami- nation showed intact brainstem reflexes, hypertonia and hyperreflexia of all four limbs with bilateral Babinski responses. A CT examination of the brain was normal. Generalised seizures were noted on the 7th post- operative day and they continued daily for 1 week. On the 5th postoperative day, the blood pressure surged upwards to 180/l 15 mmHg and whilst undergoing therapy on the same day, the patient suddenly became hypotensive, with signs of decerebrate rigidity. A repeat CT examination of the brain showed bilat- 0720-048X/90/$03.50 0 1990 Elsevier Science Publishers B.V. (Biomedical Division)
Transcript
European Journal of Radiology, 11 (1990) 46-53 Elsevier 46
EURRAD 00059
Computed tomographic changes of the brain in toxaemia of pregnancy
Taiyewo M. Kolawole ‘, Pravinchandra J. Patel’, Basim Yaqub2, Abdul Rhaman Al-Tahan2, Tajuddin Malabarey ’ and Abdul Aziz Al-Meshari
‘Departments of Radiology, ‘Medicine and ‘Obstetrics & Gynaecology. King Khalid University Hospital, King Saud University, Riyadh. Saudi Arabia
(Received 24 August 1989; accepted after revision 2 March 1990)
Four cases of toxaemia of pregnancy examined with computed tomography scans of the brain are reported. A review of the literature reveals 19 other cases with previously repored CT brain scans. The review shows intracerebral oedema as the main finding. Haemorrhage, massive or punctate was noted in four cases. The pathogenesis of the CT changes and the clinico-radiological correlation of the visual disturbances are discussed.
Introduction
Until recently, the pathophysiology of toxaemia of pregnancy was studied mainly by autopsy. In some patients the radiological contribution to the patho- physiology has been mainly through angiography. Com- puted tomography (CT), being a nearly non-invasive modality in vivo, is now used for detailed studies of internal organs, and in particular the brain, since it provides tremendous display of anatomy and pathol- ogy. However, its use has been limited in toxaemia of pregnancy. This paper reports our findings in four cases and also reviews the CT changes in toxaemia of preg- nancy in 19 others in an attempt to further elucidate the pathophysiology and correlate clinico-radiological find- ings in toxaemia in pregnancy.
Case 1
A 31-year-old woman, 38 weeks pregnant, with toxaemia in pregnancy, blood pressure being 140/90 mmHg and in labour, underwent a Caesarean section
Address for reprints: Prof. T.M. Kolawole, Radiology Department (No. 40), King Khalid University Hospital, P.O. Box 2925, Riyadh 11461, Saudi Arabia.
due to an obstruction in the second stage of labour. On the delivery of the baby, the uterus was found to be atonic with persistent and intractable bleeding. There- fore hysterectomy was performed.
During the hysterectomy there was severe blood loss. Later the patient developed cardiac arrest. Routine resuscitative measures restored circulation after three minutes. The respiratory distress caused hypoxia and hypotension. The patient regained con- sciousness 72 h after cardiac arrest, and later the blood pressure improved ranging between 130/90 and 160/100 mmHg.
On the fourth postoperative day, focal seizures in- volving the left half of the face and conjugate occular deviation to the left were noted. Neurological exami- nation showed intact brainstem reflexes, hypertonia and hyperreflexia of all four limbs with bilateral Babinski responses. A CT examination of the brain was normal.
Generalised seizures were noted on the 7th post- operative day and they continued daily for 1 week. On the 5th postoperative day, the blood pressure surged upwards to 180/l 15 mmHg and whilst undergoing therapy on the same day, the patient suddenly became hypotensive, with signs of decerebrate rigidity.
A repeat CT examination of the brain showed bilat-
Case 1 - Fig. 1. (3 scan showing high attenuation values in basal ganglia (caudate nuclei and lentiform nuclei) with normal ventricular system.
Case 2 - Fig. 2. (a) Unenhanced CT scan with bilateral low attenuation areas in the centrum ovale. (b) ‘Normal’ CT scan 2 weeks later (fogging effect).
eral haemorrhages into the caudate nuclei and lentiform nuclei. No associated low attenuation areas were noted (Fig. 1). A few days after, the patient died.
Case 2
A 22-year-old primigravid woman was admitted in her 39th week of pregnancy with an exacerbated head- ache and a 2 week history of hypertension and ankle oedema. Her blood pressure was 200/130 mmHg.
Labour was induced, but the patient devdoped generalized tonic clonic seizures and an emergency Caesarian section was performed.
On recovery, the patient complained of the inability to see. She had normal papillary reflexes and apart from some constriction of her retinal vessels, the physical examination was normal.
She had normal laboratory tests including renal functions and urinalysis. Visual evoked responses were normal. A CT scan of the brain showed bilateral cen- trum ovale low-density areas (Fig. 2a). Visual acuity became apparent within 72 h, and the repeat CT scan made 2 weeks later appeared normal with resolution of the previously low attenuation areas due to a ‘fogging effect’ (Fig. 2b).
Case 3
A 32-year-old multiparous woman was brought to a peripheral hospital in her ninth month of her third pregnancy with confusion, severe headache, vomiting and blurring of vision. She had frequent seizures on the way to hospital.
Her blood pressure was 220/120 mmHg. Apart from being a little confused, the neurological examination was normal. It was difficult to control her blood pres- sure and a Caesarian section was performed later, with delivery of normal twin babies.
The next day, the patient complained of the inability to see and shortly afterwards she was noted to have a left-sided hemiparesis. Her blood pressure was con- trolled with /?-blockers.
Two weeks later, she was transferred to our hospital (KKUH). She was responding slowly to speech, di- soriented in time and place and irritable. She had cortical blindness (the inability to appreciate light) with left-sided hemiplegia. She was anaemic with a high ESR. Her renal function tests were normal.
On admission, it was not possible to obtain visually evoked responses using flash stimulation, but she had normal evoked retinograms.
On admission, a CT scan of the brain showed bilateral hyperdense areas in the occipital regions and on the right frontal side. No enhancement was used
48
Case 3 - Fig. 3. (a) Unenhanced CT scan, symmetrical high cortical attenuation areas in the occipito-parietal regions, with less high cortical attenuation values in the fronto-parietal region more on the right side. (b) Enhanced CT scan. Cortical ribbon enhancement ofthe parieto-occipi-
tal regions (bilateral), temporal and frontal on the right.
Fig. 4. (a) Vertebral angiography demonstrating generalized narrowings of the basilar artery and its main branches. (b) Right common carotid angiogram with generalized narrowing of the intracranial branches.
She was started on sodium nitroprusside and was loaded with 1 gram of phenytoin.
(Fig. 3a). Eleven days later this was repeated with intravenous contrast medium. Marked cortical en- hancement was seen bilaterally especially in the parieto- occipital regions (Fig. 3b). By this time, vertebral and bilateral carotid angiography had revealed generalized narrowing of all the vessels with reduced intracranial vascularity (Fig. 4a and b). There was no evidence of sinus thrombosis (not shown).
There was no past history of epileptic tits or hyper- tension. Full blood count, blood sugar, renal and liver function tests, urinalysis were all within normal limits. A non-enhanced cranial CT scan showed effacement of ventricular system with a reduced subarachoid space. Three days later an enhanced CT scan was normal. She had an uneventful recovery.
Summary of previous cases
Twenty days after admission to the KKUH, evoked A synopsis of all the previously reported cases and responses using flash stimulation were of normal latent those that we saw are shown in Table I. The results but with a small amplitude. A subsequent CT revealed show a total of 19 previously reported cases, which with
TABLE I (1A)
Authors No. Age
Grimes et al., 1980 1 15
Beck and Menezes, 1981 1 26
Beeson and Duda, 1981 1 29
Gaintz et al., 1982 1 31
Kirby and Jaindi, 1984 1 28 2 32
Naheedy et al., 1985 1 30
Gra- Pari- Abor- Gestation vida ty tus period
49
bilateral temporo-occipital low-density regions with re- duced cortical density when compared with previous scans compatible with watershed infarction (Fig. 5). On discharge, the patient had improved only little. She was able to appreciate light in both eyes and to move her left limbs.
Case 4
A 20-year-old (Saudi) prim&avid woman presented in her 42nd week of pregnancy. Immediately after delivery, she convulsed. Blood pressure was 160/100 mmHg. Her neurological exam, apart from some drowsiness was normal. She was put on diazepam, and hydralazine, and was transferred to the Medical Intensive Care Unit. Three hours later, she sustained another convulsive episode while still on therapy; however, her blood pressure was not yet well under control.
Blood Neurological features pressure
(mmHg)
1 0 0
2 1 1
I 3 3
41
last trimester
36
150/108
180/130
174/l 10
Headache, total blindness
Headaches, photophobia, left occulomo- tor and bilateral abducens palsies
Blindness, convulsion, coma; CSF = 400 mm of water
1 0 0 32 150/110 Stupor, quadriparesis CSF with red blood cells
3 3 0 P.P. 3 2 0 P.P.
1 0 1 34
-
2251125
Seizures Seizures
Bi-frontal headache, right monoparesis, radionuclear scan showed left parietal region uptake
50
TABLE I (1B)
Cf findings
focal lesions
hypodensity haemorrhage bilateral
Follow-up CT Clinical WCO”k?ly
enhancement mass eff- ventricular time comment ect/brain size (...)
symmetry oedema
Occipital lobes, left occipi-
to-parietal region
+ not done normal 7/12 later
+ not done + reduced 717, 1517 and 2417 later
normal
normal
complete
complete sub-ependymal +
haemorrhage,
left & lateral basal ganglia
* Generalized white matter especially occipital & parietal lobes
Internal & external cap-
sule
White matter of occipital, parietal, left temporal, internal & exterior cap-
sule
White matter of occipital and parietal lobes
White matter of both cor- tices cerebral
t done, nil + reduced 1417 normal complete
+ + not done IO/7 later
+ done, nil + reduced 12/7 later
normal
normal
complete
complete
not mentioned + reduced 16/7 later
+ done nil t reduced 6152
normal
normal
complete
complete
+
+
TABLE I (2A)
Authors No. Age Gra- Para- Abor- Gestation Blood Neurological features vida ty tus period pressure
(mmHg)
Naheedy et al., 1985 2 21 6 5 1 term 168/l 16 Aphasia, right hemiparesis; CSF = 140 mm
31 160/96
of water, radionuclear scan - left hemis- phere uptake
Headaches, blurred vision, right facial assy- metry
ours make a total of 23 cases of toxaemia in pregnancy in which CT scans were performed [l-9]. The ages ranged from 15 to 35 years, with a mean of 27 years. Ten out of the 20 cases were primigravida (50%). The gestational age ranged from 31 weeks to term (40 weeks); and two cases were post-pa&urn. The mean gestational age was 36 weeks. The blood pressures ranged between 140-225 mmHg systotic and 130 mmHg diastolic. In 56% (13 cases) of cases the
predominant symptom was visual, ranging from blurred vision to total blindness. Photophobia was seen in one case. Other symptoms included stupor or coma in 39%) hemiplegia or paresis in 30x, and headaches in 35% (six cases).
The CT findings were positive in all cases. Bilateral lesions were seen in all cases, the lesions being symme- trical in 19 cases (83%).
There were two main CT findings. In four cases high
51
TABLE I (2B)
CT findings
focal lesions
hypodensity haemorrhage
Follow-up CT Clinical
FXO”Wy
enhancement mass eff- ventricular time comment ect/brain size (...)
bilateral symmetry oedema
White matter of both hemispheres
Frontal and parietal lobes
Basal ganglia
Posterior temporal cor-
tex (left)
Parietal lobe
Frontal lobe
Cerebellar and occipital lobes
Hematoma, right parieto-occipital lobes, left frontal lobe
Occipital lobes +
Occipital lobes +
TABLE I (3A)
+
+
+
+
+ +
+
+
+
+
+
+
+
+
+
_
+
+
not done normal 9/l later
not done nil
done, nil nil
done, nil -
done +
not done +
done, nil
not done
normal
normal
reduced
reduced
reduced
IO/7 later
9/7 later
7-14 days later
7-14 days later
nil
marked complete improvement
partial reso- lution of
macular oedema
BP normal neuropatholgy unchanged
10/7 later
marked complete improvement
normal complete
normal complete
normal complete
not done
not done
+ reduced 5152 later complete reso- complete lution
_ normal 4152 later complete reso- complete lution
Authors No. Age Gra- Para- Abor- Gestation Blood Neurological features vida ty tus period pressure
(mmHg)
Lewis et al., 1988 1 32 3 2 1 33
2 35 2 0 1 36
Kolawole et al., 1989 1 31 1 0 0 38
2 22 1 0 0 39 3 33 3 2 0 36
4 - 2 1 0 40
attenuation areas corresponding to haemorrhage occurred in the basal ganglia, subependymal or intra- cerebral in type. In the remaining cases the hypodense regions predominated, involving the entire cerebral cor-
166/150
209/l 10
Stupor, blurred vision, pupils dilated and unre- sponsive
Headache, blurred vision, diplopia flacid para- plegia; CSF = 360 mm water with xantho- chromia
180/115 Pre-eclampsia, cardiac arrest, seizures at Caesarean section
irritability with slow responses _ Eclampsia: two convulsions, one during labour,
one 6 h after delivery
tex in five cases, whilst they were focal, but in the parietal lobe, in six cases, and in the occipital lobes in nine cases; two cases had mixed multifocal lesions. In these cases the white matter was more involved than the
Basal ganglia _ + + not done + normal 617 improvement angio - complete
poor tilling of termi- nal vessels
Diffuse & immediate, left frontal - 2/7, no oedema - 4/7, anterior & pos-
terior cerebral areas
+ + not mention- nil normal 44/l narrowing of vessels, partial
ed CT unchanged
Basal ganglia +
Bilateral, occipital _
Parietal, occipital regions - +
bilaterally
+ not done nil normal _ died
+ not done nil normal normal complete
+ not done ini- nil normal l/52 CT showed bilateral partial
tially later parieto-occipital en- hancement. Angio showed generalized narrowing of all ves- sels
positive 3152 CT showed bilateral
1 week later hypodense areas in
later the parietal or occi- pital lobes
_ + + _ + slightly re- 48 h normal complete
duced later
grey matter. A mass effect as evidenced by the oblitera- tion of the sulci and cisterns and/or reduction in the size of the ventricles was present in half of the cases.
In 16 cases, enhanced CT scans were not done or mentioned. In seven others, enhanced CT scans were done; however, no enhancement was used, except in our case where it was positive 1 week later.
Clinico-radiological correlations showed that all cases with occipital lobe hypodensities had visual symptoms. The three cases with lesions in the basal ganglia complained of blindness. All the cases with hemiplegia/hemiparesis also had corresponding lesions in the contralateral parietal lobe or internal capsule.
The follow-up showed that two had died; both were cases of haemorrhage. Full clinical recovery was present in 17 cases. Amongst this group repeat CT scans were normal in 14 cases, but still abnormal in two cases; and in one case it was not recorded. Four cases had partial clinical recovery; and in these two cases generalized vascular narrowings were demonstrated by angiogra- phy. In these two cases positive CT findings were persistent. No CT scans were available for the other two. The state of clinical recovery correlated well with the CT findings.
Discussion
Toxaemia of pregnancy is a syndrome of oedema, various neurological abnormalities, hypertension and proteinuria, usually during the third trimester of preg- nancy, often referred to as pre-eclampsia occurring in 5-10% of all pregnancies especially the primigravida [3]. However, when associated with convulsions, be- fore, during or after delivery, it is termed eclampsia, which occurs in 0.05% to 0.2% of all deliveries and is fatal in 13% of cases [lo].
At surgery, the dura of the toxaemic brains was tense, with a large volume of fluid escaping after the incision [ 111, and the cerebral convolutions were flat- tened [ 121. Bleeding punctate or massive with areas of softening are noted in 89 y0 of the eclamptic brains [ 121. At autopsy, it was noted that there was fibrinoid necro- sis of the vascular wall leading to focal oedema, soften- ing, thrombosis, rupture and haemorrhage [ 13,141.
The CT findings correllate well with the above surgi- co-pathological findings. Cerebral oedema is the com- monest finding in this review and is shown by regions of low attenuation coefficient mainly involving the white matter of the brain of any lobe, and is typical of vaso- genie cerebral oedema [ 151. The internal and external capsules may be affected [ 6,8,9]. In all cases the lesions
are usually bilateral and as shown in the review usually symmetrical. The bilaterality suggests a generalised aetiology. The CT patterns replicate those seen in stroke patients. The non-haemorrhagic low-attenuation lesions usually show complete resolution in follow-up CT studies. This is supported by the total clinical recovery of most patients. However, some of the low- density areas, especially those extending into the grey matter, later turn out to be areas of infarction, hence the non-resolution of the symptoms and CT findings in some cases.
The second commonest finding relates to oedema causing increased intracranial pressure, which is evi- denced by effacement of the sulci and cisterns, and dimunition of the ventricular size.
Visual disturbances are not infrequent in toxaemia of pregnancy. Blindness occurs in l-3% of patients with eclampsia and is rare in pre-eclampsia [ 51. However, in this review, 56% of cases (13 cases) had visual dis- turbances, mainly blurred vision. Blindness occurred in five patients, two with eclampsia, the other three with pre-eclampsia; photophobia and paralysis of the occu- lar muscles also occurred.
The possible causes of blindness range from retinal lesions such as oedema, haemorrhage, detachment of the retina, as well as spasm or thrombosis of the retinal vessels, to optic nerve disturbance, central lesions such as intracranial venous thrombosis and central distur- bance of the visual center in the occipital lobes by oedema or haemorrhage [ 51. Oedema is the most com- mon cause according to this review.
White matter oedema in the occipital lobe (visual radiation) was present in 11 out of a total of 23 cases (48%) that had a CT examination, eight of which were bilateral. All cases with occipital lobe oedema which was associated with CT changes had loss of visual acuity. It is hypothesised that the increased frequency of occipital lobe oedema may be due to gravitation of fluid to the occiput in the supine position [ 21.
Cortical blindness resulting from oedema disappears with the resolution of the oedema, and usually is transient.
Haemorrhage, massive or punctate, has been report- ed in eclamptic brains [ 121. The findings in one of our cases represents frank haemorrhage (Fig. l), whilst Fig. 3 in another case typifies petechial haemorrhages within the cerebral mantle.
Vasospasm is the ‘sine qua non’ of toxaemia of pregnancy. This has been demonstrated by angiography [8], and is shown in two cases in which angiography was performed in this review. Vasospasm has been
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
Beck DW, Menezes AH. Intracranial hemorrhage in a patient with eclampsia. JAMA 1981; 246: 1442-1443. Beeson JH, Duda EE. Computed axial tomography scan demon- stration of cerebral edema in eclampsia preceded by blindness. Obstet Gynaecol 1982; 60: 529-532. Colosimo C, Fileni A, Moschini M, Guerrini P. CT findings in eclampsia. Neuroradiology 1985; 27: 313-317. Gaitz JP, Bamford CR. Unusual computed tomographic scan in eclampsia. Arch Neurol 1982; 39: 66. Grimes DA, Ekbladh LE, McCartney WH. Cortical blindness in pre-eclampsia. Int J Gynecol Obstet 1980; 17: 601-603. Kirby JC, Jaindl JJ. Cerebral CT findings in toxemia of pregnan- cy. Radiology 1984; 151: 114. Lou SPC, Chan FL, Yu YL, Woo E, Huang CY. Cortical blind- ness in toxaemia of pregnancy: findings on computed tomogra- phy. Br J Radio1 1987; 60: 347-349. Lewis LK, Hinshaw DB, Will AD, Hasso AN, Thompson JR. CT and angiographic correlation of severe neurological disease in toxemia of pregnancy. Neuroradiology 1988; 30: 59-64. Naheedy MH, Biller J, Schiffer M, Azar-Kia B, Gianopoulous J, Zarandy S. Toxemia of pregnancy: cerebral CT findings. J Comput Assist Tomogr 1985; 9: 497-501. Sibai BM, McCubbin JH, Anderson GD, Lipshitz J, Dilts PV. Eclampsia I: observations from 67 recent cases. Obstet Gynecol 1981; 58: 609-613. Chesley LC. Hypertensive disorders in pregnancy. New York: Appleton-Century-Crofts, 1978. Schmorl G. Zur Lehre von der Eklampsie. Arch Gynecol 1902; 65: 504. Govan AD. The Histology of eclamptic lesions. J Clin Path01 1976; 29: 63-69. Sheehan HL, Lynch JB. Pathology of toxemia of pregnancy. Baltimore: Williams & Wilkins, 1973; 524-584. Drayer BP, Rosenbaum AE. Brain edema defined by cranial computed tomography. J Comput Assist Tomogr 1979; 3: 317-323. Donaldson JO. Neurology of pregnancy. Philadelphia: Saunders, 1978. Landesman R, Douglas RG, Holze E. The bulbar conjunctival vascular bed in toxemias of pregnancy. Am J Obstet Gynecol 1954; 68: 170-183.
53
directly observed in the nail beds, conjunctivae and retinal vessels of eclamptics [ 16,171. Studies have also shown in patients with eclampsia a 50% increase in vascular resistance and a 20% decreased utilisation of oxygen by the brain as a result of vasospasm [ 181. It was this increase in peripheral vascular resistance, a known phenomenon in hypertension, which led to the conclusion that the neurological manifestations of eclampsia were the sequalae of hypertension [ 161. And it is significant to note that the rapid rate at which the blood pressure changed rather than the absolute systolic and diastolic values, is the primary point of importance in hypertensive encephalopathy [4]. Our cases give credence to this view.
