We present the case of a 75-year-old woman in good health, with the exception of mild arterial hypertension, for which she was being treated with antihypertensive drugs. On entering the emergency medicine unit, the patient presented with acute onset of nonfluent aphasia and code stroke protocol was followed. The subject’s past medical history was negative, except for the administration of a second dose of Pfizer-BioNTech COVID-19 vaccine (Fig. 1) 10 days before symptom onset.
In fact, two days after receiving the second dose the patient began to experience a persistent and drug-resistant headache, and focal neurological symptoms appeared approximately nine days after the aforementioned headache. In the emergency room a computed tomography (CT) scan of the head was performed with evidence of intraparenchymal hemorrhage in the left occipital lobe associated with perilesional vasogenic edema and further hemorrhagic lesions in the ipsilateral subcortical temporo-occipital site, with a round morphology.
The neurological physical examination showed nonfluent aphasia, but no sensory-motor deficits in the four limbs. CT images of the brain were sent to the on-call neurosurgeon who recommended computed tomography angiography (CTA) of intracranial circulation and antiedema therapy with mannitol and steroids.
After about 12 hours a brain CT scan was performed, which showed a significant deterioration, with numerical and dimensional increases in the hemorrhagic components of the temporal, occipital, and left parietal lobes with marked signs of perilesional edema. The CT image was also characterized by widespread hypovisualization of the cortical folds in the left hemispheric area due to the presence of edema, together with marked compression phenomena affecting the anterior and posterior horn and the trine of the left ventricular system. In the left frontoparietal region there was a subdural hematoma (SDH) with a maximum thickness of 3 mm.
The CTA showed evidence of extensive opacification defects affecting the left transverse sinus, the left sigmoid sinus, and the lower portion of the petrous rock of the left internal jugular vein, compatible with acute cerebral venous thrombosis (CVT). In addition, a focal filling defect of similar significance was also found in the right transverse sinus.
The patient was hospitalized in the neurology unit, where the following was prescribed: antiepileptic therapy with 500 mg of levetiracetam twice a day; antiedema therapy with 50 cc of mannitol four times a day for four days and subsequently 100 cc three times a day until suspension. In addition, anticoagulant therapy with enoxaparin was administered at a dosage of 6000 IU in the morning and 8000 IU in the evening.
Magnetic resonance imaging (MRI) of the brain revealed an extensive left temporo-parieto-occipital edema, corresponding to an extensive area of intraparenchymal bleeding, and confirming evidence of thrombosis of the left transverse and sigmoid sinuses of the proximal tract of the left internal jugular.
In the days that followed, the patient underwent a comprehensive series of laboratory and instrumental examinations, aimed at finding the etiology of cerebral thrombosis. Routine laboratory tests consisted of a complete blood count, coagulation screening including factors II and V Leiden, checks for the presence of neoplastic markers, and measurements of homocysteine, ferritin, beta-2-microglobulin and immunoglobin levels. There was an increase of the D-dimer (6175 ng/ml and 2885 ng/ml on the 4th and 9th day of hospitalization respectively), while the remaining parameters were within normal range, including the platelet count (Table 1).
Table 1
Routine laboratory tests performed during hospitalization.
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18/05/2021
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20/05/21
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21/05/21
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22/05/21
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24/05/21
|
27/05/21
|
31/05/21
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Leukocytes
(thousand/mm3)
|
7.6
|
15.2
|
13.1
|
8.7
|
7.9
|
6.7
|
4.9
|
Erythrocytes (million/mm3)
|
4.23
|
4.20
|
4.22
|
4.2
|
4.34
|
4.11
|
3.95
|
Hemoglobin (gr/dl)
|
13.1
|
12.9
|
12.7
|
12.8
|
13.4
|
12.4
|
12.0
|
Hematocrit (%)
|
38.7
|
37.4
|
37.8
|
37.8
|
38.3
|
37.7
|
36.2
|
Platelets (thousand/mm3)
|
256
|
246
|
205
|
209
|
212
|
235
|
270
|
I.N.R.
|
0.96
|
/
|
/
|
/
|
1.10
|
1.08
|
1.05
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PTT RATIO
|
0.80
|
/
|
/
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/
|
0.86
|
0.81
|
0.91
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Fibrinogen (mg/dl)
|
328
|
/
|
/
|
/
|
273
|
370
|
384
|
A total body CT excluded neoplastic lesions, but a pulmonary thromboembolism with filling defects in both lower lobes was found. For this reason, a venous doppler examination of the lower limbs was carried out, with evidence of voluminous deep venous thrombosis (DVT) of a peroneal vessel of the left lower limb, extending to the distal lower third of the leg up to the tibial-peroneal trunk.
During hospitalization the patient presented progressive improvement of the language impairment with regard to anomic aphasia and semantic deficit. A subsequent brain CT revealed initial phenomena of hemoglobin degradation and reduction of blood hyperdensity on the left temporo-parietal intraparenchymal hemorrhagic focus. A marked edema and hypodensity area from hypovascularization of the thrombotic area persisted.
The patient was discharged after 15 days of recovery. Two weeks after discharge another brain CT showed a complete resorption of the hemorrhagic areas, and a CTA showed post embolic rehabilitation of the petrous tract of the internal jugular vein, and persisting stable filling defects from subtotal thrombosis affecting the transverse and sigmoid sinus. In addition, a Doppler examination of the lower limbs showed complete resolution of the venous thrombosis. The patient’s therapy was changed from subcutaneous enoxaparin to warfarin, adjusted to obtain a correct PT/INR range.