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* From the Departments of Anesthesiology, CHU Brugmann Hospital, Brussels;
Neurology, CUB Erasme Hospital, Brussels;
Neuroradiology, CUB Erasme Hospital, Brussels; and
Anesthesiology, University Hospital Centre, Charleroi, Belgium.
Address correspondence to: Dr. Yota Kapessidou, Department of Anesthesiology, CHU Brugmann Hospital, 4 Place Van Gehuchten, 1020 Brussels, Belgium. Phone: +32-2-477-39-96; or +32-2-650-95-52; Fax: +32-2-477-33-45; E-mail: pkapessi{at}ulb.ac.be
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Abstract |
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Clinical features: A previously healthy 21-yr-old, primiparous, preeclamptic parturient was admitted to the hospital at 37 weeks gestation for uterine contractions. Before pregnancy she was taking no medication other than oral contraceptives and was a non-smoker. Spinal analgesia was established on the first attempt at 8 cm of cervical dilation, in the setting of rapid progression of labour. Following an uneventful delivery, on the third day postpartum, the patient experienced gradual onset of an atypical headache with unclear postural character, followed by focal neurological signs five days later. Emergency neuroimaging revealed direct evidence of thrombosis in the posterior sagittal venous sinus. Anticoagulation was initiated with iv heparin (500 UI·kg–1·day–1). The patient’s headache decreased progressively and full motor recovery was noted by day 14 postpartum. After 24 days, the patient was discharged without any neurological disability. Common inherited thrombophilic dispositions were absent, with the exception of a decrease in protein S level.
Conclusion: Central venous thrombosis, while rare, is a recognized cause of puerperium stroke. The present case highlights the importance of considering the diagnosis in the presence of postpartum atypical headache following spinal anesthesia/analgesia. Early intervention with systemic heparinization is critical when the diagnosis is confirmed.
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Introduction |
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In occidental countries, CVT is an unusual complication of pregnancy with an incidence of 1:10,000 to 1:20,000 deliveries, mainly observed during the postpartum period, and represents the main cause of puerperium stroke.1,4,5 Some case reports have associated postpartum CVT with accidental postdural puncture due to epidural analgesia.6–9 Until now, only one case report mentions CVT after spinal anesthesia for Cesarean delivery.10 We report a case of sagittal sinus thrombosis occurring after spinal analgesia for labour. The diagnosis was initially misled due to the atypical nature of the headache. Institutional approval was obtained for the publication of the personal health information in this report.
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Acceleration of labour with oxytocin was initiated 12 hr after spontaneous rupture of membranes. Her cervical dilation was 8 cm when regional analgesia was requested, three hours later. The patient did not receive any antihypertensive medication until this time, in the absence of progressive hypertension.
Considering the rapid progression of labour, a spinal analgesia technique was chosen and performed successfully on the first attempt under aseptic conditions. A 27G Whitacre spinal needle (Becton Dickinson SA, Erembodegem, Belgium) was introduced into the L3–L4 interspace and 0.5 mL of 0.5% hyperbaric bupivacaine mixed with 2.5 µg sufentanil was administered. No parenteral analgesics were added. There was no hemodynamic compromise and the patient spontaneously delivered a healthy infant 30 min later. Apgar scores were 9/10/10.
During the next three days, the patient’s arterial blood pressure varied between 120/60 mmHg and 140/90 mmHg. On the third day postpartum, the patient experienced the gradual onset of a dull throbbing frontal headache and neck pain, which were not completely relieved by recumbency. Pain was accentuated on day five postpartum, associated with dizziness in the upright position and slight photophobia. The patient was apyrexial, normotensive and had no abnormal neurological signs. Interpretation of the headache was challenging because of the unclear postural character. The diagnosis of postdural puncture headache (PDPH) was considered doubtful.
Treatment with oral analgesics, caffeine, rehydration and rest relieved the headache over the ensuing 48 hr. However, on the eighth postpartum day, the patient’s headache returned with similar intensity and localization. She developed paresthesia progressing from the left hand to the face over the distribution of the facial nerve, associated with acute left hemiparesis, blurred vision, and somnolence. The patient was not nauseated and she remained apyrexial. Fundoscopic examination revealed mild bilateral papilledema.
Cranial computed tomography (CCT) after contrast injection, revealed direct signs (empty triangle sign) of thrombosis in the posterior sagittal venous sinus, and secondary cortical venous infarctions into the left frontal and the right posterior parietal territories. Brain magnetic resonance imaging (MRI) confirmed these findings (Figure
).
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On day 11 postpartum, neurological evolution was marked by the appearance of Bravais-Jacksonian type focal seizures. Epilepsy was controlled by the addition of carbamazepine 300 mg po every eight hours. The patient’s headache resided gradually thereafter, to the point where it was managed by paracetamol on a prn basis. Full motor recovery was gained on day 14, despite persisting slow cortical activity on the electro-encephalogram (EEG). After 24 days, the patient was discharged without any neurological deficit. Of note, an EEG performed eight weeks after onset was normal. The patient was advised to avoid oral contraceptives and continue her antiepileptic medications and oral anticoagulants until the three-month follow-up visit.
During hospital stay, a complete screen was performed to exclude hereditary thrombophilia. Common inherited thrombophilic dispositions such as the factor V Leiden mutation, and the 20210 G to A mutation of the prothrombin gene were absent. Antithrombin III and protein C levels were normal. However, her protein S level was 48% of the normal value. Neither hyperhomocysteinemia nor any anticardiolipin and antiphospholipid antibodies were detected.
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Discussion |
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In current practice, spinal anesthesia is rarely identified as a cause of PDPH. The incidence of spinal headache is decreasing with improved needle technology, although data on low-frequency events such as PDPH are difficult to ascertain through randomized clinical trials because of constraints of sample size.14
In this patient, the diagnosis of spinal headache was doubtful. The puncture of the subarachnoid space was uneventful and no postdural worsening of headache occurred.
Also, preeclampsia-related headache was excluded since the patient remained normotensive after delivery. Conventional analgesic treatment and caffeine, during the next 48 hr, relieved the patient’s symptoms, but left the diagnosis in doubt. No blood patch was attempted, and the patient was kept under routine clinical follow up, without further investigations. The diagnosis was established on day eight postpartum with the appearance of a focal neurological deficit associated with seizure activity, and a diagnostic MRI.
Another reported case of CVT has been observed during the first week after normal delivery.6 Headache is the most frequent symptom encountered, and tends to be unilateral, limited to the forehead, temple, or occiput, with subacute onset.2,10 However, it can be particularly misleading when it simulates conditions such as PDPH, subarachnoid hemorrhage (thunder-clap headache) or even migraine.11,15 Subsequent neurological signs vary from focal deficits and Jacksonian type seizures, as experienced by our patient and described in 76% of peripartum CVT, to coma.1,16 Therefore, in the absence of seizures or other neurological signs in the puerperium, it is difficult to distinguish CVT-induced headache from spinal headache associated with regional anesthesia.
The diagnosis of sagittal sinus thrombosis was disclosed by radiological investigation. Diagnosis of CVT is based on neuroimaging. Cranial computed tomography is usually the first technique performed in this setting, but findings are normal in 25 to 30% of patients. The main value of CCT is to exclude hemorrhagic stroke. Direct signs of CVT, rarely seen on unenhanced CCT, include the cord sign and the dense triangle sign. However, after contrast injection, the appearance of the empty triangle or delta sign (25–30% of cases), as observed in our patient, confirms the diagnosis.1 Magnetic resonance imaging and magnetic resonance angiography are considered the most sensitive diagnostic tests, disclosing the diagnosis in 90% of cases.
Treatment with heparin must begin immediately upon confirmation of the diagnosis, even in the presence of a hemorrhagic infarct.1,11 Intravenous anticoagulation should be continued until remission of the acute stage of the disease, i.e., normal consciousness, improvement of headache and resolution of focal neurological deficits. Subsequent therapy should be converted from parenteral to oral anticoagulation for a period of three to six months. Patients with hereditary thrombophilia should be treated for a longer period (6–12 months).
Women who have suffered from a CVT while taking oral contraceptives should be counselled about alternative methods of contraception.1 Long-term follow-up of patients who have experienced pregnancy-related CVT is important, since recurrence, although rare, is possible within the first 12 months.1,19 Subsequent pregnancy is not contraindicated, although prophylactic low-dose anticoagulation should be considered, while recognizing that the risk-benefits of this therapy during pregnancy have not been established. Counselling about symptoms suggestive of CVT recurrence and neurological surveillance during pregnancy are strongly recommended. Regional anesthesia or analgesia for labour or Cesarean delivery in women with a history of CVT history is not contraindicated, while prophylactic anticoagulation is recommended in the postpartum period.1
While the pathogenesis of puerperal CVT has not been clearly elucidated, it may be related to three aspects characterizing Virchow’s classic triad: 1) stasis of intracerebral blood flow (especially in the valveless sagittal sinus); 2) vascular endothelial damage due to fluctuations in intracranial pressure (especially during delivery); and 3) the hypercoagulable state associated with dehydration and physiologic anemia of pregnancy. 20
The complex etiology may be associated with the following factors: hereditary thrombophilia, anticardiolipin antibodies, hyperhomocysteinemia, Cesarean delivery, pregnancy-related hypertension, and the use of oral contraceptives which may present a risk factor in 10% of cases.1,11,21,22 Common inherited dispositions of thrombophilia include mainly the factor V Leiden mutation (15–17% of cases) and the prothrombin-gene-mutation 20210GA (10–12% of cases), whereas antithrombin III-, protein C- and protein S-deficiency are found in only 2–6% of cases.1 In this patient, preeclampsia, decrease in protein S (even though commonly observed during pregnancy), and the use of oral contraceptives, were possible CVT-triggering factors.23
Implications of spinal anesthesia in the pathogenesis of this entity were considered in two previous case reports, but remain controversial. One report by Schou et al.,24 described the appearance of postoperative sagittal sinus thrombosis after spinal anesthesia for hemorrhoidectomy in a 35-yr-old man. Suggested mechanisms included chemical arachnoiditis and changes in intracranial pressure. A second report described a case of cortical venous thrombosis after spinal anesthesia for Cesarean delivery. Direct implications of the anesthetic technique were considered doubtful.10
Neurological complications reported after spinal anesthesia (i.e., headache and subdural hematoma) have been related to cerebrospinal fluid (CSF) leakage, leading to intracranial hypotension with subsequent venodilatation and venous stasis.25 In our case, considering the rapid progression of labour, a spinal analgesia technique was chosen and performed uneventfully. No significant hemodynamic disorders were observed after anesthesia or during delivery. Furthermore, the postpartum headache was atypical, with an unclear postural character. Therefore, leakage of CSF and important changes in intracranial pressure seem unlikely contributing factors. However, a cause-effect association is difficult to demonstrate in rare events such as CVT concomitant with spinal anesthesia, and the question is still under debate.
In summary, the present case highlights the importance of establishing a comprehensive differential diagnosis in the presence of postpartum atypical headache following spinal anesthesia/analgesia. The patient should remain under clinical follow-up and the diagnosis of CVT has to be considered. Early intervention with systemic heparinization is critical when this diagnosis is confirmed.
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2 de Bruijn SF, de Haan RJ, Stam J. Clinical features and prognostic factors of cerebral venous and sinus thrombosis in a prospective series of 59 patients. For The Cerebral Venous Sinus Thrombosis Study Group. J Neurol Neurosurg Psychiatry 2001; 70: 105–108.
3 Srinivasan K. Cerebral venous and arterial thrombosis in pregnancy and puerperium. A study of 135 patients. Angiology 1983; 34: 731–46.
4 Francois P, Fabre M, Lioret E, Jan M. Vascular cerebral thrombosis during pregnancy and post-partum. Neurochirurgie 2000; 46: 105–9.[Medline]
5 Salonen Ros H, Lichtenstein P, Bellocco R, Petersson G, Cnattingius S. Increased risks of circulatory diseases in late pregnancy and puerperium. Epidemiology 2001; 12: 456–60.[Medline]
6 Borum SE, Naul LG, McLeskey CH. Postpartum dural venous sinus thrombosis after postdural puncture headache and epidural blood patch. Anesthesiology 1997; 86: 487–90.[Medline]
7 Stocks GM, Wooller DJ, Young JM, Fernando R. Postpartum headache after epidural blood patch: investigation and diagnosis. Br J Anaesth 2000; 84: 407–10.
8 Ravindran RS, Zandstra GC, Viegas OJ. Postpartum headache following regional analgesia; a symptom of cerebral venous thrombosis. Can J Anaesth 1989; 36: 705–7.
9 Chiu CL, Chan YK. Which and what headache were we treating? Epidural blood patch for atypical headache following obstetric epidural anaesthesia. Int J Obstet Anesth 2000; 9: 273–5.[Medline]
10 Siegle JH, Dewan DM, James FM 3rd. Cerebral infarction following spinal anesthesia for cesarean section. Anesth Analg 1982; 61: 390–2.
11 Bousser MG. Cerebral venous thrombosis: diagnosis and management. J Neurol 2000; 247: 252–8.[Medline]
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14 Halpern S, Preston R. Postdural puncture headache and spinal needle design. Metaanalyses. Anesthesiology 1994; 81: 1376–83.[Medline]
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17 Isensee C, Reul J, Thron A. Magnetic resonance imaging of thrombosed dural sinuses. Stroke 1994; 25: 29–34.[Abstract]
18 Vogl TJ, Bergman C, Villringer A, Einhaupl K, Lissner J, Felix R. Dural sinus thrombosis: value of venous MR angiography for diagnosis and follow-up. AJR Am J Roentgenol 1994; 162: 1191–8.
19 Preter M, Tzourio C, Ameri A, Bousser MG. Long-term prognosis in cerebral venous thrombosis. Follow-up of 77 patients. Stroke 1996; 27: 243–6.
20 Younker D, Jones MM, Adenwala J, Citrin A, Joyce TH 3rd. Maternal cortical vein thrombosis and the obstetric anesthesiologist. Anesth Analg 1986; 65: 1007–12.
21 Lanska DJ, Kryscio RJ. Risk factors for peripartum and postpartum stroke and intracranial venous thrombosis. Stroke 2000; 31: 1274–82.
22 de Bruijn SF, Stam J, Koopman MM, Vandenbroucke JP. Case-control study of risk of cerebral sinus thrombosis in oral contraceptive users and in carriers of hereditary prothrombotic conditions. The Cerebral Venous Sinus Thrombosis Study Group. BMJ 1998; 316: 589–92.
23 Faught W, Garner P, Jones G, Ivey B. Changes in protein C and protein S levels in normal pregnancy. Am J Obstet Gynecol 1995; 172(1 Pt 1): 147–50.[Medline]
24 Schou J, Scherb M. Postoperative sagittal sinus thrombosis after spinal anesthesia. Anesth Analg 1986; 65: 541–2.
25 De Tommaso O, Caporuscio A, Tagariello V. Neurological complications following central neuraxial blocks: are there predictive factors? Eur J Anaesthesiol 2002; 19: 705–16.[Medline]
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