|Year : 2016 | Volume
| Issue : 2 | Page : 101-103
Post dural puncture headache treated with steroids progressing to cerebral venous sinus thrombosis in a postpartum female: A case report
Ashok Jadon, Neelam Sinha, Priyanka Jain
Department of Anaesthesia and Pain Relief Service, Tata Motors Hospital, Jamshedpur, Jharkhand, India
|Date of Web Publication||7-Oct-2016|
Dr. Ashok Jadon
Duplex-63, Vijaya Heritage Phase-6, Kadma, Jamshedpur - 831 005, Jharkhand
Source of Support: None, Conflict of Interest: None
Presentation of Cerebral venous sinus thrombosis (CVST) is clinically confusing. We present a case of 31 years an old postpartum woman who was treated with intravenous hydrocortisone for post dural puncture headache (PDPH) and developed CVST. We aim to present the diagnostic difficulties of such cases and the potential role of dural puncture and corticosteroids in the occurrence of CVST.
Keywords: Central venous sinus thrombosis, corticosteroids, hydrocortisone, post-dural puncture headache, spinal anesthesia
|How to cite this article:|
Jadon A, Sinha N, Jain P. Post dural puncture headache treated with steroids progressing to cerebral venous sinus thrombosis in a postpartum female: A case report. J Obstet Anaesth Crit Care 2016;6:101-3
|How to cite this URL:|
Jadon A, Sinha N, Jain P. Post dural puncture headache treated with steroids progressing to cerebral venous sinus thrombosis in a postpartum female: A case report. J Obstet Anaesth Crit Care [serial online] 2016 [cited 2021 May 10];6:101-3. Available from: https://www.joacc.com/text.asp?2016/6/2/101/191595
| Introduction|| |
Cerebral venous sinus thrombosis (CVST) is an infrequent condition associated with a variety of risk factors such as pregnancy, oral contraceptives, hypercholesterolemia, and hereditary thrombophilia. Rarely, CVST may present with post-dural puncture headache (PDPH) after epidural or spinal anesthesia. The association of dural puncture and possible role of steroids while being used for PDPH to cause CVST are not discussed elsewhere. Here, we present the case of a postpartum female who had PDPH following caesarean section under spinal anesthesia and treated with intravenous hydrocortisone for PDPH, following which she developed CVST.
| Case Report|| |
A 31-year-old multigravida with hypothyroidism was admitted for elective caesarean section under spinal anaesthesia at 38 weeks of gestation. On the 3rd postoperative day, she complained of severe fronto-occipital headache, which was aggravated in the sitting position and improved on lying down. A diagnosis of PDPH was made and she was advised plenty of oral fluids along with 1 g intravenous paracetamol and 100 mg intravenous hydrocortisone thrice daily. The pattern of the headache changed over the next day and was persistent even in the supine position. The neurology team was consulted and a computed tomography (CT) of the head was advised. However, the patient's symptoms improved over the day and CT scan was deferred due to patient's unwillingness. She was discharged on her request on the 6th postoperative day. On the 13th post-operative day, she was brought to the emergency room with complaints of episodic deviation of the angle of mouth, slurring of speech, blurred vision, headache, vomiting, and restlessness. She mentioned that her headache was on and off since discharge, for which she took an over the counter combination of paracetamol (500 mg) + aciclofenac (100 mg) and tizanidine 2 mg 3–4 tablets per day on her own. On presentation, she was conscious and oriented. Her vital signs were stable except for high blood pressure (150/90 mmHg). Examination of the nervous system was unremarkable and fundus examination showed no papilledema. A CT scan of the brain was done, which showed cerebral edema in the left fronto-parital region [Figure 1]. Meanwhile, the patient had one episode of facial twitching and complained of severe headache. Magnetic resonance imaging (MRI) of the brain was done for further evaluation, which showed multiple venous infarcts in the left fronto-parietal region. A MR venography showed irregular narrowing in the straight sinus, the left sigmoid sinus, and at the origin of the left transverse sinus, suggesting venous sinus thrombosis [Figure 2]. However, the sinuses on the right were normal. MR angiography of the brain, on the other hand, revealed atheromatous narrowing of bilateral anterior cerebral artery and M2 and M3 segments of the right middle cerebral artery. Blood investigations revealed dyslipidemia (high serum cholesterol, triglycerides and low-density lipoprotein cholesterol). Thrombophilia screen was negative and the patient denied use of a contraception. She was anticoagulated initially with heparin and then with warfarin. Heparin was tapered off once the target international normalized ratio reached a level of 2–3. She was also given fenofibrate 160 g for dyslipidemia. Her symptoms improved over the next 4–5 days, and she was completely asymptomatic and discharged from the hospital after 10 days. She is presently on follow-up for more than 5 months, and has had no further recurrence or new symptoms.
|Figure 1: Computed tomography scan of the brain showing (arrow) cerebral edema in the left frontoparietal region|
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|Figure 2: Magnetic resonance venography showed irregular narrowing in the straight sinus, the left sigmoid sinus, and at the origin of the left transverse sinus (arrows), suggesting venous sinus thrombosis|
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| Discussion|| |
CVST is an uncommon complication of pregnancy. Factors predisposing to this condition include the hypercoagulable state of pregnancy, oral contraceptives, and hereditary conditions such as factor V Leiden mutation, prothrombin gene mutation, and deficiency of protein C, protein S, and antithrombin. The present case of a previously asymptomatic patient with CVST following lumbar puncture and treatment with corticosteroids raises the question of their causative role in its development.
Dural puncture is a rare but well-documented cause of CVST., The exact mechanism is unknown, however, the possible venous dilation and stasis that follow intracranial hypotension (especially in patients with prothrombotic states) probably trigger the thrombotic process., Our patient also had predisposing conditions such as pregnancy and a probable procoagulant state, as suggested by dyslipidemia and concomitant atherosclerotic narrowing of intracerebral arteries. With the development of sinus thrombosis, cerebrospinal fluid (CSF) resorption decreases, thereby increasing the intracranial pressure. This change in CSF pressure probably explains the change in the character of the headache. She initially complained of postural headache following spinal anesthesia, which was probably caused by dural puncture. However, the constant headache and lack of postural variation with the appearance of new symptoms (seizures, facial weakness, blurred vision, vomiting) on readmission were likely produced by venous sinus thrombosis. Therefore, any PDPH that becomes constant or loses its positional character should raise the suspicion of a sinister complication such as CVST and warrant further investigation.
Another possible entity that needs further discussion is the role of corticosteroids in the development of CVST. There are reports that suggest corticosteroids to be a cause of venous sinus thrombosis, particularly in the presence of other risk factors.,, The occasional occurrence of venous thrombosis in Cushing's disease may suggest that high levels of corticosteroids may themselves be thrombogenic. Intravenous hydrocortisone have been used to treat PDPH, and we are also using it for many years with good success. However, the role of hydrocortisone to cause CVST in presence of dural puncture needs further research.
| Conclusion|| |
In the present case, the role of intravenous corticosteroids could be one of the causes for the occurrence of venous thrombosis in presence of multiple risk factors. A low pressure headache that loses its positional character should alert the treating physician that the patient may have developed CVST. In such cases, prompt MR venography should be done for early diagnosis, and anticoagulation therapy should be started because this may prevent neurological deterioration.
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Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2]