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Journal of Obstrectic Anaesthesia and Critical Care
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 Table of Contents  
CASE REPORT
Year : 2016  |  Volume : 6  |  Issue : 2  |  Page : 95-97

Postpartum cortical venous thrombosis: An unusual presentation of postdural puncture headache


Department of Anesthesiology, University of Texas Health Science Center, Lyndon B. Johnson General Hospital, Houston, TX, USA

Date of Web Publication7-Oct-2016

Correspondence Address:
Dr. Opal Raj
Department of Anesthesiology, University of Texas Health Science Center, 6431 Fannin St. MSB 5.196, Houston, TX 77030
USA
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2249-4472.191603

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  Abstract 

Headache is a common occurrence during pregnancy. A postural headache is invariably considered to be a postdural puncture headache in patients who receive neuraxial anesthesia with or without obvious or incidental dural puncture. Cerebral venous thrombosis (CVT) is rare in pregnancy and in the postpartum period, with an incidence of 1:10,000–1:25,000. Pregnancy-induced changes in coagulation result in a hypercoagulable state, which may naturally reduce the incidence of postpartum hemorrhage, but may also increase the risk of CVT. Postpartum headache being frequently encountered may complicate the diagnosis of CVT. We report a case of a woman who developed a postpartum CVT after an accidental wet tap and intrathecal catheter placement during labor.

Keywords: Cortical venous thrombosis, epidural complications, postdural puncture headache


How to cite this article:
Raj O, Rupasinghe M. Postpartum cortical venous thrombosis: An unusual presentation of postdural puncture headache. J Obstet Anaesth Crit Care 2016;6:95-7

How to cite this URL:
Raj O, Rupasinghe M. Postpartum cortical venous thrombosis: An unusual presentation of postdural puncture headache. J Obstet Anaesth Crit Care [serial online] 2016 [cited 2019 Dec 10];6:95-7. Available from: http://www.joacc.com/text.asp?2016/6/2/95/191603


  Introduction Top


Headaches are frequently encountered in the labor and delivery ward and may be misdiagnosed as a postdural puncture headache (PDPH) in patients who receive neuraxial anesthesia. There are rare, but serious causes of headaches in the postpartum period that should be on the horizon when working up a patient. We report a case of a woman who developed a postpartum cortical venous thrombosis (CVT) after an accidental wet tap and intrathecal catheter placement during labor. CVT is rare in pregnancy and in the postpartum period, with an incidence of 1:10,000–1:25,000, but has serious repercussions such as seizure and rarely death that mandate it be on the differential diagnosis. Pregnancy may induce changes in the coagulation system resulting in a hypercoagulable state, although it is helpful in reducing postpartum hemorrhage, it may also increase the risk of CVT.


  Case Report Top


A 17-year-old female G1P0 with a past medical history of sickle cell trait and obesity (body mass index of 40) arrived to triage with the complaints of vaginal spotting. She presented at approximately 34 weeks' gestational age with a quickly progressing cervical examination. She was admitted to the labor and delivery ward for observation of preterm labor and administration of steroids. The patient began to have progressively worsening contractions and requested an epidural for pain relief. An epidural was attempted by the resident anesthesiologist and attending anesthesiologist. After much struggle, an inadvertent dural puncture occurred followed by an intrathecal catheter placement as per the hospital protocol. The patient had an uncomplicated vaginal delivery approximately 3 h later and the intrathecal catheter was left in situ for 24 h.

Twenty-four hours after the delivery, the patient complained of severe neck pain and positional headache correlating with PDPH. She was offered an epidural blood patch (EBP) at this time, but refused preferring medical management instead. She was hydrated and treated with analgesics during the course of her hospital admission. Forty-eight hours after the delivery, the patient reported that her symptoms had improved with this regimen. She denied nausea, vomiting, photophobia, and had no notable neurologic deficits upon discharge. She was advised to return to the emergency department if symptoms worsened.

Later that day after being discharged from the hospital, she developed a focal left upper extremity seizure that progressed to a generalized tonic-clonic seizure. A postictal state lasting approximately 30 min ensued with unresolving left-sided weakness of her upper and lower extremities. She was taken to a nearby hospital where she experienced two more focal seizures that were treated with anticonvulsants and benzodiazepines. Her blood pressure on admission was elevated and treated with beta-blockers and magnesium. After resolution of the seizures, she continued to have left-sided hemiparesis and left-sided facial droop. She was then transferred to a tertiary care center for a higher level of care.

On admission, she was given a Glasgow coma score of 15 and continued to have weakness in the left upper and lower extremities. She also had mild slurring of her words along with left-sided facial droop. Hematology workup for vasculitis, anti-phospholipid syndrome, lupus anticoagulant, prothrombin mutation, factor V Leiden mutation, and anti-thrombin III deficiency returned negative. However, she tested positive for sickle cell trait as expected along with an elevated factor VIII level.

The severity of her clinical presentation and the resulting magnetic resonance imaging (MRI) led to the immediate diagnosis of CVT [Figure 1]. She was treated with heparin and eventually transitioned to therapeutic warfarin. Eight days after the wet tap, she was transferred to inpatient rehabilitation and shortly discharged thereafter exceeding all goals in physical, occupational, and speech therapy.
Figure 1: Magnetic resonance imaging brain without contrast: there is a large area of diffusion restriction within the high right parietal region with increased signal on diffusion-weighted imaging and corresponding decreased signal on apparent diffusion coefficient map. Abnormal fluid-attenuated inversion recovery signal is noted in the same distribution. There are multiple punctate foci of hypointensity in this region on gradient echo imaging, suggestive of the presence of abnormal blood products. On review, appearances are felt most likely to represent evidence for cortical venous thrombosis affecting the right greater than the left motor cortex

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  Discussion Top


Headache may represent a wide differential during the peripartum period. This may include migraine or tension headache, pre-eclampsia, dehydration, PDPH, subarachnoid hemorrhage, posterior reversible encephalopathy syndrome, and thrombosis among other causes.[1] Our patient was believed to have a PDPH, given the clinical picture of multiple epidural attempts and inadvertent wet tap. PDPH is typically fronto-occipital and postural in nature, worse on standing, and better when lying flat.[1] Other symptoms include a stiff neck, tinnitus, increased sensitivity to light and sound, and nausea.[1] EBP often immediately relieves these symptoms along with the accompanying severe headache. However, if the headache persists, despite this treatment, other causes must be ruled out. In our particular patient, EBP was offered, but the patient refused preferring medical management instead.

The Monro–Kellie doctrine helps to explain the pathogenesis of postural headache related to accidental dural puncture.[2] The intracranial space is a fixed space in equilibrium occupied by brain, cerebrospinal fluid (CSF), and blood; therefore, a reduction in one component must lead to an increase in another component.[3] Hence, after dural puncture and loss of CSF, two changes occur. There is an increase in the intracranial venous volume due to venous stasis and dilation of the sinuses, cortical, and spinal veins. There is also descent of the brain and brainstem structures along with distortion and stretching of veins. These structures are pain-sensitive and combined with adenosine receptor-mediated increase in cerebral blood flow, which produces the characteristic postural headache.[2]

The severity of our patient's presentation led to immediate imaging and diagnosis of cortical venous thrombosis. It is underdiagnosed in the general population and the true incidence is unknown, but it is most commonly associated with postpartum women in a hypercoagulable state and may rarely develop after neuraxial anesthesia.[1],[4],[5] It may present as an unremitting headache that may eventually include focal neurologic symptoms, seizures, and raised intracranial pressure.[1] The main difference between the headache of PDPH and CVT is that both present with a positional headache initially, but over the course of time, the headache associated with CVT becomes nonpositional in nature as happened in our patient.[4] Approximately, 2% of pregnancy-associated strokes have been attributed to CVT. MRI with venography or CT angiogram being the gold standard for diagnosis.[4]

Hypercoagulability is a common occurrence during pregnancy, representing nature's own protective mechanism against postpartum hemorrhage. Cerebral venous stasis due to traumatic injury to the dura in the presence of this postpartum hypercoagulable state may have increased the risk of CVT in our patient. This was further evidenced by a hematologic workup which confirmed sickle cell trait and elevated factor VIII levels. This has been further supported in other clinical studies. One particular study examined 16 patients with the diagnosis of CVT.[6] A hematologic workup was performed 3 months after diagnosis to eliminate confounding acute-phase reactants.[6] The most common prothrombotic risk factor found in this study was an elevated factor VIII level, which was found in 8 out of 16 patients.[6] Although the sample size was low, there does appear to be a correlation with the hypercoagulable state and CVT. Other studies reported in literature have not found a significant association between pre-eclampsia and the development of CVT. In fact, it is likely that pre-eclampsia may be associated with intracerebral hemorrhage and ischemic stroke, but it is uncommon in patients with CVT.[7]


  Conclusion Top


PDPH is an iatrogenic complication related to violation of the dura during spinal and epidural procedures. Although cortical vein thrombosis may occur during the postpartum period, as a result of hypercoagulability in pregnancy, intracranial hypotension secondary to CSF leak may increase this risk even further.

It is of paramount importance for patients to be informed of the risks of dural puncture during discharge and to have appropriate follow-up. Cortical venous thrombosis should be suspected when patients complain of headache without postural involvement and when atypical symptoms such as seizures or hemiparesis occur. Intracranial pathology should be ruled out with appropriate imaging to prevent catastrophic complications. Women who develop PDPH may also benefit from postpartum thrombo-prophylaxis, particularly in the presence of known genetic predisposition to hypercoagulability to avoid these untoward complications.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Macgregor EA. Headache in pregnancy. Continuum (Minneap Minn) 2014;20:128-47.  Back to cited text no. 1
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2.
Turnbull DK, Shepherd DB. Post-dural puncture headache: Pathogenesis, prevention and treatment. Br J Anaesth 2003;91:718-29.  Back to cited text no. 2
[PUBMED]    
3.
Kim MO, Adji A, O'Rourke MF, Avolio AP, Smielewski P, Pickard JD, et al. Principles of cerebral hemodynamics when intracranial pressure is raised: Lessons from the peripheral circulation. J Hypertens 2015;33:1233-41.  Back to cited text no. 3
    
4.
Lockhart EM, Baysinger CL. Intracranial venous thrombosis in the parturient. Anesthesiology 2007;107:652-8.  Back to cited text no. 4
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5.
Yildiz OK, Balaban H, Cil G, Oztoprak I, Bolayir E, Topaktas S. Isolated cortical vein thrombosis after epidural anesthesia: Report of three cases. Int J Neurosci 2010;120:447-50.  Back to cited text no. 5
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6.
Cakmak S, Derex L, Berruyer M, Nighoghossian N, Philippeau F, Adeleine P, et al. Cerebral venous thrombosis: Clinical outcome and systematic screening of prothrombotic factors. Neurology 2003;60:1175-8.  Back to cited text no. 6
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7.
Cantu-Brito C, Arauz A, Aburto Y, Barinagarrementeria F, Ruiz-Sandoval JL, Baizabal-Carvallo JF. Cerebrovascular complications during pregnancy and postpartum: Clinical and prognosis observations in 240 Hispanic women. Eur J Neurol 2011;18:819-25.  Back to cited text no. 7
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