A Case of Postpartum Cerebral Venous
Thrombosis
Betty Cole, Laura M. Criddle

A

bstract: Cerebral venous thrombosis, also known as
cortical venous, cerebral sinus, cerebral venous sinus,
or dural sinus thrombosis, results from clot formation in
one of the many outflow tracts of the brain. Obstruction of
flow causes venous hypertension, which is responsible for
clinical findings associated with this condition. Signs and
symptoms of cerebral venous thrombosis include headache,
nausea, mental status changes, seizures, and focal neurologic
deficits. Although cerebral venous thrombosis can occur at
any time during life, women are particularly vulnerable
before delivery and during the postpartum period because of
the hypercoagulable state that accompanies pregnancy. This
case study describes the challenging clinical course of one
postpartum patient who developed venous thrombosis of the
sagittal sinus.

Case Report
Two weeks after the uncomplicated delivery of her
fourth child, 32-year-old J. L. started experiencing
severe headaches. On the day of presentation, J. L. was
at home when she became increasingly disoriented
and developed left upper-extremity uncoordination
followed by a generalized seizure. After 911 was called,
J. L. was transported to the healthcare facility in her
rural community.
At the hospital, J. L. exhibited confusion, minimal
left-side movement, and additional seizure activity. She
was immediately intubated and sedated for seizure
management. A computed tomography (CT) scan of her
head did not detect any abnormalities, so brain magnetic
resonance imaging (MRI) was performed. The MRI scan
identified thrombosis of the anterior superior sagittal
sinus with bifrontal infarctions. An intravenous loading
dose of 5,000 units of heparin was given, followed by an
infusion of 1,000 units per hour. J. L. was then transferred
to a regional facility, where a repeat CT scan of her brain
showed hemorrhagic transformation of her right frontal
stroke. The heparin infusion was immediately discontinued, and preparations were made for fixed-wing transport to a neuroscience center in a neighboring state.
J. L. arrived at the tertiary facility intubated and sedated, with purposeful movement only in her right arm
Questions or comments about this article may be directed to Betty
Cole, BSN RN CNRN, at colebe@ohsu.edu. She is the nursing practice and education coordinator for the trauma/neurosciences intensive care unit at Oregon Health & Science University, Portland, OR.
Laura M. Criddle, MS RN CNRN, is a doctoral student at Oregon
Health & Science University, Portland, OR.
Copyright © 2006 American Association of Neuroscience Nurses
0047-2606/06/3805/00XX$5.00

350

and leg. She was quickly taken to the angiography suite,
where a microcatheter was inserted in her femoral vein
and threaded into the superior sagittal sinus to facilitate
urokinase infusion (50,000 units per hour) directly to the
site of the clot (Figs. 1, 2). This treatment was continued
for 45 hours, until repeat angiography showed the sinus
was once again patent. During fibrinolytic infusion, J. L.
was observed closely for any evidence of hemorrhage.
This observation included frequent neurologic assessment and serial CT scans to identify potential evolution
of her intracranial hemorrhage. Daily laboratory values
were monitored for changes in hemoglobin, hematocrit,
and coagulation status.
Shortly after J. L was admitted to the traumaneurosciences intensive care unit (ICU), a subarachnoid
intracranial pressure (ICP) monitoring device was placed.
J. L.’s opening pressure was higher than 40 mm Hg. During the next several days, her persistently elevated ICP
was treated with mannitol, paralytics, mechanical ventilation, and sedation (i.e., propofol, fentanyl, midazolam).
She experienced occasional seizures and remained weak
on the left side, but sedation and endotracheal intubation
made it difficult to fully assess her mental status.
One week after arrival, J. L. was extubated. She demonstrated spontaneous eye opening but could not follow
commands. On day 12, J. L. was transferred from the
ICU to the neuroscience ward, still exhibiting left-side
neglect and left-arm apraxia. Her speech was intact,
but she had no memory of recent events, including the
birth of her baby. On day 14, J. L. was stable enough for
transfer to an inpatient rehabilitation unit near her home
town. A follow-up report from her physician indicated
that J. L. was eventually able to return home and resume
care of her children.

Discussion
Pathophysiology
The cerebral venous system is unique (Fig. 3). Unlike
most vessels, the major veins of the brain are composed of dural folds called sinuses. The sinuses lack
muscular walls, cannot contract, and contain no valves.
The sinuses facilitate large amounts of venous drainage from the brain but also provide an excellent place
for blood to pool. Sinus thrombosis occurs when a
blood clot occludes one of the sinuses, obstructing
venous return. The resulting intracranial hypertension can lead to brain edema, infarction, hemorrhage,
and even death (Soleau, Schmidt, Stevens, Osborn, &
MacDonald, 2003). Cerebral venous thrombosis (CVT) is
the term collectively used to include clots not only of

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Fig 1. Cerebral angiogram showing right-sided injection (late
venous phase). Image taken approximately 36 hours after
urokinase treatment was initiated. The beaded appearance
along the sagittal sinus is indicative of partial thrombosis.

Fig 2. Cerebral angiogram (noncontrast study) showing
the catheter in the jugular vein, sigmoid sinus, transverse
sinus, and the sagittal sinus. Arrows indicate site of
thrombus.

the sagittal sinus but also of the cavernous sinus and
parietooccipital regions. This condition is also referred
to as cortical venous, cerebral sinus, cerebral venous
sinus, or dural sinus thrombosis.

normal hematologic changes as well as other conditions that may be present, such as venous stasis,
increased venous capacity, multiparity, and advanced
age, combine to produce prime conditions for clot formation during the puerperium. This hypercoagulable
state predisposes pregnant patients and new mothers
to CVT. Cases of CVT have been reported as long as
3 months after delivery (Nazziola, 2003). In this state,
the risk of a thromboembolic disease is three to four
times greater than for other women (Chan & Ginsberg, 2002). Although CVT is much less common, in
general, than deep vein thrombosis or pulmonary
embolism, gravid patients are particularly susceptible
to this condition. In some puerperal women with
CVT, a deficiency of one or more coagulation factors
was noted before pregnancy, but in most instances
prepregnancy coagulation studies were completely
normal.

Risk Factors
Three patient populations are at particular risk for CVT.
The first comprises individuals with a blood-flow disturbance that increases. For example, increased blood
viscosity can occur in patients with dehydration or
polycythemia. Cases of CVT have been reported in persons living at high altitude, who commonly experience
both polycythemia and dehydration (Basnyat, Wu, &
Gertsch, 2004). The second at-risk group includes individuals with conditions that cause infection or fibrosis
of the venous walls. Bacterial meningitis and frontal
sinusitis are the most common sources of infection. The
third at-risk group comprises patients who have an
increased thrombotic tendency that is due to an inherited or acquired clotting disorder, such as the factor-V
Leiden gene or antiphospholipid syndrome, or due to
pregnancy (Horne & McCloskey, 2006).
Gravid patients have an elevated CVT risk because
of the normal alterations in the coagulation process
associated with pregnancy. During pregnancy, the
patient experiences dramatic hematologic changes
that prevent hemorrhage at the time of delivery, and
these changes persist for several weeks postpartum.
Fibrinogen, platelets, and most factor levels (VII,
VIII, IX, X, and XII) are elevated, and fibrinolytic
activity is reduced (Bousser & Russell, 1997). These

Clinical Findings
Cases of CVT have been documented in the medical
literature since the early 1940s. However, until the mid1980s, the diagnosis was made postmortem (Bousser &
Russell, 1997). Symptoms produced by venous hypertension included headache, nausea, vomiting, motor
weakness, decreased level of consciousness, visual
complaints, photophobia, aphasia, ataxia, and seizures.
The clinical presentation of CVT varies greatly; findings are not distinct, and they resemble those of many
other neurologic conditions. In some patients, headache is the sole complaint.

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351

Fig 3. Diagram showing the pattern of distribution of the
major dural venous sinuses and their connection to the
internal jugular veins. From Cerebral Venous Thrombosis, by M.-G. Bousser and R. R. Russell (p. 175), 1997,
Philadelphia: Saunders. Copyright 1997 by Elsevier.
Reprinted with permission.
One published case (Nazziola, 2003) illustrates how
difficult it can be to establish a diagnosis of CVT when
patients present with vague initial symptoms. A postpartum woman arrived in an emergency department complaining of headache and nausea. She had no alteration
in level of consciousness and no focal neurologic deficits.
The patient was discharged home when her brain CT scan
was interpreted as normal. This woman returned to the
emergency department the following day, complaining of
the same symptoms. Once again, she was sent home after
a normal lumbar puncture. On the third day, the woman
arrived by ambulance following a generalized seizure. A
repeat CT scan of the brain (with and without contrast)
showed some ischemic changes. A magnetic resonance
venogram was performed next; it revealed thrombosis of
both the transverse and sigmoid sinuses. As this incident
illustrates, because CVT symptoms can be vague, variable, and nonspecific, adequate radiologic imaging is
essential. In one small series, 60% of CVT patients whose
only presenting symptom was headache had initial CT
scans that were interpreted as negative (Cumurciuc,
Crassard, Sarov, Valade, & Bousser, 2005).
Nursing Interventions
Nursing care of the individual with a CVT is similar to that
of other patients with central nervous systems disorders
and must be tailored to individual needs. In J. L.’s case,
we used mechanical ventilation to ensure adequate oxygenation. Cerebral perfusion was supported by keeping
the head of J. L.’s bed at 30 degrees, minimizing external
stimulation, and maintaining her mean arterial pressure
above 70 mm Hg. Intracranial pressure was monitored
with a subarachnoid bolt. Spikes in ICP were treated
352

with mannitol, paralytics, sedation, analgesics, and positioning. These interventions were effective in keeping
J. L.’s cerebral perfusion pressure within the target range.
Other interventions for intracranial hypertension that are
sometimes used in CVT patients include corticosteroids,
diuretics, and barbiturate-induced coma.
Dysphagia is a common complication of CVT. To prevent aspiration, J. L. was given nothing by mouth for
the first few days following extubation. Nutritional support was initiated early in the course of her illness and
provided by tube feedings. Our patient’s care included
seizure prophylaxis with phenytoin (Dilantin); serum
levels were monitored daily to ensure they remained in
a therapeutic range. While she was receiving thrombolytic therapy, J. L. required regular nursing assessment
to monitor for signs of blood in her gastrointestinal or
urinary tracts. To prevent iatrogenic coagulopathies,
J. L.’s prothrombin time–international normalized ratio
(PT/INR) and partial thromboplastin time (PTT) were
monitored daily. Ongoing discussions of prognosis and
plans for long-term rehabilitation were held during frequent conferences with J. L.’s husband and family.
Medical Interventions
Heparin administration is the standard treatment for
CVT. Although lysis of the sinus thrombus does not
occur with systemic anticoagulation, prevention of
new thrombus formation is essential. The goal of
heparin therapy is to halt clot proliferation and prevent
worsening of clinical symptoms (Bousser & Russell,
1997; Chow et al., 2000). Heparin is generally continued until the patient stabilizes (Bousser & Russell).
However, intracranial hemorrhage (as occurred in
J. L.’s case) is a significant potential consequence of this
therapy, and the benefits of anticoagulation must be
carefully weighed against the risks.
Fibrinolytic drug therapy for CVT is provided by
using a microcatheter to infuse a clot-dissolving agent
into the dural sinus. This technique has been shown to be
highly effective; however, access to therapy is currently
limited to tertiary care centers, and this intervention is
commonly reserved for patients with significant neurologic deficits.
Mechanical thrombolysis, with or without fibrinolytic drug therapy, can be accomplished by several
mechanisms. Guidewires have been used for mechanical interruption of the thrombus. Interventional neuroradiologists can insert microcatheter balloons (e.g.,
coronary artery balloons) to dislodge or compress clots.
Rheolytic thrombectomy catheters are also a treatment
option for patients with CVT. The AngioJet ®, the most
commonly used rheolytic catheter, is a 5-french, 140cm device that uses small saline jets to disrupt the clot.
Mechanical intervention is indicated for patients in
whom fibrinolytics are contraindicated, and for those
who demonstrate poor response to local urokinase infusion or experience rapid neurological decline. When

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interventional radiologic techniques are not available,
craniectomy and thrombectomy have sometimes been
used. It is important to note that many of these invasive
procedures are still considered investigational (Baker,
Opatowsky, Wilson, Glazier, & Morris, 2001).
Long-term medical therapy for CVT patients includes
systemic anticoagulation with warfarin for an average of
6 months (Cakmak et al., 2003). Fortunately, the risk of
CVT recurrence during subsequent pregnancies is low
(Mehraein et al., 2003), and patients are not routinely
counseled against future pregnancies. At present, insufficient data exists to determine the benefit of prophylactic
anticoagulation in the gravid patient with a history of
CVT (van der Stege, Engelen, & van Eyck, 1997).
Prognosis
CVT associated with pregnancy is reported to have a
better prognosis than CVT arising from other causes,
with a mortality rate of approximately 10% (van der
Stege et. al., 1997). Researchers have estimated allcause CVT mortality as 10%−30% (Baker et. al., 2001;
Chow et al., 2000). In a retrospective review of 170
peripartum patients with CVT, Lanska and Kryscio
(2000) reported that more than 93% of patients were
discharged home, and there were no deaths in their
series. Although many CVT patients experience some
persistent neurologic deficits, most will return to their
previous level of function.

Summary
Nursing care of the postpartum patient with CVT is
similar to that of other patients with CVT. Neuroscience
nurses caring for these patients can be instrumental in
the prevention of secondary brain insult by performing
frequent neurological assessments for signs of change,
providing rapid interventions as appropriate, and carefully monitoring coagulation studies to prevent complications associated with anticoagulation therapies.

End-of-Life Concepts

References
Baker, M. D., Opatowsky, M. J., Wilson, J. A., Glazier, S. S., & Morris,
P. P. (2001). Rheolytic catheter and thrombolysis of dural venous
sinus thrombosis: A case series. Neurosurgery, 48, 487–493.
Basnyat, B., Wu, T., & Gertsch, J. H. (2004). Neurological conditions
at altitude that fall outside the usual definition of altitude sickness.
High Altitude Medical Biology, 5(2), 171–179.
Bousser, M. G., & Russell, R. R. (1997). Cerebral venous thrombosis.
London: Saunders.
Cakmak, S., Derex, L., Berruyer, M., Nighoghossian, N., Philippeau,
F., Adeleine, P., et al. (2003). Cerebral venous thrombosis: Clinical
outcome and systematic screening of prothrombotic factors. Neurology, 60, 1175–1178.
Chan, W. S., & Ginsberg, J. S. (2002). Diagnosis of deep vein thrombosis and pulmonary embolism in pregnancy. Thrombosis Research,
107, 85–91.
Chow, K., Gobin, Y. P., Saver, J., Kidwell, C., Dong, P., & Vinuela, F.
(2000). Endovascular treatment of dural sinus thrombosis with
rheolytic thrombectomy and intra-arterial thrombolysis. Stroke,
31, 1420–1425.
Cumurciuc, R., Crassard, I., Sarov, M., Valade, D., & Bousser, M. G.
(2005). Headache as the only neurological sign of cerebral venous
thrombosis: A series of 17 cases. Journal of Neurology, Neurosurgery, and Psychiatry, 76, 1084–1087.
Horne, M. K., & McCloskey, D. J. (2006). Factor V Leiden as a common genetic risk factor for venous thromboembolism. Journal of
Nursing Scholarship, 38(1), 19–25.
Lanska, D. J., & Kryscio, R. J. (2000). Risk factors for peripartum and
postpartum stroke and intracranial venous thrombosis. Stroke, 31,
1274–1282.
Mehraein, S., Ortwein, H., Busch, M., Weih, M., Einhaupl, K., &
Masuhr, F. (2003). Risk of recurrence of cerebral venous and sinus
thrombosis during subsequent pregnancy and puerperium. Journal of Neurology, Neurosurgery, and Psychiatry, 74, 814–816.
Nazziola, E. (2003). Dural sinus thrombosis presenting three months
postpartum. Annals of Emergency Medicine, 42, 592–595.
Soleau, S. W., Schmidt, R., Stevens, S., Osborn, A., & MacDonald, J. D.
(2003). Extensive experience with dural sinus thrombosis. Neurosurgery, 52, 542–544.
van der Stege, J. G., Engelen, M. J. A., & van Eyck, J. (1997). Uncomplicated pregnancy and puerperium after puerperal CVT. European
Journal of Obstetrics, Gynecology, and Reproductive Biology, 71,
99–100.

continued from page 348

References
American Association of Colleges of Nursing. (1998). Peaceful death:
Recommended competencies and curricular guidelines for end-oflife nursing care. Washington, DC: Author.
Cassel, C. K., & Foley, K. M. (1999). Principles of care of patients at
the end-of-life: An emerging consensus among the specialties of
medicine. New York: Milbank Memorial Fund.
City of Hope. (1999). End-of-life care content guideline. Duarte, CA:
Author.
English, N., & Yocum, C. (1996). Guidelines for curriculum development on end-of-life and palliative care in nursing education.
Alexandria, VA: National Hospice Organization.
Ferrell, B. R., & Coyle, N. (2002). An overview of palliative nursing
care. Lippincott’s Case Management, 7, 163–168.
Ferrell, B. R., Virani, R., & Grant, M. (1999a). Analysis of symptom
assessment and management content in nursing textbooks. Journal of Palliative Medicine, 2, 161–172.
Ferrell, B. R., Virani, R., & Grant, M. (1999b). Analysis of end-oflife content in nursing textbooks. Oncology Nursing Forum, 26,
869–876.

Ferrell, B. R., Virani, R., & Grant, M. (1999c). Review of communication and family caregiver content in nursing texts. Journal of
Hospice and Palliative Nursing, 1, 97–107.
Field, M. J., & Cassel, C. K. (Eds.). (1997). Approaching death: Improving care at the end of life. Washington, DC: National Academy
Press.
Joint Commission on the Accreditation of Healthcare Organizations.
(1999). New JCAHO standards, intents, examples, and scoring
questions for pain assessment and management in hospitals. Oakbrook Terrace, IL: Author.
Lewis, L. (2001). Toward a good death in the nursing home: Pain management and hospice are key. Caring for the Ages, 2(7), 24–26.
National Consensus Project. (2004). Clinical practice guidelines for
quality palliative care. Brooklyn, NY: Author.
Rabow, M. W., Hardie, G. E., Fair, J. M., & McPhee, S. J. (2000). An
evaluation of end-of-life care content in 50 textbooks from multiple specialties. Journal of the American Medical Association, 283,
771–778.

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