|Year : 2015 | Volume
| Issue : 1 | Page : 5-8
Postoperative cerebral venous infarction
Deepak Agrawal, Vikas Naik
Department of Neurosurgery, Neurosciences Centre, All India Institute of Medical Sciences, New Delhi, India
|Date of Web Publication||2-Apr-2015|
Neurosciences Center, All India Institute of Medical Sciences, New Delhi - 110 029
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Background: Postoperative cerebral venous infarction (POCVI) is not an uncommon complication in cranial surgeries. However, literature is sparse on the epidemiology and management of postoperative venous infarcts. Aims and Objectives: The aim was to study the incidence and clinico-radiological course of POCVI in patients in a tertiary level neurosurgical unit and compare the outcome between pediatric and adult patients following POCVI. Materials and Methods: In this prospective study carried out over an 8 month period, consecutive patients undergoing elective major cranial surgeries were monitored neurologically and with serial computed tomography (CT) of the head for POCVI in the postoperative period. All patients had at least one CT head done within 24 hours of surgery. Diagnosis of hemorrhagic POCVI was based on the presence of subcortical, multifocal hyperdensities with irregular margins and or low density areas in the perioperative fields. Nonhemorrhagic POCVI was diagnosed if CT showed a localized hypodensity poorly demarcated in the subcortical white matter with/without mass effect, along with the presence of fresh neurological deficits. Observations and Results: A total of 376 patients were enrolled in the study period. Of these, 26 (7%) developed POCVI. The male: female ratio was 1.2:1 and age ranged from 6 to 68 years with 12 (46%) being under the age of 18 years. Sixteen (61%) patients developed hemorrhagic POCVI and 10 (39%) patients developed nonhemorrhagic POCVI. The mean time to POCVI detection was 72 hours (range 24-144 hours). Seventeen (66%) patients were managed conservatively, and nine (34%) patients underwent decompressive craniectomy as an additional procedure for management of POCVI. In five patients (all with hemorrhagic POCVI), the infarction was an incidental finding. Of the 21 patients with symptomatic POCVI, 13 (61.9%) patients improved neurologically and were discharged with residual deficits. Two (9.5%) showed no neurological improvement till discharge, and 6 (28.5%) died during the hospital stay following POCVI. Conclusions: Children constitute a significant population (46% in our study) of the patients who develop POCVI with poor outcome similar to that seen in adult patients.
Keywords: Cerebral, complication, cranial, incidence, management, surgery, venous infarction
|How to cite this article:|
Agrawal D, Naik V. Postoperative cerebral venous infarction. J Pediatr Neurosci 2015;10:5-8
| Introduction|| |
With the advent of microneurosurgery, sinuses and bridging veins are more frequently encountered with an increased risk of postoperative complications following interruption of the venous circulation. However, as the clinical symptomatology and prognosis of intraoperative cerebral vein occlusion are known to be quite variable, little information is actually available regarding the pathophysiology and management of this potentially catastrophic complication. In contrast, there is a plethora of literature available on venous sinus thrombosis.  The incidence of postoperative cerebral venous infarction (POCVI) is difficult to determine due to an unclear definition, apparent rarity of complications, variability of symptoms, and the inclusion of other factors like brain retraction during the operation itself.  Kageyama et al.,  reported postoperative venous infarction in 13% of the 120 cases operated by them and Al-Mefty and Krisht showed that brain edema occurred in 10% of the cases in which the superficial sylvian vein was sacrificed.  In another study Kuboto reported that 40% of the patients with vein sacrifice during an interhemispheric approach suffered from brain damage.  In contrast, Robertson quoted an extremely low complication rate of venous insufficiency at 1.5/1000 cases of skull base surgery.  In this study, we attempted to study the incidence and clinico-radiological course of POCVI in a tertiary level neurosurgical unit.
| Materials and Methods|| |
This was a prospective study carried out in one unit of the department of Neurosurgery at our hospital over an 8-month period. Approval from the departmental Ethics Committee was obtained for the study and informed consent taken from all patients. Consecutive patients undergoing elective cranial surgery were enrolled in this study. Patients undergoing emergency surgery, reexploration, surgery for traumatic brain injury, shunts, biopsies or burr-hole procedures, as well as spinal procedures, were excluded from the study.
Patients were evaluated clinically preoperatively, and pertinent radiology (computed tomography (CT) head/magnetic resonance imaging brain) reviewed to document any preexisting infarcts. Postoperatively all patients underwent a CT scan of the head within 24 h. Patients were monitored for neurological deterioration and CT scan was repeated as required by the attending neurosurgeon.
As previously described, POCVI was divided into hemorrhagic and nonhemorrhagic types. , The diagnosis of hemorrhagic POCVI was based on the presence of subcortical, multifocal hyperdensities with irregular margins and or low density areas in the perioperative fields. Nonhemorrhagic POCVI was diagnosed if CT showed a localized hypodensity poorly demarcated in the subcortical white matter with/without mass effect, along with the presence of fresh neurological deficits. These criteria have been modified from the original criteria, which were based purely on radiology, to better exclude patients with possible retraction injury.
| Results|| |
A total of 376 patients were enrolled in the study period. Of these, 26 (7%) developed POCVI. The male: female ratio was 1.2:1 and age ranged from 6 to 68 years with 12 (46%) being under the age of 18 years. Majority (76%, n = 20) of the patients operated were for intracranial tumors, followed by vascular pathology in 15%. There was one case each of intra cranial abscess and cerebrospinal fluid rhinorrhea. Of those with tumors, meningioma constituted 45% (n = 9) of the cases, followed by glioma (25%) and acoustic neuroma (20%), There was one each of craniopharyngioma and colloid cyst. Perilesional edema on CT scan was seen in 16 (61%) patients.
One patient had frontal venous sinus injury; however no major cortical vein injury was documented in any of these patients. 17 (65%) patients had dura tense on opening, 7 (26%) patients had retraction, which was considered excess by the operating surgeon.
Postoperative cerebral venous infarction
Ten (39%) patients developed nonhemorrhagic POCVI [Figure 1]a and b and 16 (61%) patients developed hemorrhagic POCVI [Figure 2]a and b. The mean time to POCVI detection was 72 h (range 24-144 h).
|Figure 1: (a) Plain computed tomography (CT) head of the patient who was noticed to have upper limb monoplegia in the postoperative period, showing the development of a nonhemorrhagic venous infarct. The differentiation between peritumoral edema (a) and infarction may be difficult on CT scans and presence of neurological deficits strongly favors the latter diagnosis (b) plain CT head (same patient) done on postoperative day 4, showing hemorrhagic transformation of the venous infarct|
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|Figure 2: (a) Plain computed tomography (CT) head of a patient showing bifrontal venous hemorrhagic infarcts following bifrontal retraction. (b) Plain CT head of a patient showing left frontal venous hemorrhagic infarcts following pterional approach|
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Five patients (19%) were asymptomatic and found to have venous infarct on a routine postoperative CT scan head. 21 (80.76%) had symptomatic POCVI. Of these, 3 (11%) patients had focal deficit as presenting manifestation, 13 (50%) had altered sensorium, and 5 (19%) had both.
Seventeen (66%) patients were managed conservatively and nine (34%) patients underwent decompressive craniectomy as an additional procedure for management of POCVI. In those who were managed conservatively (n = 17), dose of mannitol was increased in 11 (64%) patients and in 15 (88%) the dose of steroid was increased. Hospital stay ranged from a mean of 4 days in asymptomatic to a mean of 20 days in symptomatic patients. Following treatment, 13 (61.9%) of the 21 symptomatic patients improved neurologically and were discharged with residual deficits. Two (9.5%) (one adult and one of pediatric age group) showed no neurological improvement till discharge, and 6 (28.5%) (of which 3 were of pediatric age group) died during the hospital stay following POCVI.
| Discussion|| |
Literature on POCVI is sparse and nonexistent for pediatric population. Robertson divided venous infarction into two types: The acute form and the chronic form. The acute form manifests in the postoperative period and can be life-threatening. The chronic form manifests itself months or years postoperatively with headaches, disequilibrium and visual disturbances due to papilledema. Nakase further divided the acute form of venous infarction into the mild and the severe types. The mild type has a slow neurological deterioration by gradual thrombus evolution and can be treated conservatively. The patient is usually conscious initially and deteriorates neurologically after a variable lag period ranging from 2 to 5 days. In the severe type, the patient has altered sensorium or focal neurological deficits from the immediate postoperative period and may require aggressive management, which may include decompressive surgery and barbiturate therapy.
It is believed the mere sacrifice of the anastomotic or bridging vein usually does not lead to venous infarction. This is attributed to the absence of valves in the cerebral veins, which facilitates recruitment of collateral pathways during the early phase of venous occlusion.  The severity of cerebral venous compromise therefore depends upon the availability of individual venous collaterals. It is well-known that brain retraction can have disastrous ischemic sequelae in the territory of the compressed brain, and it has been shown that, compared with vein occlusion or brain compression alone, the accumulated episode caused severe ischemia and increased the vulnerability of tissue to damage.  Venous congestion produces interstitial edema [Figure 3], which can lead to hypoperfusion and infarction. Due to its widespread availability and use, CT head remains the initial diagnostic modality of choice for detecting postoperative venous infarction and can be classified as nonhemorrhagic and hemorrhagic infarcts. , Contrary to common belief, venous infarcts are most often nonhemorrhagic on CT examination and can be further differentiated into two groups:  Nonenhancing infarcts which are relatively rare and show localized hypodensity, usually poorly demarcated, affecting the subcortical white matter and producing a slight mass effect on the ventricular system. This hypodensity is usually due to localized cerebral edema. The second type is the enhancing type and these are the most common type in which gyral and cortical enhancement is seen close to the hypodensity with mass effect. The hypodensity is most commonly subcortical but can be cortical and subcortical.  Although in most cases, the enhancement appears gyral and cortical or immediately subcortical, it can also be round or patchy-and in these cases it is often located in the subcortical white matter or deep grey matter.
|Figure 3: Preoperative magnetic resonance imaging head, T2-weighted, axial view of a patient with convexity meningioma showing the perilesional edema. This edema may predispose to development of venous infarction in the postoperative period|
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However, in our study, the hemorrhagic type predominated. These are visible as large subcortical hematomas or fluffy, petechial hemorrhages within the area of hypodensity.
The large hemorrhages are subcortical, multifocal with irregular margins. Interestingly, most of these lesions, whether or not they are hemorrhagic on the CT scan, disappear with time. This could reflect the inherent insensitivity of CT to follow the evolution of infarction or could imply an ischemic rather than an infarctive process. The hemorrhage however, is usually seen to disappear by 1-month and the enhancement and edema by 2 months.
In spite of the advances in the understanding of the contribution of ischemic mechanisms in postoperative venous infarction, prevention remains the best form of management. It cannot be overemphasized that minimizing brain retraction and avoiding injury to bridging veins remains the mainstay in preventive measures. However, due to the nature of the surgery, this may not always be possible. Tsutsumi et al.,  have shown that while planning interhemispheric approach, some kinds of venous infarction can be predicted by the pattern and reserve capacity of venous return on preoperative angiograms: Type A, in which large collateral veins are located anterior to the collateral suture, is unlikely to present complications in sacrificing the bridging veins. In type C, which has no definite vein in the frontal lobe, sacrifice of the bridging vein could easily lead to venous infarction. Type B, in which collaterals are located in the middle position between types A and C, would pose an intermediate risk for the development of venous infarction. Therefore, preoperative knowledge of venous anatomy can be crucial in deciding the side and type of approach.
Following injury to cerebral veins intraoperatively, however, the management remains ill-defined. Medical management, including cerebral perfusion pressure monitoring, hyperosmolar therapy and steroids have been tried with varying results. Controlled human trials with any of the above modalities are however lacking. Heinmann et al.,  examined the role of hyperosmolar therapy using single bolus hypertonic saline on ischemic areas in a rat cortical vein occlusion model. They found that compared to normal saline and 10% hydroxyethyl starch, a 4 min infusion of 7.5% saline administered 30 min after cortical vein occlusion had both an immediate and a long-term beneficial effect on cerebral blood flow that corresponded to smaller infarct size.
In established infarcts, the management options become limited and one may have to resort to decompressive craniectomy to decrease intracranial pressure and improve cerebral perfusion. Excision of infarcted tissue has no place in the management armamentarium as this may cause damage to the tissue which is in the quiescent zone.
In our study, a significant percentage (38%) of patients with symptomatic POCVI had poor outcome (death or severe disability).
| Conclusions|| |
The incidence of POCVI in this study, although comparable to previous studies, remains high in the current era of modern neurosurgery. Children constitute a significant population (46% in our study) of the patients who develop POCVI with poor outcome similar to that seen in adult patients.
| References|| |
Agrawal D, Mahapatra A. Traumatic dural venous sinus thrombosis. In: Mahapatra A, editor. Textbook of Head Injury. 2 nd
ed. Delhi: Modern Publishers; 2005.
Nakase H, Shin Y, Nakagawa I, Kimura R, Sakaki T. Clinical features of postoperative cerebral venous infarction. Acta Neurochir (Wien) 2005;147:621-6.
Kageyama Y, Watanabe K, Kobayashi S. Postoperative brain damage due to cerebral vein disorders resulting from the pterional approach. New York, Tokyo: Springer, Berlin Heidelberg; 1996.
Al-Mefty O, Krisht A. The danger veins. New York, Tokyo: Springer, Berlin Heidelberg; 1996.
Kubota M, Ono J, Saeki N. Postoperative brain damage due to sacrifice of bridging veins during the anterior interhemispheric approach. New York, Tokyo: Springer, Berlin Heidelberg; 1996.
Roberson JB Jr, Brackmann DE, Fayad JN. Complications of venous insufficiency after neurotologic-skull base surgery. Am J Otol 2000;21:701-5.
Chiras J, Bousser MG, Meder JF, Koussa A, Bories J. CT in cerebral thrombophlebitis. Neuroradiology 1985;27:145-54.
Chiras J, Dubs M, Bories J. Venous infarctions. Neuroradiology 1985;27:593-600.
Tsutsumi K, Shiokawa Y, Sakai T, Aoki N, Kubota M, Saito I. Venous infarction following the interhemispheric approach in patients with acute subarachnoid hemorrhage. J Neurosurg 1991;74:715-9.
Heimann A, Takeshima T, Alessandri B, Noppens R, Kempski O. Effects of hypertonic/hyperoncotic treatment after rat cortical vein occlusion. Crit Care Med 2003;31:2495-501.
[Figure 1], [Figure 2], [Figure 3]