Venous Injuries and Cerebral Edema in Cranial Surgery




Highlights





  • The exact consequences of “venous injury,” inadvertently caused during the course of routine neurosurgical operations, find scant mention in neurosurgical literature.



  • Numerous so-called “unpredictable” postoperative complications in neurosurgery are related to the lack of prevention or nonrecognition of venous injury.



  • The factors responsible for devastating postoperative venous complications are a combination of intraoperative venous compromise, iatrogenic brain injury, and prolonged lobe retraction.



  • The frequency of postoperative venous infarction after manipulation/sacrifice of venous structures during cranial surgery is reportedly higher in older patients than in younger patients.



  • There is no intraoperative test available to determine whether postoperative venous infarction will occur if we injure or sacrifice a particular vein during surgery.



  • The unpredictable response of the brain to venous injury causes catastrophic complications in a few patients; to avoid these, meticulous venous preservation should be an aim in all neurosurgical procedures.





Background


Complications related to the intracranial venous system, especially the cerebral venous drainage, have received comparatively less attention in the neurosurgical literature. Consequently, venous complications are not given due recognition, even though most practicing neurosurgeons would agree that they are not uncommon. Numerous so-called “unpredictable” postoperative complications in neurosurgery are most likely related to the lack of prevention or to the nonrecognition of venous problems, especially damage to the dangerous venous structures—namely the major dural sinuses, the deep cerebral veins, and some of the dominant superficial veins like the vein of Labbé, vein of Trolard, or the superior petrosal vein.


Frequent variations exist in the size and connections of the intracranial veins, and this has made it difficult to define their normal pattern. Hence, there is ambiguity in reporting the damage to the venous anatomy that usually occurs during the course of an intracranial surgery. Apart from the treatise on the neurosurgical perspective of the intracranial venous system published by Hakuba and the extensive reviews published by Sindou and Auque, the neurologic literature on venous injury and its consequences is scant.




Incidence of Venous Injury and Its Sequelae


Kageyama et al. reported postoperative venous infarction (POVI) in 13% of the 120 cases operated on by them. Saito et al. reported POVI in 2.6% of cases after the frontotemporal bridging vein was cut during the pterional approach, and Al-Mefty and Krisht showed that brain edema occurred in 10% of cases after sacrifice of the superficial sylvian vein. Kubota reported that 4 of 10 patients with vein sacrifice during an interhemispheric approach suffered from brain damage. Roberson et al. reported that the complication rate of venous insufficiency was 1.5 per 1000 cases of neurologic–skull base surgery. Agrawal and Naik studied a total of 376 patients undergoing elective major cranial surgeries over a period of 8 months. In their study, 26 (7%) patients developed POVI, out of which 16 (61%) patients developed hemorrhagic POVI and 10 (39%) patients developed nonhemorrhagic POVI.


The exact consequences of “venous injury,” inadvertently caused during the course of routine neurosurgical operations, find scant mention in neurosurgical literature; some publications even suggest that veins could be sacrificed without any significant neurologic damage. The reasons can be manifold. When we consider the postoperative computed tomography (CT) or magnetic resonance imaging (MRI) scan and visualize an area of cerebral contusion or hypodensity, adjacent to the operative site or in the trajectory of the neurosurgical approach, we tend to attribute it to several factors—namely retraction injury, retraction edema, pial transgression by the surgeon, arterial injury, presence of preoperative tumor edema, and after-effects of tumor manipulation. The extent of brain damage from venous cause is rarely quantifiable, and this may be due to the interplay of the above-mentioned confounding factors.




Consequences of Venous Injury


The incidence of intraoperative venous injury and subsequent POVI is difficult to determine due to an unclear definition, myriad postoperative neurologic presentations, and the inclusion of other factors during the operation itself (for example, brain retraction).


Roberson et al. divided venous infarction into two types: the acute form and the chronic form. The acute form manifests itself in the immediate postoperative period and can, at times, be life-threatening. The chronic form manifests itself months or years postoperatively with headaches, disequilibrium, and visual changes due to papilledema. In this setting, venous thrombosis from intraoperative venous injury progresses to the dural sinuses, thus influencing cerebrospinal fluid (CSF) absorption and eventually presenting as communicating hydrocephalus.


Nakase et al. further described two types of perioperative (acute) venous infarction in their study: severe and mild types. The severe type requires extensive treatment like internal decompression and barbiturate therapy immediately after the operation. The mild type has a slow clinical deterioration by gradual thrombus evolution and can be treated conservatively. In all the severe cases documented in their series, the sacrificed cortical vein was the petrosal vein.


The variability of the intracranial venous system makes it difficult to predict the exact course and amount of flow in a particular draining vein during surgical approaches. The absence of valves in the veins and the presence of collateral drainage systems make it possible for the venous drainage to adapt to an intraoperative venous injury and limit the amount of brain damage. This is often used as an excuse by neurosurgeons to sacrifice veins during the surgical approach. However, it should be borne in mind that it is very difficult to predict the dominant venous drainage from a particular cerebral region intraoperatively and that sacrificing this dominant drainage can have disastrous consequences for the brain.


The fact that sacrifice of the individual cortical veins only infrequently leads to venous infarction, hemorrhage, swelling, and neurologic deficits is attributed to the diffuse anastomoses between the veins. The intraoperative sacrifice of the anastomotic or bridging vein usually does not lead to venous infarction due to the absence of cerebral valves. The recruitment of collateral pathways occurs during the early phase of venous occlusion. The severity depends on the availability of individual venous collaterals. Only when the collateral venous flow is compromised by additional compression or under extraordinary physiologic conditions—for example, intraoperative brain retraction, excessive changes of systemic blood pressure, and an elderly patient—does venous infarction occur. Although the brain may tolerate occlusion of the nondominant channels to a large extent, the occlusion of a dominant venous channel carries significant risk of POVI.




Types of Postoperative Venous Complications


Based on the published literature on this subject and on our current understanding of the venous system, the postoperative venous complications can be classified into the following categories.


Acute Decompensated Venous Injury


This injury is analogous to the severe acute venous infarction described by Nakase et al. and manifests immediately postoperatively as a hemorrhagic cerebral infarction in the territory of the injured draining vein. This usually presents with severe cerebral edema with consequent midline shift and may require extensive measures like decompressive surgery or barbiturate coma to manage the raised intra-cranial pressure (ICP).


Acute Compensated Venous Injury


When the venous injury results in the occlusion of the nondominant venous channels or in the occlusion of the dominant venous channel in a favorable setting (without the added insult of brain retraction or preexisting cerebral edema), the recruitment of venous collaterals may compensate for the venous injury and thus limit the damage to the brain. This usually manifests as mild to moderate cerebral edema and may resolve with cerebral protection strategies and antiedema measures.


Chronic Venous Insufficiency


In this entity, the intraoperative venous injury may go unnoticed or may manifest as mild cerebral edema. However, venous thrombosis due to intraoperative venous injury may progress to the dural sinuses, causing chronic dural venous thrombosis. Over time, this influences CSF absorption and may eventually present as a form of communicating hydrocephalus.

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Jun 29, 2019 | Posted by in NEUROSURGERY | Comments Off on Venous Injuries and Cerebral Edema in Cranial Surgery

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