Controlling the AVMs intraoperative bleeding requires attention to certain tenants. Let's review these tenants in the case of one of my patients, who is a 56-year-old female who presented with a sudden headache and left-sided visual field dysfunction. Imaging revealed small amount of hemorrhage around the area of arteriovenous malformation. This malformation is located in the parieto-occipital area, primarily fed by the branches of the posterior cerebral artery. The drainage pattern joins this superior sagittal sinus. You can see that these deep feeding vessels are primarily cortical and not necessarily white matter and should be readily amenable to bipolar coagulation. Some of the finer vessels that are at the apex of the malformation are most likely the deep white matter feeders or the red devils that are very problematic to control via any tool, let alone bipolar coagulation, since they lack robust walls. Especially on the right parieto-occipital craniotomy in the lateral position. A paramedian incision was used. You can see the midline is located here. The is quite forceful and has an intense amount of flow. You can see the bone flap is pulsating. The dura was open in curvilinear fashion based over the superior sagittal sinus, a couple of sutures were placed over the superior aspect of the falx to mobilize the sagittal sinus. Here's the configuration of the malformation and ICG can clearly identify the deep white matter feeders and the large draining vein joining the superior sagittal sinus. The AVM was circumferentially disconnected. The arachnoid bands were carefully dissected. The cortical vessels at the depth of the sulci were identified, coagulated, and cut. Here, you can see some of the large cortical vessels that have robust walls. Some of the larger feeding vessels are also disconnected, some of the deep white matter feeders own a very thin wall. However, those vessels that are located over the area of the interhemispheric fissure and interface the pial surface are very amenable to coagulation. However, inadequate coagulation and avoidance of the clips when necessary can lead to torrential bleeding. The control of bleeding is important. The forceps have to be used exactly at the site of the bleeding, indiscriminate coagulation should be avoided. This is one of my residents who is attempting to control the immense bleeding, in this case. A larger suction is most likely necessary so he can clearly see the source of bleeding. Again, the bleeding from these cortical vessels is quite controllable via the use of bipolar coagulation since the arteries own a very robust wall and collapse and are coagulable using the bipolar forceps. After a series of attempts, I took over the next maneuvers within the operative field in a moment another forceps was used. But again, this was unsuccessful. Here is the technique of grabbing the vessel more perpendicular along its axis to control the bleeding. After these cortical vessels are carefully managed, some of the deeper vessels from the posterior cerebral artery can be found, clip ligated and further coagulated and subsequently transected. Therefore, large vessels with robust walls do require the clips in addition to the bipolar forceps for their adequate control. The vessel is first skeletonized, even though it's somewhat located within the white matter, this vessel owns a very robust wall. One of the distal branches of PCA leading to the malformation is first coagulated. I typically use very small aneurysm clips. Next, the vessel is disconnected. The AVM is subsequently mobilized and its apex is also disconnected from some of the smaller, more robust feeding vessels. Again, the clips are used. Most of the flow for this AVM came from robust vessels that acted like cortical vessels. Some of the deep white matter feeders can be obviously more problematic to control. Here's part of the thrombotic draining vein. Most of the AVM is now disconnected except the large primary draining vein joining the superior sagittal sinus. I continue to work under the vein to disconnect the malformation along the interhemispheric fissure. Temporary occlusion of the vain reveals no evidence of tension within the malformation, therefore, the vein is coagulated and subsequently clipped and transected. Hemostasis is secured. And post-operative angiogram demonstrates adequate removal of the arteriovenous malformation. So the learning points are really the differentiation between deep white matter feeders that lack robust walls versus cortical vessels that face the pial surfaces or may reside in the white matter, but still own very solid walls and are amenable to coagulation. Some of the larger vessels in this category require the clips in addition to bipolar coagulation for their efficient control and transection. Thank you.
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