|Year : 2018 | Volume
| Issue : 12 | Page : 984-987
Intractable brain swelling during cerebral arteriovenous malformation surgery due to contralateral acute subdural haematoma
Ankur Khandelwal, Arvind Chaturvedi, Gyaninder Pal Singh, Rajeeb Kumar Mishra
Department of Neuroanaesthesiology and Critical Care, All India Institute of Medical Sciences, New Delhi, India
|Date of Web Publication||10-Dec-2018|
Dr. Gyaninder Pal Singh
Room No. 711, Department of Neuroanaesthesiology and Critical Care, Neurosciences Centre, All India Institute of Medical Sciences, New Delhi - 110 029
Source of Support: None, Conflict of Interest: None
Severe brain swelling during routine neurosurgery can herald serious consequences. Failure to control brain swelling despite adequate measures warns of a surgical cause and should be dealt efficiently. We report a case of an adult female who developed intraoperative acute subdural haematoma (SDH) and consequent intractable brain swelling during surgery of supratentorial arteriovenous malformation (AVM). Such a manifestation of contralateral acute SDH during supratentorial AVM surgery has not been reported earlier.
Keywords: Acute subdural haematoma, anaesthesia, arteriovenous malformation, brain swelling, intraoperative
|How to cite this article:|
Khandelwal A, Chaturvedi A, Singh GP, Mishra RK. Intractable brain swelling during cerebral arteriovenous malformation surgery due to contralateral acute subdural haematoma. Indian J Anaesth 2018;62:984-7
|How to cite this URL:|
Khandelwal A, Chaturvedi A, Singh GP, Mishra RK. Intractable brain swelling during cerebral arteriovenous malformation surgery due to contralateral acute subdural haematoma. Indian J Anaesth [serial online] 2018 [cited 2021 Jan 24];62:984-7. Available from: https://www.ijaweb.org/text.asp?2018/62/12/984/247125
| Introduction|| |
Brain relaxation is an important aspect of neurosurgical anaesthesia and is relevant to operating conditions, retraction injury, and likely patient outcome. Mild to moderate brain swelling is relatively common and the incidence is reported to be as high as 30%. On the other hand, profound cerebral swelling, although relatively uncommon (0.7%–6.1%), can impose serious consequences. We report a case of intractable intraoperative brain swelling during left temporal arteriovenous malformation (AVM) surgery, the cause of which was postoperatively identified as contralateral acute subdural haematoma (SDH).
| Case Report|| |
A 23-year-old female weighing 60 kg presented with recurrent episodes of generalised tonic-clonic seizures since the past 1 year. The patient was a known case of left temporal AVM and had undergone gamma knife therapy 15 years ago. Magnetic resonance imaging (MRI) of brain showed a cavity in the left temporal region surrounded by haemorrhagic residues [Figure 1]a. Digital subtraction angiography confirmed residual AVM in the left temporal region [Figure 1]b. There were feeders to AVM from distal branches of left middle cerebral artery and it drained to subtemporal vein and sylvian vein. Embolisation was not done as there were multiple feeders and normal cortical branches arising from the feeder artery. Thus, craniotomy and excision of AVM (Spetzler Martin Grade III) was planned. On evaluation, the patient was American Society of Anesthesiologists classification physical status class II with Glasgow Coma Scale of 15/15 and no neurological deficit. Preoperatively, the patient received oral levetiracetam 1 g twice daily and phenytoin 300 mg at bed time. In the operating room, induction of general anaesthesia was achieved with intravenous (iv) with fentanyl 120 μg and propofol 140 mg, and iv rocuronium 50 mg was used to facilitate tracheal intubation. Anaesthesia was maintained with iv fentanyl (60 μg/h), rocuronium (15 mg/h), and propofol (200–300 mg/h) infusions titrated to maintain bispectral index value between 40 and 50 and ventilated with O2:air (1:1) mixture. The patient was placed supine with neck flexed and head turned to the right side. The head was stabilised on 3-pin Mayfield skull fixation holder. Once craniotomy was done, the surgeon complained of severe brain swelling. However, there were no associated fluctuations in systemic blood pressure and/or heart rate. We elevated the head end of patient by 30°. Furthermore, we asked the surgeon to reduce neck flexion and rotation even though there was no increase in airway pressures from baseline. Moreover, we also ensured normocapnia (PaCO2 35–40 mmHg) and systemic blood pressures close to baseline. But brain swelling persisted. We commenced intravenous mannitol (1 g/kg) at the beginning of dural opening to facilitate brain relaxation. In addition, frusemide 20 mg intravenous was also administered. These manoeuvres attenuated brain swelling but not up to the surgeon's satisfaction. As a result, we instituted mild hyperventilation ensuring PaCO2 not less than 30 mmHg (as measured by arterial blood gas analysis). Clearly, brain swelling subsided and surgery continued uneventfully. AVM was resected completely. PaCO2 was then gradually increased to around 35–36 mmHg. However, yet again, brain swelling was noticed at the time of dural closure. This raised suspicion for surgical cause and demanded urgent evaluation. We facilitated dural closure by mild hyperventilation (PaCO2 30–32 mmHg). Following completion of the surgery, the patient was shifted for noncontrast computed tomography (NCCT) scan of brain which revealed new-onset right frontoparietal thin acute SDH [Figure 1]c. Since it was a thin SDH, neurosurgeon decided to manage it without surgical intervention. The patient was electively ventilated overnight and sedated with fentanyl 50 μg/h and midazolam 1 mg/h. A repeat coagulation profile done at this time was also normal. NCCT brain repeated at 6 h [Figure 1]d and postop day 1 [Figure 1]e showed progressive reduction in the size of SDH. On postop day 1, trachea was extubated as the patient had full sensorium, intact airway reflexes, no neurological deficit, and stable haemodynamics. The patient was discharged home on postop day 7 after her brain CT scan showed substantial reduction in the size of SDH [Figure 1]f. At the time of discharge, the patient was stable without any neurological deterioration.
|Figure 1: Images of the brain. (a) Gradient echo sequence showing cavity in left temporal region with surrounding haemorrhagic residue. (b) Digital subtraction angiography showing arteriovenous malformation in the left temporal region fed by left distal middle cerebral artery branches. (c-f) Noncontrast computed tomography showing thin acute subdural haematoma in the right frontoparietal region: (c) immediate postoperative, (d) 6 h postoperative, (e) first postoperative day, and (f) seventh postoperative day and its progressive reduction in size from 1c to 1f|
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| Discussion|| |
AVMs are abnormalities of the vessels that constitute a connection between the arterial and venous systems and lack an intervening capillary bed. AVMs display an annual average haemorrhage rate of 2.8%–4.6% and is associated with significant morbidity and mortality. Acute SDH can coexist with a parenchymal haematoma as a result of AVM rupture. However, development of intraoperative acute SDH at a remote site is extremely rare. To the best of our knowledge, contralateral acute SDH during supratentorial AVM surgery has not been reported before.
In our case, though it is difficult to pinpoint the exact aetiology of acute SDH, the most plausible explanation seems to be the acute shift in brain parenchyma following craniotomy causing stretching and possibly tearing of the bridging veins on the opposite side. Furthermore, AVM resection had a decompressive impact that caused further tearing of the stretched bridging veins and released a tamponade effect. Consequently, an acute SDH was formed on the contralateral side. In addition, rotation and flexion of the neck causing impairment of venous drainage and thereby causing increase in intracranial venous pressure could have been the contributing factor. Studies have mentioned increased subdural intracranial pressure as the strongest predictor of intraoperative brain swelling. Acute SDH resulting from arterial ruptures is generally located in the temporoparietal region when compared with those caused by bridging vein ruptures which are typically located in frontoparietal region. In our case too, acute SDH occurred in the frontoparietal region suggesting venous origin. In addition, loose adhesions between dura and skull inner table at both frontal and parietal lobes is considered to be one of the reasons for SDH to frequently occur at these areas.
Another possible cause for acute brain swelling in AVM surgeries can be ‘normal perfusion pressure breakthrough’. This phenomenon leads to acute hyperaemia in the surrounding normal brain following resection of AVM thereby causing brain swelling. However, in our case this was not the cause as the brain swelling was noted immediately after removal of bone, before resection of AVM. Though this phenomenon may have further aggravated brain swelling at the time of dural closure.
Rarely, acute SDH can result from traumatic rupture of the bridging veins by excessive penetration of the headrest pin. However, the conical shape of the pin is designed in a way to minimise lacerations and the pin pressure is recommended not to exceed 60 psi for the Mayfield head clamps. We excluded this probability as the pins were tightened to keep the pin pressure within the range and there was no obvious fracture of the skull clinically or on radiology. Moreover, acute SDH in our case did not correlate with the site of pin insertion. Other possible causes such as bleeding disorders, disseminated intravascular coagulation, and hypertensive episodes during surgery were also excluded. In our case, we preferred propofol-based total intravenous maintenance anaesthesia to ensure brain relaxation from the beginning of the surgery. However, the measures, after initial success, proved insufficient and the brain suddenly bulged uncontrollably and inexplicably. Thus, we had to resort to other strategies including elevating head end, reducing neck flexion, and rotation, ensuring adequate depth of anaesthesia, instituting hyperosmolar therapy and loop diuretic, and finally controlled hyperventilation. The presence of chronic hypotension does not necessarily result in vasoparalysis in the arteriolar resistance bed. There is generally a preserved responsiveness to CO2 pre- and postsurgical resection, which lends further support to the notion of intact autoregulatory capacity. It is also important to consider and suspect surgical factor to be the cause of sustained or recurrent intraoperative brain swelling if anaesthesia-related causes are ruled out and multiple measures to reduce brain swelling prove inadequate. Intraoperative modalities available to investigate surgical cause of brain swelling include intraoperative MRI and brain ultrasound. Since the majority of the remote haemorrhages develop during or soon after surgery, postoperative routine CT study has been recommended.
| Conclusion|| |
Haemorrhage occurring at areas remote from the site of intracranial surgery comprises an uncommon entity. The pathophysiology is incomprehensive, despite several theories trying to explain it. Awareness among the neurosurgeons and anaesthesiologists is important for early recognition of this rare but potentially dreadful complication. Unexpected intraoperative brain swelling should always be dealt meticulously.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
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Conflicts of interest
There are no conflicts of interest.
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