Brain edema after cranioplasty

Brain edema after cranioplasty

Some authors have reported a rare unexplained complication of sudden death in association with massive brain edema immediately after cranioplasty.

Causes of cerebral edema and hemorrhage immediately after cranioplasty include reperfusion, reduction of automatic adjustment function, sinking skin flap syndrome, negative pressure due to s.c. drain, venous stasis, vascular damage following restoration of midline shift, and allergic reaction1).

Once the computed tomography scan shows malignant cerebral swelling, the patient is expected to have a poor prognosis 2) 3).

It is hypothesized that intracranial hypotension (IH) caused stagnation of venous flow. Neurosurgeons should be aware that fatal venous congestion induced by IH may occur after cranioplasty. To avoid this, tight dural closure should be obtained, and avoidance of the use of subcutaneous drains should be considered 4).


Zhang et al., reported one fatal case and analyze the possible mechanism of this complication.

The patient was a 40-year-old man who had a severe right basal ganglia hemorrhage and underwent DC ∼ 2 months before. One day before scheduled cranioplasty, a External lumbar cerebrospinal fluid drainage was placed. The cranioplasty itself was uneventful. However, he gradually fell into a coma, and his right pupil was moderately dilated 20 hours after the surgery. A brain computed tomography (CT) scan indicated massive right cerebral edema with compressed right midbrain. The patient did not regain consciousness, and he remained quadriplegic.

It is necessary to increase awareness of complications of cranioplasty in high-risk patients. The lessons learned from this case include avoiding excessive drainage of cerebrospinal fluid. Patients with low-density lesions in the brain need to be treated with caution. Once the CT scan shows massive cerebral swelling, the patient has a poor prognosis 5).


A 51-year-old man who was a victim of traumatic brain injury underwent emergency clot removal and decompression craniectomy. His neurologic condition improved with subsequent rehabilitation therapy, and he had left sinking skin flap syndrome where the skull was defective. Six months after the initial surgery, he underwent a cranioplasty; however, he did not recover from the uneventful anesthesia. A vacuum suction drain showed 300 mL of flow outflow had drained when his pupils dilated and fixed. An immediate computed tomography scan showed ipsilateral diffuse cerebral swelling with diffuse cerebral hemorrhage. Despite all approaches that were considered, the cerebral swelling continued to worsen until death 6).


Two cases of critical brain swelling after otherwise uneventful cranioplasty. Both cases had subarachnoid hemorrhage and extremely similar clinical courses. They underwent decompressive craniotomy and clipping in the acute phase and had cranioplasty in the chronic phase, resulting in serious cerebral swelling and death. Deep venous sinus thrombosis was revealed in the autopsy for one case. Although no venous occlusion was identified in the other case, radiological findings suggested venous congestion. In both cases, intraoperative cerebrospinal fluid leakage was massive and was prolonged by a drain 7).


A 64-year-old man was admitted with the diagnosis of cerebral hemorrhage, and emergency surgery for hemorrhage removal and decompressive craniotomy were performed. One month after surgery, cranioplasty was performed using a titanium mesh plate. Sixteen hours after the surgery, the patient became comatose with bilateral dilated pupils followed by blood pressure lowering. Computed tomography of the brain showed bilateral massive cerebral edema. The titanium mesh plate was immediately removed, however, the patient’s neurological condition did not recover and he died 7 days after the surgery. We speculated that the negative pressure difference and increase in cerebral blood flow after cranioplasty may have attributed to the fatal cerebral swelling 8).


A 84-year-old man with subarachnoid hemorrhage underwent craniotomy and clipping with external decompression. Perfusion magnetic resonance imaging showed subclinical sinking skin flap syndrome, and he underwent cranioplasty on postoperative day 58. No problems occurred during the operation, but cerebral edema and hemorrhage were recognized on immediate postoperative computed tomography. Edema continued to progress, but edema and bleeding eventually improved without additional surgery.

Neurological symptoms improved to presurgical baseline and stabilized 9).


A 50-year-old female was admitted with sudden onset of stuporous consciousness. A brain computed tomography (CT) revealed a subarachnoid hemorrhage with intracranial hemorrhage and subdural hematoma. Emergency decompressive craniectomy and aneurysmal neck clipping were performed. Following recovery, the decision was made to proceed with an autologous cranioplasty. The cranioplasty procedure was free of complications. An epidural drain was placed and connected to a suction system during skin closure to avoid epidural blood accumulation. However, following the procedure, the patient had a seizure in the recovery room. An emergency brain CT scan revealed widespread cerebral edema, and the catheter drain was clamped. The increased intracranial pressure and cerebral edema were controlled with osmotic diuretics, corticosteroids, and antiepileptic drugs. The edema slowly subsided, but new low-density areas were noted in the brain on follow-up CT 1 week later. They speculated that placing the epidural drain on active suction may have caused an acute decrease in intracranial pressure and subsequent rapid expansion of the brain, which impaired autoregulation and led to reperfusion injury 10).


Sviri reported on 4 patients who underwent cranioplasty after DC between January 2005 and August 2010 and died because of massive cerebral edema immediately after uneventful surgery and anesthesia. All 4 of the new cases reported involved young male patients who underwent decompressive hemicraniectomy after traumatic brain injury. They developed massive cerebral swelling immediately after uneventful cranioplasty (3 patients) or after removal of an epidural hematoma several hours after surgery (1 patient). All 4 patients had a large skull defect and significantly sunken craniotomy site, and all were treated with a closed vacuum suction system that was placed under the scalp and kept open at the end of the cranioplasty procedure. After surgery, the patients’ pupils became fixed and dilated, and brain CT scans showed massive brain edema. Despite emergency DC, the patients did not recover, and all 4 died. A MEDLINE search showed 8 similar cases that were reported previously. Fatal cerebral swelling after uneventful cranioplasty is a distinct clinical entity, although it is unpredictable. It is postulated that a negative pressure difference from the elimination of atmospheric pressure that had been chronically applied on the injured sinking brain in combination with the negative pressure applied by the closed subgaleal suction drain may lead to a massive brain shift toward the cranioplasty site and initiate a fatal vasomotor reaction 11).

References

1) , 9)

Kato A, Morishima H, Nagashima G. Unexpected complications immediately after cranioplasty. Acute Med Surg. 2017 Feb 22;4(3):316-321. doi: 10.1002/ams2.260. eCollection 2017 Jul. PubMed PMID: 29123881; PubMed Central PMCID: PMC5674471.
2) , 6)

Shen L, Zhou Y, Xu J, Su Z. Malignant Cerebral Swelling After Cranioplasty: Case Report and Literature Review. World Neurosurg. 2018 Feb;110:4-10. doi: 10.1016/j.wneu.2017.10.102. Epub 2017 Oct 28. Review. PubMed PMID: 29101073.
3) , 5)

Zhang X, Pan B, Ye Z, Li Z, Mo F, Wang X. Massive Brain Swelling after Cranioplasty: A Case Report. J Neurol Surg A Cent Eur Neurosurg. 2019 May 10. doi: 10.1055/s-0039-1688726. [Epub ahead of print] PubMed PMID: 31075809.
4)

Nomura M, Ota T, Ishizawa M, Yoshida S, Hara T. Intracranial Hypotension-associated Cerebral Swelling following Cranioplasty: Report of Two Cases. Asian J Neurosurg. 2017 Oct-Dec;12(4):794-796. doi: 10.4103/1793-5482.185070. PubMed PMID: 29114315; PubMed Central PMCID: PMC5652127.
7)

Nomura M, Ota T, Ishizawa M, Yoshida S, Hara T. Intracranial Hypotension-associated Cerebral Swelling following Cranioplasty: Report of Two Cases. Asian J Neurosurg. 2017 Oct-Dec;12(4):794-796. doi: 10.4103/1793-5482.185070. PubMed PMID: 29114315; PubMed Central PMCID: PMC5652127.
8)

Kaneshiro Y, Murata K, Yamauchi S, Urano Y. Fatal cerebral swelling immediately after cranioplasty: A case report. Surg Neurol Int. 2017 Jul 25;8:156. doi: 10.4103/sni.sni_137_17. eCollection 2017. PubMed PMID: 28808605; PubMed Central PMCID: PMC5535512.
10)

Lee GS, Park SQ, Kim R, Cho SJ. Unexpected Severe Cerebral Edema after Cranioplasty : Case Report and Literature Review. J Korean Neurosurg Soc. 2015 Jul;58(1):76-8. doi: 10.3340/jkns.2015.58.1.76. Epub 2015 Jul 31. PubMed PMID: 26279818; PubMed Central PMCID: PMC4534744.
11)

Sviri GE. Massive cerebral swelling immediately after cranioplasty, a fatal and unpredictable complication: report of 4 cases. J Neurosurg. 2015 Jun 19:1-6. [Epub ahead of print] PubMed PMID: 26090828.

Pediatric cerebral arteriovenous malformation

Pediatric cerebral arteriovenous malformation

Although brain arteriovenous malformations (bAVMs) account for a very small proportion of cerebral pathologies in the pediatric population, they are the cause of roughly 50% of spontaneous intracranial hemorrhages. Pediatric bAVMs tend to rupture more frequently and seem to have higher recurrence rates than bAVMs in adults 1) 2) 3) 4) 5) 6) 7).

Natural History

The natural history of untreated cerebral AVMs in children is worse than in adults, in relation to a longer life expectation, a higher annual risk of AVM bleeding (3.2% vs. 2.2%) and a higher incidence of posterior fossa and basal ganglia AVMs, most of which present with massive haemorrhages 8).

Treatment

The management of pediatric bAVMs is particularly challenging. In general, the treatment options are conservative treatment, microsurgeryendovascular therapy (EVT), gamma knife radiosurgery (GKRS), proton-beam stereotactic radiosurgery (PSRS), or a combination of the above.


In 2019 Meling et al., performed a systematic review, according to the PRISMA guidelines, with the result that none of the options seem to offer a clear advantage over the others when used alone. Microsurgery provides the highest obliteration rate, but has higher incidence of neurological complications. EVT may play a role when used as adjuvant therapy, but as a stand-alone therapy, the efficacy is low and the long-term side effects of radiation from the multiple sessions required in deep-seated pediatric bAVMs are still unknown. GKRS has a low risk of complication, but the obliteration rates still leave much to be desired. Finally, PSRS offers promising results with a more accurate radiation that avoids the surrounding tissue, but data is limited due to its recent introduction. Overall, a multi-modal approach, or even an active surveillance, might be the most suitable when facing deep-seated bAVM, considering the difficulty of their management and the high risk of complications in the pediatric population 9).


In 2016 El-Ghanem et al., published a Review of the Existing Literature:

Microsurgical resection remains the gold standard for the treatment of all accessible pediatric AVMs. Embolization and radiosurgery should be considered as an adjunctive therapy. Embolization provides a useful adjunct therapy to microsurgery by preventing significant blood loss and to radiosurgery by decreasing the volume of the AVM. Radiosurgery has been described to provide an alternative treatment approach in certain circumstances either as a primary or adjuvant therapy 10).

Outcome

Intracranial haemorrhage is the presenting clinical manifestation in 75-80% of paediatric patients and is associated with a high morbidity and mortality 11).

Case series

A prospectively maintained database of children between January 1997 and October 2012 for bAVMs was retrospectively queried to identify all consecutive ruptured bAVMs treated by surgery, embolization, and radiosurgery. The impact of baseline clinical and bAVM characteristics on clinical outcome, rebleeding rate, annual bleeding rate, and bAVM obliteration was studied using univariate and multivariate Cox regression analysis.

One hundred six children with ruptured bAVMs were followed up for a total of 480.5 patient-years (mean, 4.5 years). Thirteen rebleeding events occurred, corresponding to an annual bleeding rate of 2.71±1.32%, significantly higher in the first year (3.88±1.39%) than thereafter (2.22±1.38%; P<0.001) and in the case of associated aneurysms (relative risk, 2.68; P=0.004) or any deep venous drainage (relative risk, 2.97; P=0.002), in univariate and multivariate analysis. Partial embolization was associated with a higher annual bleeding rate, whereas initial surgery for intracerebral hemorrhage evacuation was associated with a lower risk of rebleeding.

Associated aneurysms and any deep venous drainage are independent risk factors for rebleeding in pediatric ruptured bAVMs. Immediate surgery or total embolization might be advantageous for children harboring such characteristics, whereas radiosurgery might be targeted at patients without such characteristics 12).

References

1) , 8) , 11)

Di Rocco C, Tamburrini G, Rollo M. Cerebral arteriovenous malformations in children. Acta Neurochir (Wien). 2000;142(2):145-56; discussion 156-8. PubMed PMID: 10795888.
2)

Millar C, Bissonnette B, Humphreys RP. Cerebral arteriovenous malformations in children. Can J Anaesth. 1994;41:321–331.
3)

Kiris T, et al. Surgical results in pediatric Spetzler-Martin grades I–III intracranial arteriovenous malformations. Childs Nerv Syst. 2005;21:69–74. discussion 75–76.
4)

Hoh BL, et al. Multimodality treatment of nongalenic arteriovenous malformations in pediatric patients. Neurosurgery. 2000;47:346–357. discussion 357–358.
5)

Kondziolka D, et al. Arteriovenous malformations of the brain in children: a forty year experience. Can J Neurol Sci. 1992;19:40–45.
6)

11. Wilkins RH. Natural history of intracranial vascular malformations: a review. Neurosurgery. 1985;16:421–430.
7)

Jankowitz BT, et al. Treatment of pediatric intracranial vascular malformations using Onyx-18. J Neurosurg Pediatr. 2008;2:171–176.
9)

Meling TR, Patet G. What is the best therapeutic approach to a pediatric patient with a deep-seated brain AVM? Neurosurg Rev. 2019 Apr 13. doi: 10.1007/s10143-019-01101-8. [Epub ahead of print] Review. PubMed PMID: 30980204.
10)

El-Ghanem M, Kass-Hout T, Kass-Hout O, Alderazi YJ, Amuluru K, Al-Mufti F, Prestigiacomo CJ, Gandhi CD. Arteriovenous Malformations in the Pediatric Population: Review of the Existing Literature. Interv Neurol. 2016 Sep;5(3-4):218-225. Epub 2016 Sep 1. Review. PubMed PMID: 27781052; PubMed Central PMCID: PMC5075815.
12)

Blauwblomme T, Bourgeois M, Meyer P, Puget S, Di Rocco F, Boddaert N, Zerah M, Brunelle F, Rose CS, Naggara O. Long-term outcome of 106 consecutive pediatric ruptured brain arteriovenous malformations after combined treatment. Stroke. 2014 Jun;45(6):1664-71. doi: 10.1161/STROKEAHA.113.004292. Epub 2014 May 1. PubMed PMID: 24788975.
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