Recurrent hemifacial spasm after microvascular decompression

Recurrent hemifacial spasm after microvascular decompression

Microvascular decompression (MVD) is a highly effective treatment for hemifacial spasm (HFS), but even if the root exit zone (REZ) from the brainstem is adequately decompressed, residual spasms after surgery or early reappearance of spasms are not uncommon 1) 2) 3) 4) 5)

Return of symptoms after a period of complete resolution of hemifacial spasm occurs in up to 10% of patients, 86% of recurrences happen within 2 yrs of surgery, and the risk of developing recurrence after 2 yrs of post-op relief is only ≈ 1% 6).


Among more than 2500 patients who underwent microvascular decompression for hemifacial spasm, 23 patients received a second MVD in the Kyung Hee University Hospital from January 2002 to December 2017. Three-dimensional time of flight magnetic resonance angiography and reconstructed imaging were used to identify the culprit vessel and its conflict upon root exit zone (REZ) of the facial nerve. They reviewed patients’ medical records and operation videos to identify the missing points of the first surgery.

8 patients had incomplete decompression, such as single-vessel decompression of multiple offending vessels. Teflon was not detected at the REZ, but was found in other locations in 12 patients. Three patients had severe adhesion with previous Teflon around the REZ. Nineteen patients had excellent surgical outcomes at immediate postoperative evaluation; 20 patients showed spasm disappearance at 1 year after surgery and 3 patients showed persistent symptoms. Neuro-vascular contacts around REZ of facial nerve were revealed on MRI of incomplete decompression and Teflon malposition patient groups. There were no clear neuro-vascular contacts in the patients with severe Teflon adhesion.

The decision on secondary MVD for persistent or recurrent spasm is troubling. However, if the neurovascular contact was observed in the MRI of the patient and there were offending vessels, the surgical outcome might be favorable 7).

References

1)

Fukushima T: Microvascular decompression for hemifacial spasm: results in 2890 cases, in Carter LP, Spetzler RF, editors. (eds): Neurovascular Surgery. New York, McGraw-Hill, 1995, pp 1133–1145
2)

Huang CI, Chen IH, Lee LS: Microvascular decompression for hemifacial spasm: analyses of operative findings and results in 310 patients. Neurosurgery 30: 53– 56; discussion 56–57, 1992.
3)

Ishikawa M, Nakanishi T, Takamiya Y, Namiki J: Delayed resolution of residual hemifacial spasm after microvascular decompression operations. Neurosurgery 49: 847– 854; discussion 854–856, 2001.
4)

Li CS: Varied patterns of postoperative course of disappearance of hemifacial spasm after microvascular decompression. Acta Neurochir (Wien) 147: 617– 620; discussion 620, 2005.
5)

Shin JC, Chung UH, Kim YC, Park CI: Prospective study of microvascular decompression in hemifacial spasm. Neurosurgery 40: 730– 734; discussion 734–735, 1997.
6)

Payner TD, Tew JM. Recurrence of Hemifacial Spasm After Microvascular Decompression. Neurosurgery. 1996; 38:686–691
7)

Park CK, Lee SH, Park BJ. Surgical Outcomes of Revision Microvascular Decompression for Persistent or Recurrent Hemifacial Spasm after Surgery: Analysis of radiological and intraoperative findings. World Neurosurg. 2019 Aug 2. pii: S1878-8750(19)32107-2. doi: 10.1016/j.wneu.2019.07.191. [Epub ahead of print] PubMed PMID: 31382068.

Unplanned hospital readmission after cranial neurosurgery

Unplanned hospital readmission after cranial neurosurgery

Many readmissions may be preventable and occur at predictable time intervals. The causes and timing of readmission vary significantly across neurosurgical subgroups. Future studies should focus on detecting specific complications in select cohorts at predefined time points, which may allow for interventions to lower costs and reduce patient morbidity 1).

In a single-center Canadian experience. Almost one-fifth of neurosurgical patients were readmitted within 30 days of discharge. However, only about half of these patients were admitted for an unplanned reason, and only 10% of all readmissions were potentially avoidable. This study demonstrates unique challenges encountered in a publicly funded healthcare setting and supports the growing literature suggesting 30-day readmission rates may serve as an inappropriate quality of care metric in neurosurgical patients. Potentially avoidable readmissions can be predicted, and further research assessing predictors of avoidable readmissions is warranted 2).

A study of Elsamadicy et al. suggested that infection, altered mental status, and new sensory/motor deficits were the primary complications leading to unplanned 30-day readmission after cranial neurosurgery 3).


The preponderance of postdischarge mortality and complications requiring readmission highlights the importance of posthospitalization management 4).


Obstructive sleep apnea (OSA) is known to be associated with negative outcomes and is underdiagnosed. The STOP-Bang questionnaire is a screening tool for OSA that has been validated in both medical and surgical populations. Given that readmission, after surgical intervention is an undesirable event, Caplan et al. sought to investigate, among patients not previously diagnosed with OSA, the capacity of the STOP-Bang questionnaire to predict 30-day readmissions following craniotomy for a supratentorial tumor.

For patients undergoing craniotomy for treatment of a supratentorial neoplasm within a multiple-hospital academic medical center, data were captured in a prospective manner via the Neurosurgery Quality Improvement Initiative (NQII) EpiLog tool. Data were collected over a 1-year period for all supratentorial craniotomy cases. An additional criterion for study inclusion was that the patient was alive at 30 postoperative days. Statistical analysis consisted of simple logistic regression, which assessed the ability of the STOP-Bang questionnaire and additional variables to effectively predict outcomes such as 30-day readmission, 30-day emergency department (ED) visit, and 30-day reoperation. The C-statistic was used to represent the receiver operating characteristic (ROC) curve, which analyzes the discrimination of a variable or model.

Included in the sample were all admissions for supratentorial neoplasms treated with craniotomy (352 patients), 49.72% (n = 175) of which were female. The average STOP-Bang score was 1.91 ± 1.22 (range 0-7). A 1-unit higher STOP-Bang score accurately predicted 30-day readmissions (OR 1.31, p = 0.017) and 30-day ED visits (OR 1.36, p = 0.016) with fair accuracy as confirmed by the ROC curve (C-statistic 0.60-0.61). The STOP-Bang questionnaire did not correlate with 30-day reoperation (p = 0.805) or home discharge (p = 0.315).

The results of this study suggest that undiagnosed OSA, as assessed via the STOP-Bang questionnaire, is a significant predictor of patient health status and readmission risk in the brain tumor craniotomy population. Further investigations should be undertaken to apply this prediction tool in order to enhance postoperative patient care to reduce the need for unplanned readmissions 5).


Lopez Ramos et al., from the Department of Neurological Surgery, University of California San Diego, La Jolla, CA, USA, examined clinical risk factors and postoperative complications associated with 30-day unplanned hospital readmissions after cranial neurosurgery.

They queried the American College of Surgeons National Surgical Quality Improvement Program database from 2011-2016 for adult patients that underwent a cranial neurosurgical procedure. Multivariable logistic regression with backwards model selection was used to determine predictors associated with 30-day unplanned hospital readmission.

Of 40,802 cranial neurosurgical cases, 4,147 (10.2%) had an unplanned readmission. Postoperative complications were higher in the readmission cohort (18.5% vs 9.9%, p <0.001). On adjusted analysis, clinical factors predictive of unplanned readmission included hypertension, COPD, diabetes, coagulopathy, chronic steroid use, and preoperative anemia, hyponatremia, and hypoalbuminemia (all p ≤ 0.01). Higher ASA class (III-V), operative time >216 minutes, and unplanned reoperation were also associated with an increased likelihood of readmission (all p ≤0.001). Postoperative complications predictive of unplanned readmissions were wound infection (OR 4.90, p <0.001), pulmonary embolus (OR 3.94, p <0.001), myocardial infarction/cardiac arrest (OR 2.37, p <0.001), sepsis (OR 1.73, p <0.001), deep venous thrombosis (1.50, p=0.002), and urinary tract infection (OR 1.45, p=0.002). Female sex, transfer status, and postoperative pulmonary complications were protective of readmission (all p <0.05)

Unplanned hospital readmission after cranial neurosurgery is a common event. Identification of high-risk patients who undergo cranial procedures may allow hospitals to reduce unplanned readmissions and associated healthcare costs 6).


Cusimano et al., conducted a systematic review of several databases; a manual search of the Journal of NeurosurgeryNeurosurgeryActa NeurochirurgicaCanadian Journal of Neurological Sciences; and the cited references of the selected articles. Quality review was performed using the STROBE (Strengthening the Reporting of Observational Studies in Epidemiology) criteria. Findings are reported according to the PRISMA(Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines.

A total of 1344 articles published between 1947 and 2015 were identified; 25 were considered potentially eligible, of which 12 met inclusion criteria. The 30-day readmission rates varied from 6.9% to 23.89%. Complications arising during or after neurosurgical procedures were a prime reason for readmission. Race, comorbidities, and longer hospital stay put patients at risk for readmission.

Although readmission may be an important indicator for good care for the subset of acutely declining patients, neurosurgery should aim to reduce 30-day readmission rates with improved quality of care through systemic changes in the care of neurosurgical patients that promote preventive measures 7).

References

1)

Taylor BE, Youngerman BE, Goldstein H, Kabat DH, Appelboom G, Gold WE, Connolly ES Jr. Causes and Timing of Unplanned Early Readmission After Neurosurgery. Neurosurgery. 2016 Sep;79(3):356-69. doi: 10.1227/NEU.0000000000001110. PubMed PMID: 26562821.
2)

Wilson MP, Jack AS, Nataraj A, Chow M. Thirty-day readmission rate as a surrogate marker for quality of care in neurosurgical patients: a single-center Canadian experience. J Neurosurg. 2018 Jul 1:1-7. doi: 10.3171/2018.2.JNS172962. [Epub ahead of print] PubMed PMID: 29979117.
3)

Elsamadicy AA, Sergesketter A, Adogwa O, Ongele M, Gottfried ON. Complications and 30-Day readmission rates after craniotomy/craniectomy: A single Institutional study of 243 consecutive patients. J Clin Neurosci. 2018 Jan;47:178-182. doi: 10.1016/j.jocn.2017.09.021. Epub 2017 Oct 12. PubMed PMID: 29031542.
4)

Dasenbrock HH, Yan SC, Smith TR, Valdes PA, Gormley WB, Claus EB, Dunn IF. Readmission After Craniotomy for Tumor: A National Surgical Quality Improvement Program Analysis. Neurosurgery. 2017 Apr 1;80(4):551-562. doi: 10.1093/neuros/nyw062. PubMed PMID: 28362921.
5)

Caplan IF, Glauser G, Goodrich S, Chen HI, Lucas TH, Lee JYK, McClintock SD, Malhotra NR. Undiagnosed obstructive sleep apnea as a predictor of 30-day readmission for brain tumor patients. J Neurosurg. 2019 Jul 19:1-6. doi: 10.3171/2019.4.JNS1968. [Epub ahead of print] PubMed PMID: 31323636.
6)

Lopez Ramos C, Brandel MG, Rennert RC, Wali AR, Steinberg JA, Santiago-Dieppa DR, Burton BN, Pannell JS, Olson SE, Khalessi AA. Clinical Risk Factors and Postoperative Complications Associated with Unplanned Hospital Readmissions After Cranial Neurosurgery. World Neurosurg. 2018 Jul 24. pii: S1878-8750(18)31614-0. doi: 10.1016/j.wneu.2018.07.136. [Epub ahead of print] PubMed PMID: 30053566.
7)

Cusimano MD, Pshonyak I, Lee MY, Ilie G. A systematic review of 30-day readmission after cranial neurosurgery. J Neurosurg. 2017 Aug;127(2):342-352. doi: 10.3171/2016.7.JNS152226. Epub 2016 Oct 21. PubMed PMID: 27767396.

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.
WhatsApp WhatsApp us
%d bloggers like this: