© Springer Science+Business Media Dordrecht 2016
Shi-Ting Li, Jun Zhong and Raymond F. Sekula, Jr. (eds.)Microvascular Decompression Surgery10.1007/978-94-017-7366-9_1515. Perioperative Adverse Events of Microvascular Decompression: Review and a Personal Experience of 2263 Cases
(1)
Department of Neurosurgery, Samsung Medical Center, Sungkyunkwan University, School of Medicine, 81 Irwon-ro, Gangnam-gu, Seoul, 135-710, South Korea
Abstract
Background
Microvascular decompression (MVD) is effective treatment modality for the treatment of trigeminal neuralgia and hemifacial spasm. However, there are potential risks of MVD generally related to the surgical technique and particularly to manipulation around the cranial nerve. The purpose of this study was to identify possible adverse events after MVD and to establish the strategies to minimize the complications after MVD.
Methods
We reviewed the literatures focusing on the adverse events after MVD and analyzed our personal series of 2263 cases.
Results
The complications after MVD include facial palsy, middle ear effusion, hearing loss, dysgeusia, other cranial nerve deficits, thromboembolic or hemorrhage complication, etc. The complications can be classified into transient and permanent deficits. For transient complications, patient’s reassurance is important, and for permanent form, we should keep in mind the disciplined surgical technique, collaborative intraoperative monitoring, and development of modern equipments.
Conclusion
We believe that a significant proportion of these complications can be avoidable through development and testing of standardized protocols to incorporate monitoring technologies and specific technical practices, teamwork and communication, and concentrated volume and specialization.
Keywords
MVDComplicationsAvoidableStandard protocolsTechniquesMicrovascular decompression (MVD) is considered the treatment of choice for trigeminal neuralgia and hemifacial spasm and is a safe and effective treatment option for definitive cure. However, there are potential risks of MVD generally related to the surgical technique and particularly to manipulation around the cranial nerve. Common complications included facial palsy, hearing impairment, cerebrospinal fluid leaks and fistulas, cranial nerve deficits, and cerebrovascular events. In particular, cerebrovascular events, although relatively rare, remains a significant problem. Hemorrhagic complications carry by far the highest risk of devastating neurological outcome in functional neurosurgery. Estimating the predictive risk factors of postoperative complications is a challenging issue. Increased regionalization, more stringent volume requirements, and greater standardization and more rapid assimilation of standardized devices may prove beneficial for the more technical complications of surgery, but these strategies have not been adequately evaluated. This study reviews the factors that may predict susceptibility to post-MVD complications and addresses therapeutic choices, adjunctive therapies, and technological applications that may help with complication avoidance.
15.1 Transient and Permanent Deficits
Postoperative complications after MVD can be classified into transient and permanent deficits. Transient complications include facial palsy, hearing deficit, and cerebrospinal fluid leak. Permanent complications include hearing loss, facial palsy, and hemorrhagic/thromboembolic events (Miller and Miller 2012; Huh et al. 2008). Transient complications can be overcome by close follow-up of symptom change, appropriate warning for possible conversion to the permanent deficits, and simultaneously reassuring the patients. Huh et al. published in 2008 that postoperative complications were noted in 545 (35.8 %) patients. Among them, facial palsy, hearing deficit, and low cranial nerve palsies were found in 18.6 % (n = 283), 7.2 % (n = 109), and 2.8 % (n = 43), respectively. However, permanent facial weakness, hearing deficit, and lower cranial nerve palsies such as hoarseness and dysphagia were encountered in 1.2 % (n = 18), 2.1 % (n = 32), and 0.1 % (n = 2), respectively (Huh et al. 2008). Therefore, 1-year or longer follow-up monitoring is required before determination of “permanence” with respect to cranial nerve dysfunction (Huh et al. 2008).
There are some differences of the incidence of complications after MVD between trigeminal neuralgia and hemifacial spasm. In our series of 2263 patients undergoing MVD (under submission), the most common complications after MVD for trigeminal neuralgia was middle ear effusion (MEE) (5.38 %), followed by hearing impairment (1.35 %), dysgeusia (1.35 %), and wound complications (1.35 %). After MVD for hemifacial spasm, the most common complications were facial nerve palsy (8.19 %), followed by MEE (5.38 %) and hearing deficits (3.63 %). In the following sections, we are to discuss each complication of MVD, which we can encounter commonly.
15.1.1 Facial Palsy
Facial palsy is the most common complication of MVD for hemifacial spasm. The incidence of facial palsy is reported to be 14.3–18.6 % (Miller and Miller 2012; Huh et al. 2008). Facial palsy can be classified into two groups based on the mode of onset. Immediate facial palsy occurs immediately after surgery within 24 h, where delayed facial palsy usually occurs over a 24-h to 7-day period after the operation (Hongo et al. 1985). Recent literatures showed that the rate for incurring delayed facial palsy following MVD is 2.8–8.3 % (Lovely et al. 1998; Rhee et al. 2006; Furukawa et al. 2003; Han et al. 2012) and was reversible in almost all the cases. Recently, in our 2263 cases series, we found that facial palsy occurred in 169 (7.47 %) cases. Eighteen patients (0.80 %) exhibited immediately after surgery, and 151 patients (6.67 %) had facial palsy after a delayed period. Severity of immediate-onset facial palsy was higher than delayed-onset facial palsy. In cases of trigeminal neuralgia, there was no incidence of immediate-onset facial palsy, but two cases had delayed-onset facial palsy.
The accurate mechanism of postoperative facial palsy remains unclear. Possible etiologies of facial palsy include direct injury in the exit zone of facial nerve injury by the Teflon felt, delayed facial nerve edema by manipulation, or disturbance of microcirculation due to vasospasm (Huh et al. 2008; Lovely et al. 1998; Rhee et al. 2006). Finding that most cases of facial palsy occur in the hemifacial spasm rather than trigeminal neuralgia showed evidence that immediate-onset facial palsy is caused by direct injury to facial nerve. During the surgical field, any degree of stretching force on the nerve can be added by cerebellar retraction to secure operation field. In general, the facial weakness can resolve spontaneously, with excellent outcomes (Lovely et al. 1998; Rhee et al. 2006; Samii et al. 2002; Kondo 1998). Cause of delayed-onset facial palsy is unknown. The theory of viral origin may have reliable rationale (Lovely et al. 1998; Rhee et al. 2006; Furukawa et al. 2003; Hung et al. 2002; Badr-El-Dine et al. 2002). The manipulation of the nerve could stimulate a dormant virus, possibly localized in the geniculate ganglion. Postoperative facial palsy is usually managed with extensive rehabilitation, and reoperations are rarely required (Lovely et al. 1998; Rhee et al. 2006; Furukawa et al. 2003; Han et al. 2012; Dannenbaum et al. 2008; Jeon et al. 2010).
15.1.2 Hearing Impairment
Hearing impairment is a relatively infrequent but significant risk of the MVD caused by damage to the vestibulocochlear nerve. In general, hearing impairment is defined as either an increase of more than 15 dB of average pure tone audiogram (0.5, 1, 2 K) threshold according to bone conduction or an increase of more than 20 % of speech discrimination scale related to baseline hearing. Excessive and forceful retraction of the cerebellum is supposed to be a major reason of hearing impairment after MVD. Profound sensorineural hearing loss is a recognized complication of MVD for hemifacial spasm with a reported incidence of 1.9–20 % (Miller and Miller 2012; Dannenbaum et al. 2008; Chung et al. 2001; Fritz et al. 1988; Hatayama and Moller 1998; Hyun et al. 2010; Jannetta and Hirsch 1993; Jannetta et al. 1986; Jo et al. 2011, 2013; Moffat et al. 2005; Moller and Jannetta 1983; Park et al. 2009; Rosseau et al. 1993; Sekiya et al. 1991; Shah et al. 2012; Vasama et al. 1998). These reports may underestimate the true incidence of hearing loss because preoperative and postoperative audiograms are not always available for comparison.
15.2 Possible Mechanism of Hearing Loss
Hearing loss after MVD may occur for the following reasons (Miller and Miller 2012; Dannenbaum et al. 2008; Chung et al. 2001; Fritz et al. 1988; Hatayama and Moller 1998; Hyun et al. 2010; Jannetta and Hirsch 1993; Jannetta et al. 1986; Jo et al. 2011, 2013; Moffat et al. 2005; Moller and Jannetta 1983; Park et al. 2009; Rosseau et al. 1993; Sekiya et al. 1991; Shah et al. 2012; Vasama et al. 1998):
1.
Stretching of the 8th nerve when retracting the cerebellum; the manipulation of the nerve is likely to lead to the stretching or spasm of the vasa nervorum and consequent ischemic phenomena.
2.
Manipulation of the labyrinthine artery and/or the anteroinferior cerebellar artery; the cochlea receives its blood supply from the internal auditory artery. Damage to the artery leads to cochlear ischemia or infarction which may affect wave I.
3.
Direct trauma to the nerve by instruments or nearby coagulation.
4.
5.
Recently, we reported a new possible mechanism of hearing loss due to increased intracranial pressure from overinfusion of saline with dural closure (Jo et al. 2013); intradural compression due to overinfusion of saline may lead to postoperative hearing loss, although the incidence is low, and immediate decompression by drainage may be required.
Recently, Ying et al. (2013) suggested that high-frequency hearing loss occurs in a significant number of patients following MVD surgery for hemifacial spasm. Drill-induced noise and transient loss of CSF during surgery may impair hearing in the high-frequency ranges on both the ipsilateral and contralateral sides.
Considering the flocculus covering the VII–VIII nerves complex, it is difficult to directly approach in a dorsoventral direction and completely observe the root exit zone of facial nerve. Cerebellar retraction may be mandatory to observe the exit zone of facial nerve, and it is sometimes closely associated with postoperative hearing deterioration. In the recent literature, Lee et al. (2015) suggested that preoperative assessment of pathological anatomy by MR imaging can predict the degree of cerebellar retraction intraoperatively and attempted to show indirectly the correlation of cerebellar retraction with BAEP change.
Rarely, sudden deterioration in brainstem auditory evoked potentials (BAEP) occurs during or immediately after craniectomy, probably caused by an edema in the intracanalicular tract of the nerve. The vibrations caused by drilling for craniotomy is transmitted to the rocca petrosa and may lead to edema and subsequent ischemia of the cochlear nerve, resulting in a reversible blockade of its transmission capacities (Lee et al. 2015). Grundy et al. suggested that hypoperfusion should be considered as a contributing factor, when decreasing of the amplitude without prolongation of the latency (Grundy et al. 1982). The amplitude of BAEP can depend upon the individual situation such as recording conditions, electrode impedance, and a number of unknown factors (Moller 1995).
15.3 Role of BAEP
Intraoperative monitoring of brainstem auditory evoked potentials (BAEP) is useful for reducing the risk of hearing impairment in patients undergoing the cerebellopontine angle (CPA) surgery including MVD (Hatayama and Moller 1998; Lee et al. 2009; Sindou et al. 1992). The surgical procedure most frequently associated with BAEP deterioration is traction and/or compression of the nerve during the course of the maneuvers to release the nerve structures from the vascular loop. These BAEP changes may reflect direct mechanical or thermal damage to the brainstem, brainstem compression, or ischemia or infarction resulting from vascular compromise. Our experience supported that during MVD surgery, if the decrease of amplitude and prolongation of latency in wave V are rapid and the changes do not recover with correction, the possibility of hearing loss is high (Ying et al. 2013).
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