Intracranial pressure monitoring in children

Intracranial pressure monitoring in children

Protocols for treatment of children with severe traumatic brain injury incorporate intracranial pressure monitoring as part of a comprehensive plan to minimize secondary injuries, using either ICP and/or cerebral perfusion pressure (CPP) as the therapeutic target 1).

At least 500 children enrolled in 9 studies have demonstrated at least some association between ICP and outcome 2) 3) 4) 5) 6) 7) 8) 9) 10).

As a result, most centers adopted ICP monitoring years ago, while some have argued against the need for such an approach 11).

Data suggest that there is a small, yet statistically significant, survival advantage in patients who have ICP monitors and a GCS score of 3. However, all patients with ICP monitors experienced longer hospital length of stay, longer intensive care unit stay, and more ventilator days compared with those without ICP monitors. A prospective observational study would be helpful to accurately define the population for whom ICP monitoring is advantageous 12).

EVD and IP measurements of ICP were highly correlated, although intermittent EVD ICP measurements may fail to identify ICP events when continuously draining cerebrospinal fluid. In institutions that use continuous cerebrospinal fluid diversion as a therapy, a two-monitor system may be valuable for accomplishing monitoring and therapeutic goals 13).


In the search for a reliable, cooperation-independent, noninvasive alternative to invasive intracranial pressure monitoring in children, various approaches have been proposed, but at the present time none are capable of providing fully automated, real-time, calibration-free, continuous and accurate intracranial pressure estimates. Fanelli et al. investigated the feasibility and validity of simultaneously monitored arterial blood pressure(ABP) and middle cerebral artery (MCA) cerebral blood flow velocity (CBFV) waveforms to derive noninvasive ICP (nICP) estimates.

Invasive ICP and ABP recordings were collected from 12 pediatric and young adult patients (aged 2-25 years) undergoing such monitoring as part of routine clinical care. Additionally, simultaneous transcranial Doppler (TCD) ultrasonography-based MCA CBFV waveform measurements were performed at the bedside in dedicated data collection sessions. The ABP and MCA CBFV waveforms were analyzed in the context of a mathematical model, linking them to the cerebral vasculature’s biophysical properties and ICP. The authors developed and automated a waveform preprocessing, signal-quality evaluation, and waveform-synchronization “pipeline” in order to test and objectively validate the algorithm’s performance. To generate one nICP estimate, 60 beats of ABP and MCA CBFV waveform data were analyzed. Moving the 60-beat data window forward by one beat at a time (overlapping data windows) resulted in 39,480 ICP-to-nICP comparisons across a total of 44 data-collection sessions (studies). Moving the 60-beat data window forward by 60 beats at a time (nonoverlapping data windows) resulted in 722 paired ICP-to-nICP comparisons.

Greater than 80% of all nICP estimates fell within ± 7 mm Hg of the reference measurement. Overall performance in the nonoverlapping data window approach gave a mean error (bias) of 1.0 mm Hg, standard deviation of the error (precision) of 5.1 mm Hg, and root-mean-square error of 5.2 mm Hg. The associated mean and median absolute errors were 4.2 mm Hg and 3.3 mm Hg, respectively. These results were contingent on ensuring adequate ABP and CBFV signal quality and required accurate hydrostatic pressure correction of the measured ABP waveform in relation to the elevation of the external auditory meatus. Notably, the procedure had no failed attempts at data collection, and all patients had adequate TCD data from at least one hemisphere. Last, an analysis of using study-by-study averaged nICP estimates to detect a measured ICP > 15 mm Hg resulted in an area under the receiver operating characteristic curve of 0.83, with a sensitivity of 71% and specificity of 86% for a detection threshold of nICP = 15 mm Hg.

This nICP estimation algorithm, based on ABP and bedside TCD CBFV waveform measurements, performs in a manner comparable to invasive ICP monitoring. These findings open the possibility for rational, point-of-care treatment decisions in pediatric patients with suspected raised ICP undergoing intensive care 14).


Noninvasive quantitative measures of the peripapillary retinal structure by SD-OCT were correlated with invasively measured intracranial pressure. Optical coherence tomographic parameters showed promise as surrogate, noninvasive measures of intracranial pressure, outperforming other conventional clinical measures. Spectral-domain OCT of the peripapillary region has the potential to advance current treatment paradigms for elevated intracranial pressure in children 15).

References

1)

Adelson PD, Bratton SL, Carney NA, Chesnut RM, du Coudray HE, Goldstein B, Kochanek PM, Miller HC, Partington MP, Selden NR, Warden CR, Wright DW; American Association for Surgery of Trauma; Child Neurology Society; International Society for Pediatric Neurosurgery; International Trauma Anesthesia and Critical Care Society; Society of Critical Care Medicine; World Federation of Pediatric Intensive and Critical Care Societies. Guidelines for the acute medical management of severe traumatic brain injury in infants, children, and adolescents. Chapter 19. The role of anti-seizure prophylaxis following severe pediatric traumatic brain injury. Pediatr Crit Care Med. 2003 Jul;4(3 Suppl):S72-5. PubMed PMID: 12847355.
2)

Alberico AM, Ward JD, Choi SC, Marmarou A, Young HF. Outcome after severe head injury. Relationship to mass lesions, diffuse injury, and ICP course in pediatric and adult patients. J Neurosurg. 1987;67(5):648–656.
3)

Barzilay Z, Augarten A, Sagy M, Shahar E, Yahav Y, Boichis H. Variables affecting outcome from severe brain injury in children. Intensive Care Med. 1988;14(4):417–421.
4)

Chambers IR, Treadwell L, Mendelow AD. Determination of threshold levels of cerebral perfusion pressure and intracranial pressure in severe head injury by using receiver-operating characteristic curves: an observational study in 291 patients. J Neurosurg. 2001;94(3):412–416.
5)

Downard C, Hulka F, Mullins RJ, Piatt J, Chesnut R, Quint P, Mann NC. Relationship of cerebral perfusion pressure and survival in pediatric brain-injured patients. J Trauma. 2000;49(4):654–658. discussion 658-659.
6)

Eder HG, Legat JA, Gruber W. Traumatic brain stem lesions in children. Childs Nerv Syst. 2000;16(1):21–24.
7)

Esparza J, J MP, Sarabia M, Yuste JA, Roger R, Lamas E. Outcome in children with severe head injuries. Childs Nerv Syst. 1985;1(2):109–114.
8)

Kasoff SS, Lansen TA, Holder D, Filippo JS. Aggressive physiologic monitoring of pediatric head trauma patients with elevated intracranial pressure. Pediatr Neurosci. 1988;14(5):241–249.
9)

Michaud LJ, Rivara FP, Grady MS, Reay DT. Predictors of survival and severity of disability after severe brain injury in children. Neurosurgery. 1992;31(2):254–264.
10)

Shapiro K, Marmarou A. Clinical applications of the pressure-volume index in treatment of pediatric head injuries. J Neurosurg. 1982;56(6):819–825.
11)

Salim A, Hannon M, Brown C, Hadjizacharia P, Backhus L, Teixeira PG, Chan LS, Ford H. Intracranial pressure monitoring in severe isolated pediatric blunt head trauma. Am Surg. 2008 Nov;74(11):1088-93. PubMed PMID: 19062667.
12)

Alkhoury F, Kyriakides TC. Intracranial Pressure Monitoring in Children With Severe Traumatic Brain Injury: National Trauma Data Bank-Based Review of Outcomes. JAMA Surg. 2014 Jun;149(6):544-8. doi: 10.1001/jamasurg.2013.4329. PubMed PMID: 24789426.
13)

Exo J, Kochanek PM, Adelson PD, Greene S, Clark RS, Bayir H, Wisniewski SR, Bell MJ. Intracranial pressure-monitoring systems in children with traumatic brain injury: combining therapeutic and diagnostic tools. Pediatr Crit Care Med. 2011 Sep;12(5):560-5. doi: 10.1097/PCC.0b013e3181e8b3ee. PubMed PMID: 20625341; PubMed Central PMCID: PMC3670608.
14)

Fanelli A, Vonberg FW, LaRovere KL, Walsh BK, Smith ER, Robinson S, Tasker RC, Heldt T. Fully automated, real-time, calibration-free, continuous noninvasive estimation of intracranial pressure in children. J Neurosurg Pediatr. 2019 Aug 23:1-11. doi: 10.3171/2019.5.PEDS19178. [Epub ahead of print] PubMed PMID: 31443086.
15)

Swanson JW, Aleman TS, Xu W, Ying GS, Pan W, Liu GT, Lang SS, Heuer GG, Storm PB, Bartlett SP, Katowitz WR, Taylor JA. Evaluation of Optical Coherence Tomography to Detect Elevated Intracranial Pressure in Children. JAMA Ophthalmol. 2017 Apr 1;135(4):320-328. doi: 10.1001/jamaophthalmol.2017.0025. PubMed PMID: 28241164; PubMed Central PMCID: PMC5470406.

Hemifacial spasm etiology

Hemifacial spasm etiology

Although classical hemifacial spasm (HFS) has been attributed to an atraumatic pulsatile vascular compression around the root exit zone (REZ) of the facial nerve, rare tumor-related HFS associated with meningiomas, epidermoid tumors, lipomas, and schwannomas in the cerebellopontine angle have been reported. The exact mechanism and the necessity of microvascular decompression for tumor-induced HFS is not clear, especially for vestibular schwannomas.

In clinical pediatric neurosurgery practice, fourth ventricle tumor and cerebellar tumors are not rare. However, reports of secondary refractory hemifacial spasm are very rare. No report is currently available on the treatment of hemifacial spasm secondary to fourth ventricle and cerebellar tumors in China. Zamponi et al. [Childs Nerv Syst 2011 Jun;27(6):1001-5] reported that these lesions can occur in neonates and infants, and surgical resection is effective 1).


Imaging data of 341 patients with a HFS who underwent microvascular decompression were reviewed retrospectively and compared with 360 controls. The hemodynamics of typical anatomical variations of the vertebral artery (VA) were analyzed using computational fluid dynamics (CFD) software.

Asymmetry of the left and right VAs was prevalent, and the left VA was the most dominant VA. A dominant VA was more prevalent in the HFS group than in the control group (p=0.026). A Left HFS had a significantly higher proportion of a left dominant VA, and a right HFS had a significantly higher proportion of right dominant VA (p<0.001). CFD models showed that angulation and tortuosity of vessels caused remarkable pressure difference between vascular walls of opposite sides. Dynamic clinical observations showed the mode of vessel transposition coincided with biomechanical characteristics.

Anatomical variations and hemodynamics of the vertebrobasilar arterial system are likely to contribute to vascular compression formation in a HFS2).


Liu et al. retrospectively analyzed 10 patients with vestibular schwannomas out of 5218 cases of hemifacial spasm between 2004 and 2014.

Hemifacial spasm occurred ipsilateral to the vestibular schwannoma in 9 patients and contralateral to the lesion in 1 patient. The mean follow-up period was 86 months (range, 22-140 months). All patients underwent surgery for resection of the vestibular schwannoma. Following the principle of neurovascular compression, offending vessels were found in 7 patients, no offending vessels in 2 patients, and a tumor with the displacement of brain stem contributing to contralateral facial nerve compression in 1 patient. HFS was relieved immediately postoperatively in 9 patients, whereas it improved gradually and then resolved after one month in one patient with a contralateral vestibular schwannoma.

For HFS induced by vestibular schwannomas in this study, the majority of cases are caused by a combination of tumor and vascular co-compression at the REZ. Surgical intervention resulted in resolution of symptoms. For HFS with ipsilateral vestibular schwannoma, exploration of the facial nerve root for vascular compression should be performed routinely after tumor resection. It is critical to check that no vessel is contact with the entire nerve root 3).


During the period from October 1984 to October 2008, Han et al. treated 6,910 HFS patients using a microsurgical procedure. Of these HFS patients, 55 cases were associated with cerebellopontine angle tumors. A small craniectomy was performed in order to excise the tumor. All tumors were found to compress the root exit zone (REZ) of the facial nerve to different extents, but concomitant vascular compression of the facial nerve was observed in a majority of cases, and microvascular decompression of the facial nerve at REZ was conducted in 43 of 55 patients (78.2%) by displacing the co-compressing vasculature away from the REZ and retaining it using a Teflon pad. Intraoperative findings and postoperative pathological examinations suggested that the tumors were epidermoid cysts, meningiomas, and Schwannomas. Follow-up in 48 of 55 patients for 4-230 months after surgery showed that the clinical symptoms of HFS disappeared in 43 cases, improved in two cases, and recurred in three cases. Ten patients had sequelae associated with the operation. They concluded from this study that the majority of cases of tumor-related HFS are caused by combined tumor and vascular co-compression at the REZ, and tumor removal and microvascular decompression are required in order to relieve the symptoms 4).


Kindling-like hyperactivity of the facial motor nucleus induced by constant stimulation of compressing artery is considered as the predominant mechanism underlying the pathogenesis of Hemifacial spasm (HFS).

Trigeminal neuralgia, hemifacial spasm, vestibulocochlear neuralgia and glossopharyngeal neuralgia represent the most common neurovascular compression syndromes.

In nearly all cases, primary hemifacial spasm is related to arterial compression of the facial nerve at root exit zone (REZ). The offending arterial loops originate from the posterior inferior cerebellar artery (PICA), anterior inferior cerebellar artery (AICA), or vertebrobasilar artery (VB). In as many as 40% of the patients, neurovascular conflicts are multiple. The cross-compression is almost always seen on magnetic resonance imagingcombined with magnetic resonance angiography.


Hemifacial spasm (HFS) associated with type 1 Chiari malformation is particularly uncommon and is limited to isolated case report.

Li et al retrospectively evaluated 13 patients who had simultaneously HFS and type 1 Chiari malformation among 675 HFS patients. Clinical features and radiological findings were collected from each patient and analyzed. All these 13 patients were surgically treated with MVD through retro-mastoid microsurgical approach, and postoperative outcomes were evaluated. A review of literature about this association was also provided. In this study, the frequency of type 1 Chiari malformation in HFS patients was 1.9 %. The clinical profile of this series of patients did not differ from typical form of primary HFS. MVD achieved satisfactory results in 11 patients (85 %) in short- and long-term follow-up. There was no mortality or severe complication occurred postoperatively. Although rare, clinician should be aware of the association of HFS and type 1 Chiari malformation and consider MVD as an effective surgical management 5).

References

1)

Cai Y, Ge M, Qi X, Sun H, Zhang D. Ocular Dyskinesia and Hemifacial Spasm Secondary to Fourth Ventricular Tumor: Report of 4 Cases and Review of the Literature. Pediatr Neurosurg. 2019 Aug 22:1-8. doi: 10.1159/000501915. [Epub ahead of print] PubMed PMID: 31437843.
2)

Wang QP, Yuan Y, Xiong NX, Fu P, Huang T, Yang B, Liu J, Chu X, Zhao HY. Anatomical variation and hemodynamic evolution of vertebrobasilar arterial system may contribute to the development of vascular compression in hemifacial spasm. World Neurosurg. 2018 Dec 26. pii: S1878-8750(18)32897-3. doi: 10.1016/j.wneu.2018.12.074. [Epub ahead of print] PubMed PMID: 30593967.
3)

Liu J, Liu P, Zuo Y, Xu X, Liu H, Du R, Yu Y, Yuan Y. Hemifacial Spasm as Rare Clinical Presentation of Vestibular Schwannomas. World Neurosurg. 2018 Aug;116:e889-e894. doi: 10.1016/j.wneu.2018.05.124. Epub 2018 May 28. PubMed PMID: 29852302.
4)

Han H, Chen G, Zuo H. Microsurgical treatment for 55 patients with hemifacial spasm due to cerebellopontine angle tumors. Neurosurg Rev. 2010 Jul;33(3):335-9; discussion 339-40. doi: 10.1007/s10143-010-0250-0. Epub 2010 Mar 9. PubMed PMID: 20217169.
5)

Li N, Zhao WG, Pu CH, Yang WL. Hemifacial spasm associated with type 1 Chiari malformation: a retrospective study of 13 cases. Neurosurg Rev. 2016 Jul 15. [Epub ahead of print] PubMed PMID: 27422274.

Neurosurgical Review: For Daily Clinical Use and Oral Board Preparation

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