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 » Case Report
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Table of Contents    
CASE REPORT
Year : 2022  |  Volume : 70  |  Issue : 4  |  Page : 1665-1667

Near-Infrared Spectroscopy–Guided Hyperventilation for Transient Intracranial Pressure Control during Anesthesia Induction in a Patient with Impending Uncal Herniation


Department of Anesthesiology, Neuro Anesthesia Division, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, Kerala, India

Date of Submission18-Dec-2021
Date of Decision09-Feb-2022
Date of Acceptance13-Mar-2022
Date of Web Publication30-Aug-2022

Correspondence Address:
Ranganatha Praveen
Associate Professor, Department of Anesthesiology, Neuro Anesthesia Division, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, Kerala - 695 011
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.355096

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 » Abstract 


Near-infrared spectroscopy (NIRS) is known to determine the adequacy of regional cerebral oxygen supply. NIRS values during anesthetic induction depends upon various factors such as anesthetic agents, inspired oxygen fraction, blood carbon dioxide levels and systemic blood pressure. Also high intracranial pressure (ICP) can lead to reduced NIRS values, secondary to increased cerebral vascular resistance induced decrease in cerebral blood flow. However optimal hyperventilation instituted as a bridge to definitive ICP management is difficult to ascertain as hypocapnia due to poorly titrated hyperventilation can potentially worsen ICP. Here we describe a novel application of NIRS-guided hyperventilation during anesthesia induction in a brain tumor patient with raised ICP features and impending uncal herniation as suggested by computed tomography (CT) scan, with ipsilateral baseline reduced NIRS values. These ipsilateral NIRS values further reduced significantly during anesthesia induction even before profound bradycardia occurred, which promptly improved to baseline following hyperventilation.


Keywords: Hyperventilation, intra cranial pressure, near infrared spectroscopy, regional cerebral oxygen saturation, uncal herniation
Key Message: Drop in NIRS values well ahead of profound bradycardia, can reflect ICP surge during anesthesia induction in brain tumor patients with features of raised ICP and reduced ipsilateral NIRS values at baseline. However, hyperventilation promptly improved NIRS values in them.


How to cite this article:
Varma S, Praveen R, Hrishi AP, Sethuraman M. Near-Infrared Spectroscopy–Guided Hyperventilation for Transient Intracranial Pressure Control during Anesthesia Induction in a Patient with Impending Uncal Herniation. Neurol India 2022;70:1665-7

How to cite this URL:
Varma S, Praveen R, Hrishi AP, Sethuraman M. Near-Infrared Spectroscopy–Guided Hyperventilation for Transient Intracranial Pressure Control during Anesthesia Induction in a Patient with Impending Uncal Herniation. Neurol India [serial online] 2022 [cited 2022 Oct 2];70:1665-7. Available from: https://www.neurologyindia.com/text.asp?2022/70/4/1665/355096




The usefulness of near infrared spectroscopy (NIRS) in conditions of raised intracranial pressure (ICP) is described.[1] Intracranial hypertension increases cerebral vascular resistance, ultimately leading to ischemia which is detected as a fall in regional cerebral oxygen saturation (rSO2) on NIRS.[1] This is also true for brain tumor–related raised ICP, wherein ipsilateral reduction in rSO2 occurs.[2] This rSO2 variability during anesthetic induction may reflect worsening ICP and could be applied in clinical management and is not previously described to the best of our knowledge.


 » Case Report Top


A 27-year-old male (weighing 60 kgs) presented with profound headache, vomiting and seizures for a week with a Glasgow coma score (GCS) of 15, heart rate (HR) 62 min-1, blood pressure (BP) 140/90 mmHg, respiratory rate (RR) of 12-14 min-1, without any neurological deficits. His laboratory investigations were normal. Computed tomography (CT) brain showed a 6.8 × 5.46 × 3 cm lesion in the right temporal lobe with mass effect in the form of midline shift, lateral ventricle effacement and impending uncal herniation [Figure 1]a and [Figure 1]b. After administering intravenous (IV) levetiracetam and confirming the fasting status, he was taken up for emergency tumor decompression.
Figure 1: (a) CT brain showing a 6.8 × 5.46 × 3 cm lesion in the right temporal lobe with mass effect and impending uncal herniation; (b) CT brain showing lesion in the right side with midline shift and effacement of right lateral ventricle

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After placing standard monitors, radial artery was cannulated under local infiltration of 2% lignocaine. Baseline, rSO2 (Root with O3 monitor; Masimo Corporation, USA) values from forehead probes were 72% and 53% on left (lrSO2) and right (rrSO2) respectively on room air, while peripheral oxygen saturation (SpO2) was 100%. Adequate preoxygenation with 100% inspired oxygen fraction (FiO2) was performed following which lrSO2 remained 74% and rrSO2 56%.

Anesthesia was induced with intravenous fentanyl 2 mcg.kg-1, propofol 2 mg.kg-1 and atracurium 0.5 mg.kg-1. Bag and mask ventilation with 100% oxygen/sevoflurane with a tidal volume of approximately 450 ml and RR of 16 was administered. Post induction, rrSO2 dropped to 41% while lrSO2 remained at 72% [Figure 2], with HR 55 min-1, BP 120/70 mmHg, end tidal carbon dioxide 32 and SpO2 100%. Mephentermine 3 mg boluses increased BP to 142/88 mmHg, however the rrSO2 dropped to 28% [Figure 2], indicating probable tumor side impaired autoregulation and raised ICP. Heart rate remained 52 min-1. On instituting hyperventilation to a RR of 22 min-1, rrSO2 value improved to 54% (lrSO2 74%) with HR of 58 min-1. Trachea was intubated and anesthesia maintained with air/oxygen mixture (1:1), propofol, fentanyl and atracurium infusion titrated to a bi-spectral index of 40 to 60. Ventilation was titrated real time to maintain normocarbia. Surgery was uneventful with lrSO2 of 68–72 and rrSO2 60–64 throughout. BP was maintained within 10% of baseline. Patient was extubated in neuro intensive care unit with preoperative GCS. No neurological deficits were observed and further postoperative recovery was uneventful.
Figure 2: Trends in rSO2 values on NIRS monitor

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 » Discussion Top


NIRS determines the adequacy of regional cerebral oxygen supply.[3] Various factors can influence its intraoperative values. Anesthesia induction (by causing cerebral metabolic suppression), hypercapnia and increasing inspired oxygen to 100% from room air, increase rSO2 values,[2],[3] while hypotension and hypocapnia causes its decrease.[3],[4]A fall in rSO2 below an absolute value of 50% is associated with cerebral ischemia.[4] Hemispheric difference in rSO2 values was seen in our case; the rSO2 ipsilateral to the tumor was 53%, with only minimal change following 100% oxygen and declined to 41% following anesthesia induction. Optimization of rSO2 was attempted by delivering 100% oxygen, augmenting BP and achieving normocarbia.[3] The rSO2 declined to 28% despite these maneuvers. Finally, hyperventilation was instituted which led to the return of rSO2 to baseline. Our concern was that acute cerebral desaturation could have been a precursor to cerebral ischemia secondary to increase in ICP (preoperative CT brain concerning for raised ICP) which was promptly reversed with hyperventilation. The fact that there was no improvement in rrSO2 values from 41%, rather a further drop to 28%, even after optimizing various systemic factors including augmentation of BP, points towards the possibility of impaired autoregulation on the tumor (which was large, >5 mm midline shift) side,[5] leading to worsening of ICP. This situation responded to hyperventilation as seen in our case. Also, seizure as a cause of ipsilateral rSO2 decline,[6] secondary to increased cerebral metabolic demand might not be a possibility here, as hyperventilation would have worsened seizure and therefore rSO2.

Induction of anesthesia in such patients with critically low intracranial compliance is challenging as even a minimal increase in the ICP can be catastrophic, especially in the presence of a mass lesion that can cause impending uncal herniation.[7] Hyperventilation is instituted as a bridge to definitive ICP management with bradycardia (component of Cushing's reflex) as a marker for raised ICP in this setting.[8] However, the optimal hyperventilation needed to prevent further ICP surge is difficult to ascertain. Indeed hypocapnia due to poorly titrated hyperventilation can be deleterious by itself with potential worsening of intracranial compliance.[7] The use of NIRS monitoring in the setting of anesthesia induction can be twofold: Firstly, a critical asymmetrical reduction in NIRS can be used as a trigger to institute hyperventilation, and secondly, its return to baseline could indicate its endpoint.

NIRS monitoring during induction of anesthesia can detect subtle changes in cerebral oxygenation as a surrogate for ICP changes in patients with raised ICP, such as our patient (who had radiological features of raised ICP). This can help guide management as illustrated from our case wherein precipitous drop in rSO2 value, which was postulated to be a harbinger of impending uncal herniation occurred even before profound bradycardia. Furthermore, it improved following hyperventilation. Thus, in the appropriate setting, this can be a trigger for timely intervention such as hyperventilation as a bridge to definitive management of ICP. Also, Brain Trauma Foundation recommends invasive brain tissue oxygen tension– or jugular venous oxygenation–guided hyperventilation as a temporary measure to reduce the increased ICP, whenever instituted.[9] The use of NIRS as a non-invasive monitor, including in this area, however, remains less explored.


 » Conclusion Top


The use of NIRS during induction of anesthesia in this setting is not previously described. The novel application of NIRS can be complementary to standard monitoring and can facilitate safe anesthetic management in this cohort. This use of NIRS however, remains unexplored and perhaps our report paves way for further studies to elucidate its role in this setting.


 » Consent Top


Written informed consent was obtained from the brother of the patient.

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.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
 » References Top

1.
Kampfl A, Pfausler B, Denchev D, Jaring HP, Schmutzhard E. Near infrared spectroscopy (NIRS) in patients with severe brain injury and elevated intracranial pressure. Acta Neurochir Suppl 1997;70:112-4.  Back to cited text no. 1
    
2.
Zuluaga MT, Esch ME, Cvijanovich NZ, Gupta N, McQuillen PS. Diagnosis influences response of cerebral NIRS to intracranial hypertension in children. Pediatr Crit Care Med 2010;11:514-22.  Back to cited text no. 2
    
3.
Weber F, Scoones GP. A practical approach to cerebral near-infrared spectroscopy (NIRS) directed hemodynamic management in noncardiac pediatric anesthesia. Pediatr Anesth 2019;29:993–1001.  Back to cited text no. 3
    
4.
Picton P, Shanks A, Dorje P, Mashour GA. The influence of basic ventilation strategies on cerebral oxygenation in anesthetized patients without vascular disease. J Clin Monit Comput 2010;24:421–5.  Back to cited text no. 4
    
5.
Sharma D, Bithal PK, Dash HH, Chouhan RS, Sookplung P, Vavilala MS. Cerebral autoregulation and CO2 reactivity before and after elective supratentorial tumor resection. J Neurosurg Anesthesiol 2010;22:132–7.  Back to cited text no. 5
    
6.
Sokol DK, Markand ON, Daly EC, Leurssen TG, Malkoff MD. Near infrared spectroscopy (NIRS) distinguishes seizure types. Seizure 2000;9:323–7.  Back to cited text no. 6
    
7.
Seder DB, Riker RR, Jagoda A, Smith WS, Weingart SD. Emergency neurological life support: Airway, ventilation, and sedation. Neurocrit Care 2012;17(Suppl 1):S4–20.  Back to cited text no. 7
    
8.
Tan TK, Cheng MH, Sim EY. Options for managing raised intracranial pressure. Proc Singapore Healthc 2015;24:156–64.  Back to cited text no. 8
    
9.
Carney N, Totten AM, O'Reilly C, Ullman JS, Hawryluk GW, Bell MJ, et al. Guidelines for the management of severe traumatic brain injury, fourth edition. Neurosurgery 2017;80:6-15.  Back to cited text no. 9
    


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