A Patient With a Subarachnoid Hemorrhage After Endovascular Coiling and a Malfunctioning Ventriculostomy

A Patient With a Subarachnoid Hemorrhage After Endovascular Coiling and a Malfunctioning Ventriculostomy

[ Ultrasound Corner ] A Patient With a Subarachnoid Hemorrhage After Endovascular Coiling and a Malfunctioning Ventriculostomy Gabriel Wardi, MD, M...

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Ultrasound Corner

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A Patient With a Subarachnoid Hemorrhage After Endovascular Coiling and a Malfunctioning Ventriculostomy Gabriel Wardi, MD, MPH; Jacob Wouden, MD; Jeffrey E. Thomas, MD; and Daniel A. Sweeney, MD

CHEST 2017; 151(4):e81-e84

A man in his 50s with a medical history of hypertension and methamphetamine abuse presented to an outside hospital with a severe headache and was diagnosed with a high-grade subarachnoid hemorrhage (SAH) (Hunt and Hess grade 3, Fisher grade 4) complicated by acute hydrocephalus. While being transported to a triage center by helicopter, the patient’s condition deteriorated, as flexor posturing, hypertension, and relative bradycardia developed, for which he was intubated and administered IV mannitol. On arrival, his Glasgow Coma Scale score was 3, and an emergent external ventricular drain (EVD) was placed. Immediately after the procedure he began to move all extremities and attempted to sit up in bed. He remained intubated and sedated, and the next day he underwent coiling of a basilar-tip aneurysm. His postoperative course was complicated by hypoxemic respiratory failure and a possible seizure for which he remained intubated and sedated on a continuous infusion of propofol. On postoperative day 3, a transcranial Doppler study exhibited no evidence of vasospasm, and a noncontrast head CT scan showed that the ventricles were smaller when compared with his initial CT scan. Two days later, the EVD stopped functioning (no

AFFILIATIONS: From the Division of Pulmonary, Critical Care, and Sleep Medicine (Drs Wardi and Sweeney), Department of Internal Medicine, and the Department of Emergency Medicine (Dr Wardi), University of California, San Diego, La Jolla; and Washington Hospital (Drs Wouden and Thomas), Fremont, CA. The work was performed at the University of California, San Diego, La Jolla, CA and Washington Hospital, Fremont, CA. CORRESPONDENCE TO: Gabriel Wardi, MD, MPH, 200 W Arbor Dr, San Diego, CA 92103; e-mail: [email protected] Copyright Ó 2017 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved. DOI: http://dx.doi.org/10.1016/j.chest.2016.07.049

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Figure 1 – Coronal view of the left orbit. The optic nerve sheath diameter (ONSD) is 4.3 mm.

drainage or waveform). His neurologic examination was limited secondary to sedation and mechanical ventilation. His pupils were 2 to 3 mm, equal, and sluggishly reactive to light, and he withdrew to noxious stimuli. A point-of-care ultrasonographic (POCUS) examination of his left optic nerve sheath was performed by placing a linear probe at the lateral canthus; a coronal image was used to measure the optic nerve sheath diameter (ONSD) (Fig 1). The same examination was attempted on the right eye (Video 1).

Question: What is the significance of the POCUS examination findings, and is there a syndrome associated with this patient’s condition? e81

Answer: Increased intracranial pressure and Terson syndrome (vitreous hemorrhage in the presence of a subarachnoid hemorrhage) Based on the POCUS examination and the ambiguous neurologic examination, the EVD was replaced. Of note, noncontrast head CT imaging performed immediately prior to this procedure showed that the original EVD was well positioned and the size of the ventricles were stable compared with prior scans (Fig 2). Nonetheless, the neurosurgeon reported increased intracranial pressure (ICP) at the time the EVD was replaced. Repeated ultrasonography performed 15 hours later showed that his left ONSD had decreased from 4.3 mm to 3.3 mm (Fig 3). An ophthalmologic consult was obtained the next day, and a dilated fundus examination showed multiple intraretinal blot hemorrhages, preretinal hemorrhages, and vitreous hemorrhages in each eye. The right vitreous hemorrhage was so significant that the retina could not be adequately examined. The remainder of the patient’s 31/2-month hospital course was complicated by respiratory failure secondary to pneumonia and suspected neurogenic pulmonary edema necessitating tracheostomy, the need for percutaneous endoscopic gastrostomy, and Clostridium difficile infection. Otherwise, his recovery was remarkable in that at the time of discharge, his tracheostomy tube had been removed, and he was alert, oriented, and conversant. He was wheelchair bound secondary to deconditioning, and unfortunately his visual acuity was limited, as he was only able to make out shapes and was not able to read text at 18 inches.

Figure 2 – Noncontrast head CT scan obtained immediately prior to replacement of the external ventricular drain (EVD).

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Discussion Terson syndrome was first described in 1881 and was later named after the French ophthalmologist Albert Terson.1 The definition includes any intraocular hemorrhage associated with any form of intracranial hemorrhage.2 Terson syndrome in the setting of an SAH has a reported incidence of 8% to 46% and is associated with worse prognostic markers and a higher mortality rate.1 The pathogenesis is not fully understood but is theorized to be a function of sudden increased ICP leading to intraocular hemorrhage.3 CT imaging can identify Terson syndrome; however, many hospital protocols avoid imaging involving the orbit given that radiation exposure is associated with the development of cataracts.4 Ultrasonography avoids both the need for a dilated eye examination and exposure to radiation. Ultrasonography cannot identify all intraocular hemorrhage, but it has been shown to identify vitreous hemorrhages, the subset that is most associated with a poor prognosis and most likely to require surgery at a later date.1 This case is also significant for the fact that POCUS—with a linear probe placed at the lateral canthus to obtain a coronal axis measurement of the ONSD—raised clinical suspicion for increased ICP when the CT scan was not suggestive of such a pathologic condition. This information resulted in replacement of the EVD, with clinical improvement. Repeated bedside ultrasonography performed 15 hours later showed a decrease in the left ONSD. Controversy exists as to the optimal view for measuring the diameter of the optic nerve sheath, that is, in the visual axis with the probe placed on the upper eyelid, in the coronal axis with the probe placed at the lateral canthus, or in the coronal axis through an infraorbital approach.5-7 In the patient, a linear probe was placed at the lateral canthus as demonstrated in Video 2 and Discussion Video. A step-by-step example of how to measure the optic nerve sheath through the coronal view is seen in Figures 4-6. There are numerous studies involving primarily patients with traumatic brain injury in whom visual axis imaging of the ONSD (cutoff range of 4.8-5.9 mm) has been shown to correlate with increased ICP, defined as a pressure $ 20 mm Hg.8,9 Nonetheless, this approach can be technically challenging, and some investigators have questioned whether this view actually identifies the optic nerve or whether this image represents an artifact, possibly a shadow cast by the lamina cribrosa, the optic disc, or the optic nerve

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Figure 3 – Coronal view of left orbit after replacement of the external ventricular drain EVD. The optic nerve sheath diameter (ONSD) is 3.3 mm.

sheath itself.10 The lateral approach to obtain a coronal view of the optic nerve has historically been used by ophthalmologists. Using this technique with an endocavitary probe, the average ONSD was 3.4 mm (95% CI, 3.18-3.61 mm) in a study of 27 healthy subjects, which is similar to measurements obtained at autopsy.5 The coronal view in the patient was obtained by placing a linear probe (SonoSite, Inc.; 13-6 MHz,

Figure 4 – Placement of the ultrasonographic probe to measure the optic nerve sheath diameter (ONSD) in the coronal axis. The probe is placed vertically at the lateral canthus with the marker dot cephalad and the ultrasound beam aimed nasally.

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Figure 5 – Image of the optic nerve sheath in the coronal axis just posterior to the globe. The image is optimized by obtaining a view in which the cross-sectional shape of the optic nerve and nerve sheath are circular and not oval to avoid making a falsely enlarged measurement based on an oblique cut.

depth of 3.7 cm) oriented vertically with the indicator cephalad and positioned at the lateral canthus. At the point that the optic nerve appeared circular (as opposed to oval, which would represent an oblique cut), the ONSD was measured medial to lateral, outer edge to outer edge, as seen in Figures 1 and 3. We report the patient having an ONSD of 4.3 mm prior to EVD replacement, which improved to 3.3 mm within 15 hours after the procedure, suggesting that the coronal view of the ONSD is time sensitive to changes in ICP. A coronal axis measurement of the ONSD using an infraorbital approach has been described.6 Measurements of the ONSD in healthy volunteers (n ¼ 42) using this technique were similar to measurements made in the visual axis; however, the images were obtained in less time (200 s vs 152 s; P < .05).

Figure 6 – Measurement of the optic nerve sheath in the coronal axis. The optic nerve sheath was measured medial to lateral, outer edge to outer edge (4.2 mm). Measurement of the optic nerve sheath cephalad to caudal, outer edge to outer edge, has also been previously described.5

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Reverberations 1. Point-of-care ocular ultrasonographic measurements of ONSD have been shown to correlate with increased ICP; nonetheless, controversy surrounding this approach remains. This case report suggests that a coronal view of the ONSD may also be predictive of ICP. 2. Terson syndrome in the setting of SAH is likely underdiagnosed. Vitreous hemorrhages can be identified in the process of performing a POCUS examination of the optic nerve sheath.

Acknowledgments Financial/nonfinancial disclosures: None declared. Other contributions: CHEST worked with the authors to ensure that the Journal policies on patient consent to report information were met. Additional information: To analyze this case with the videos, see the online version of this article.

References 1. Czorlich P, Skevas C, Knowpe V, et al. Terson syndrome in subarachnoid hemorrhage, intracerebral hemorrhage, and traumatic brain injury. Neurosurg Rev. 2015;38(1):129-136; discussion 136.

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2. Manschot W. Subarachnoid hemorrhage: intraocular symptoms and their pathogenesis. Am J Ophthalmol. 1954;38(4):501-505. 3. Ogawa T, Dake T, Amemiya T. Terson syndrome: a case report suggesting the mechanism of vitreous hemorrhage. Ophthalmology. 2001;108(9):1654-1656. 4. Koskela E, Pekkola J, Kivisaari R, et al. Comparison of CT and clinical findings of Terson’s syndrome in 121 patients: a 1-year prospective study. J Neurosurg. 2014;120(5):1172-1178. 5. Blehar DJ, Gaspari RJ, Montoya A. Correlation of visual axis and coronal axis measurements of the optic nerve sheath diameter. J Ultrasound Med. 2008;27(3):407-411. 6. Amini R, Stolz A, Patanwala A, et al. Coronal axis measurement of the optic nerve sheath diameter using a linear transducer. J Ultrasound Med. 2015;34(9):1607-1612. 7. Soldatos T, Chatzimichail K, Papathanasiou M, et al. Optic nerve sonography: a new window for the non-invasive evaluation of intracranial pressure in brain injury. Emerg Med J. 2009;26(9): 630-634. 8. Rajajee V, Vanaman M, Fletcher J, et al. Optic nerve ultrasound for the detection of raised intracranial pressure. Neurocrit Care. 2011;15(3):506-515. 9. Geeraerts T, Merceron S, Benhamou D, et al. Non-invasive assessment of intracranial pressure using ocular sonography in neurocritical care patients. Intensive Care Med. 2008;34(11): 2062-2067. 10. Copetti R, Cattarossi L. Optic nerve ultrasound: artifacts and real images. Intensive Care Med. 2009;35(8):1488-1489; author reply 1490-1491.

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