In Part I we covered the basics of neuroprotective care following traumatic brain injury, and discussed how the majority of interventions are possible in the field - without requiring high level equipment. Detecting and monitoring raised intracranial pressure (ICP) also need not require high level equipment or even a high level of technical skill. It's been shown that US special operations combat medic course (SOCM) candidates can obtain ultrasonographic measurements that do not statistically significantly differ from those of emergency physicians [1]. The important thing to remember is that the difficult skill is interpreting and integrating that information.
Identifying raised ICP can be difficult. Early symptoms like severe headache or vomiting are non-specific, and physical findings like papilloedema are all very well and good if you've got an ophthalmoscope and know how to wield it (I'll eat my hat if anyone carries an ophthalmoscope in the field, much less anyone who's identified retinal venous engorgement or a loss of venous pulsations on field fundoscopy). An altered level of consciousness is the crucial one, because other signs occur late - signs like an ipsilateral mydriasis ("blown pupil") from oculomotor nerve compression, which often precedes the classic “down-and-out” gaze palsy, and finally Cushing’s triad (hypertension as a compensatory response to brainstem compression, bradycardia as a vagal response to the hypertension, and irregular breathing due to direct compression of respiratory centres).
In minor head injury we want to be able to detect if there is a raised ICP. This is because the signs and symptoms of raised ICP are the canary in the mine - they portend the intracranial pathology that would require CT and/or neurosurgical input. Assessing whether there is evidence of raised ICP therefore forms a large part of your clinical assessment in the head injured patient. In the field this assumes greater significance because it informs the decision to initiate evacuation and retrieval (though note - this is still only one very small piece of the puzzle, to be interpreted alongside the mechanism and history of the injury, past medical history, anticoagulation status, and other examination findings).
In severe head injury, we want to be able to monitor the ICP, because this patient sub-group is often intubated, meaning serial GCS measurement is no longer possible. Evacuation measures are likely already well underway at this point, but we want to know if the ICP is shooting up because that portends badness. Being able to identify a worsening ICP assists us in optimising our MAP (and therefore our CPP) but also guides whether we need to be escalating our analgesia or sedation, and informs decisions about when to start using osmotherapeutic agents like hypertonic saline or mannitol.
(Image from Tan et al [2])
In either case - whether it's part of identification in the minor injury, or monitoring in the severe injury - an early, rapid, and non-resource intensive method of ICP estimation would be a very useful tool to have at your disposal.
Ocular ultrasound
Using a high-frequency linear probe (at least 7.5-10 MHz), scan the (closed) eye. You can use a Tegaderm or similar to cover the eye to protect it from ultrasound gel if you so wish (being careful not to trap air pockets beneath it that will interfere with image acquisition). Obviously don't do ocular ultrasound if the patient has a globe rupture, and in all patients try to keep your acoustic output as low as reasonably achievable.
(image adapted from Sinai EM)
Optic nerve sheath diameter
The sheath surrounding the optic nerve is continuous with the dura mater and so the pressure within it should closely approximate intracranial pressure. Because the optic nerve is surrounded by CSF - as pressure increases, so too should the volume of the sub-arachnoid space surrounding it. We can measure this volume through a surrogate marker: diameter.
By convention, ONSD is measured 3mm posterior to the retina - this is because the contrast between the echogenicity of structures is often most pronounced here, and because cadaveric studies seem to suggest this area is the most expansile part of the sheath (and therefore, theoretically, the most sensitive place to measure) [3]. Measure from one edge of the hypoechoic sheath to the other, and do this in 2 planes, transverse and sagittal - taking the average of the two values. Repeat this for the other eye.
(Images obtained by the author using a Butterfly iQ+ using 16Hz (TIs 0.01, MI 0.2))
So what's our cut off for a "raised ICP"? A lot of studies have attempted to answer this question - and full disclosure - the answer varies. Like, a lot. ROC curve analysis has shown the optimal threshold for declaring a "raised ICP" could be anywhere between 4.85mm [4] and 5.9mm [5]. This is very confusing, but these studies were all quite small in nature, and used different frequency probes with differing image quality. Probably the best evidence comes from the meta-analysis by Ohle et al (n=478) [6]. When compared to CT-proven raised ICP (which is not necessarily the gold standard for ICP measurement), an ONSD >5mm had a sensitivity of 95.6% (95%CI, 87.7%-98.5%) and a specificity of 92.3% (95%CI, 77.9%-98.4%). If expressing this in a more Bayesian way gets you going on those long nights alone, then this equates to a +LR of 12.4 and a -LR of 0.05 for this 5mm cut-off (that's pretty good!)
Given the heterogenous nature of the literature, this still wasn't quite good enough for the folks at PulmCrit [7] - who felt while 5mm had sufficient sensitivity, 6mm had greater specificity, and so while <5mm would likely be sufficient in ruling out elevated ICP, only >6mm was sufficient to rule it in.* They suggest using the presence or absence of papilloedema as the deciding factor for those trapped in the clinical nether-regions betwixt the two (discussed further in its own section below).
Some centres have tried to further increase the accuracy of this technique by adjusting for confounders like patient size. This is done by expressing ONSD as a proportion of eyeball transverse diameter (ETD), which can be obtained by simply finding and measuring the point of maximal eyeball width in the transverse plane.
One very large study that obtained baseline data in healthy volunteers was Kim et al (n=585) [8], who found a mean ONSD of 4.11mm and the mean ONSD/ETD ratio of 0.18. Zhu et al (n=104) [9] compared comatose patients with supratentorial space-occupying lesions (ONSD/ETD 0.27) and healthy controls (ONSD/ETD 0.22). This shows some promise as a clinical parameter, but at the time of writing no large studies have been conducted to inform what cut-off value is most useful. One small study on paediatric head trauma found that a cut-off of 0.22 had a sensitivity of 100% and specificity of 88% [10] - I doubt this would be generalisable to adults if the results of Zhu et al are to be believed.
The important point here is that a single measurement is less important than a dynamic change. Studies have shown fair-to-good interobserver reliability between emergency physicians, ultrasonographers, and ophthalmologists when measuring ONSD [11], but the best test will be a single observer taking serial measurements. Take a baseline measurement as part of your initial assessment, and subsequent measurements as part of on-going periodic neurological observations. Studies performed on patients immediately before and after lumbar puncture seem to suggest ONSD does react to changes in ICP in real time, so what you're measuring likely does represent the contemporaneous ICP [12]. Serial ONSD measurements have been used in the identification of high altitude cerebral oedema (HACE) - one case report demonstrated an increase in ONSD from 6mm to 7mm when ascending from 3840m to 4321m [13].
Papilloedema
Unlike ONSD, which is a continuous variable, whether there's papilloedema or not is rather binary. It's either there or it isn't - you kind of just have to (if you'll pardon the pun) eyeball it. Bear in mind that oedema doesn't develop immediately, so an acute rise in ICP may not yet manifest itself in the form of papilloedema, but for established elevations in ICP, ultrasonographic papilloedema does seem to be a fairly sensitive and specific finding [14,15,16].
Notes:
*Note that paediatric cut-offs differ again.
References:
[1] Betcher J, Becker TK, Stoyanoff P, Cranford J, Theyyunni N. Military trainees can accurately measure optic nerve sheath diameter after a brief training session. Mil Med Res. 2018;5(1):42.
[2] Tan TK, Cheng MH, Sim EY. Options for managing raised intracranial pressure. SAGE Open Med. 2015. Available from: https://doi.org/10.1177/2010105815598444
[3] Helmke K, Hansen HC. Fundamentals of transorbital sonographic evaluation of optic nerve sheath expansion under intracranial hypertension. I. Experimental study. Pediatr Radiol. 1996;26(10):701-5.
[4] Amini A, Eghtesadi R, Feizi AM, et al. Sonographic optic nerve sheath diameter as a screening tool for detection of elevated intracranial pressure. Emerg (Tehran). 2013;1(1):15-9.
[5] Geeraerts T, Launey Y, Martin L, et al. Ultrasonography of the optic nerve sheath may be useful for detecting raised intracranial pressure after severe brain injury. Intensive Care Med. 2007;33(10):1704-11.
[6] Ohle R, McIsaac SM, Woo MY, Perry JJ. Sonography of the optic nerve sheath diameter for detection of raised intracranial pressure compared to computed tomography: a systematic review and meta-analysis. J Ultrasound Med. 2015;34(7):1285-94.
[7] PulmCrit. Algorithm for diagnosing ICP elevation with ocular sonography. 2017. Available from: https://emcrit.org/pulmcrit/pulmcrit-algorithm-diagnosing-icp-elevation-ocular-sonography/.
[8] Kim DH, Jun JS, Kim R. Ultrasonographic measurement of the optic nerve sheath diameter and its association with eyeball transverse diameter in 585 healthy volunteers. Sci Rep. 2017;7(1):15906.
[9] Zhu S, Cheng C, Zhao D, et al. The clnical and prognostic values of optic nerve sheath diameter and optic nerve sheath diameter/eyeball transverse diameter ratio in comatose patients with supratentorial lesions. BMC neurol. 2021;21(1):259.
[10] Şık N, Ulusoy E, Çitlenbik H, et al. The role of sonographic optic nerve sheath diameter measurements in pediatric head trauma. J Ultrasound. 2022;25(4):957-63.
[11] Le A, Hoehn ME, Smith ME, et al. Bedside sonographic measurement of optic nerve sheath diameter as a predictor of increased intracranial pressure in children. Ann Emerg Med. 2009;53(6):785-91.
[12] Chen L, Wang L, Hu Y, et al. Ultrasonic measurement of optic nerve sheath diameter: a non-invasive surrogate approach for dynamic, real-time evaluation of intracranial pressure. Br J Ophthalmol. 2019;103(4):437-41.
[13] Wipplinger F, Holthof N, Lienert J, et al. Point-of-care ultrasound diagnosis of acute high altitude illness: a case report. Wilderness Environ Med. 2021;32(2):204-9.
[14] Lochner P, Brio F, Zedde ML, et al. Feasibility and usefulness of ultrasonography in idiopathic intracranial hypertension or secondary intracranial hypertension. BMC Neurol. 2016;16:85.
[15] Bäuerle J, Nedelmann M. Sonographic assessment of the optic nerve sheath in idiopathic intracranial hypertension. J Neurol. 2011;258(11):2014-9.
[16] Carter SB, Pistilli M, Livingston KG, et al. The role of orbital ultrasonography in distinguishing papilledema from pseudopapilledema. Eye (Lond). 2014;28(12):1425-30.
[17] Marchese RF, Mistry RD, Scarfone RJ, Chen AE. Identification of optic disc elevation and the crescent sign using point-of-care ocular ultrasound in children. Pediatr Emerg Care. 2015;31(4):304-7.