Journal of Emergencies, Trauma, and Shock
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Year : 2020  |  Volume : 13  |  Issue : 3  |  Page : 175-176
What's new in emergencies trauma and shock – Diagnosing intracranial hypertension

1 Department of Medicine, IGMC, Shimla, Himachal Pradesh, India, India
2 Department of Emergency Medicine, Sarasota Memorial Hospital, Sarasota, Florida, USA

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Date of Submission12-Sep-2020
Date of Acceptance12-Sep-2020
Date of Web Publication18-Sep-2020

How to cite this article:
Chauhan V, Galwankar S. What's new in emergencies trauma and shock – Diagnosing intracranial hypertension. J Emerg Trauma Shock 2020;13:175-6

How to cite this URL:
Chauhan V, Galwankar S. What's new in emergencies trauma and shock – Diagnosing intracranial hypertension. J Emerg Trauma Shock [serial online] 2020 [cited 2022 Oct 4];13:175-6. Available from:

Cranium is a rigid structure that houses brain, cerebrospinal fluid (CSF), and blood. Changes in the quantity of any of these substances can alter the pressure inside the cranium. This pressure is called intracranial pressure (ICP), and when elevated above 20 mmHg, intracranial hypertension (IH). The Monroe-Kellie Doctrine says that elevation in any one component of the cranium will lead to decrease in one or two of the other components.[1] IH decreases the cerebral perfusion pressure (CPP) and is defined by the given formula: CPP = mean arterial pressure − ICP. Therefore, it becomes extremely important to diagnose and treat IH at the earliest to prevent herniation and death.

Etiological classification of IH is given:

  • Increase in brain volume: Trauma, ischemic stroke, uremia, and hyponatremia
  • Mass effect: Hematoma, tumor, abscess, and intracranial hemorrhage
  • Excess CSF production: choroid plexus tumor
  • CSF reabsorption defects: Obstructive hydrocephalus, meningitis
  • Excess blood volume: Hypercarbia, aneurysms, venous sinus thrombosis, and raised central venous pressure
  • Miscellaneous: Benign intracranial hypertension, hypervitaminosis A, and tetracycline use.

The traditional methods of diagnosing IH include history and clinical examination findings such as headache, vomiting, altered mental status, visual disturbance, and sixth nerve palsy. Extremes of IH with pending herniation may present as hypertension, bradycardia, and irregular respiration also called as Cushing's triad.[1] Invasive methods have been used to measure ICP that include lumbar puncture and manometry which can lead to sudden drop of ICP, resulting in brain herniation.[1] The procedure requires certain expertise, intensive care setup, can result in infection, and is contraindicated in patient with coagulopathy.[2]

Noninvasive radiological investigations such as magnetic resonance imaging (MRI), computed tomography (CT), and point-of-care ultrasonography (USG) are other modalities that reliably predict IH.[2],[3],[4],[5] The typical findings on CT and MRI are evident at very high ICP, and these include effacement of ventricles, basal cisterns, sulci and gyri, midline shift, loss of grey and white matter differentiation, and brain herniation. These changes are not easily quantifiable, and therefore, their sensitivity and specificity cannot be relied upon.

Measurement of optic nerve sheath diameter (ONSD) is a relatively newer diagnostic modality for raised ICP that is easily quantifiable using MRI, CT, or USG.[2],[3],[4],[5] Optic nerve is surrounded by a sheath that contains CSF communicating with the arachnoid space, and therefore, any change in the CSF pressure is reflected in the measurement of ONSD. The experimental studies done on optic nerve preparations that were obtained postmortem showed that that a maximum change of 60% occurs in the ONSD at 3 mm behind the optic nerve head, while it was only 35% at 10 mm distance.[6] ONSD can be measured reliably in patients of head trauma undergoing a CT scan or MRI.[2],[3] Alternatively, USG measurement of ONSD is also quite sensitive and specific for IH.[7],[8],[9] The choice of newer radiological modalities depends upon the availability of radiological investigations at hand. While USG is quick, its interpretation may vary from person to person, and even the same operator may have variation in the estimation of ONSD upon repeated attempts.

Once estimation of ONSD has been done using any of the methods, the next step is to compare it with the established normal range of ONSD in a particular population. ONSD was only associated with the eyeball transverse diameter that was measured using MRI.[2] The measured ONSD on MRI had poor association with age, gender, height, weight, body mass index, mean arterial blood pressure, or intraocular pressure.[2]

On USG, the upper limit of normal for ONSD as measured inner-edge to inner-edge is:

  • Up to 4 mm in infants
  • Up to 4.5 mm in children
  • Up to 5 mm in adults.

Measurements above 5 mm (bilaterally) correspond with elevations in the ICP above 20 mmHg, and further elevation of ICP results in a linear increase in ONSD up to 7.5 mm, at which the diameter plateaus.[10] Whether higher ONSD is because of an elevated ICP can be answered by doing a 30° test. ONSD is measured in primary gaze and then 30° from the primary gaze. A decrease in ONSD by over 15% on 30° eccentric gaze is quite specific for IH as the etiology of the elevated ONSD, while a negative test (no change in nerve sheath diameter on eccentric gaze suggests an alternative etiology for elevated ONSD).[10] Acute and chronic IH may be differentiated with the help of the crescent sign on USG (seen in papilledema), which indicates chronicity.[8]

The current issue of Journal of Emergencies, Trauma and Shock has two articles focused on two different radiological modalities for diagnosing IH, specifically in head trauma patients.[11],[12] One of these describes the use of CT in head injury patients that showed that the receiver operating curve (ROC) for ONSD at a cutoff value of 5.6 mm detects ICH (measured using invasive ICP monitoring) with sensitivity of 72.2% and specificity of 50%.[11] The other article used USG to measure ONSD in head injury patients, and when compared with CT-based diagnosis of raised ICT using a cutoff value for ONSD of >5.0 mm for raised ICP, they had area under the ROC curve to be 90%.[12] These studies add to the literature on successful use of radiology for diagnosis of IH not only in head trauma, but these modalities are equally good for the various etiologies of IH described above.

To conclude, IH is a life-threatening condition with varied etiologies that must be diagnosed early using any of the easily accessible imaging modalities. USG, in the hands of an expert, is a reliable, quick, noninvasive, radiation-free modality and is now being used commonly by the residents in emergency medicine departments for quick diagnosis of IH. However, if a patient of head trauma is planned to undergo CT scan or MRI, it is advisable to request simultaneous good measurements of ONSD 3 mm behind the globe as an additional quantitative marker of raised ICP. USG has an edge over CT and MRI for being useful in performing repeated measurement of ONSD to document the progression of raised ICP.

   References Top

Pinto VL, Tadi P, Adeyinka A. Increased Intracranial Pressure. In: StatPearls. 1st ed.. Treasure Island (FL): StatPearls Publishing; 2020.  Back to cited text no. 1
Kim DH, Jun JS, Kim R. Measurement of the optic nerve sheath diameter with magnetic resonance imaging and its association with eyeball diameter in healthy adults. J Clin Neurol 2018;14:345-50.  Back to cited text no. 2
Vaiman M, Abuita R, Bekerman I. Optic nerve sheath diameters in healthy adults measured by computer tomography. Int J Ophthalmol 2015;8:1240-4.  Back to cited text no. 3
Amini A, Kariman H, Arhami Dolatabadi A, Hatamabadi HR, Derakhshanfar H, Mansouri B, et al. Use of the sonographic diameter of optic nerve sheath to estimate intracranial pressure. Am J Emerg Med 2013;31:236-9.  Back to cited text no. 4
Wang LJ, Chen LM, Chen Y, Bao LY, Zheng NN, Wang YZ, et al. Ultrasonography assessments of optic nerve sheath diameter as a noninvasive and dynamic method of detecting changes in intracranial pressure. JAMA Ophthalmol 2018;136:250-6.  Back to cited text no. 5
Helmke K, Hansen HC. Fundamentals of transorbital sonographic evaluation of optic nerve sheath expansion under intracranial hypertension. I. Experimental study. Pediatr Radiol 1996;26:701-5.  Back to cited text no. 6
Beare NA, Kampondeni S, Glover SJ, Molyneux E, Taylor TE, Harding SP, et al. Detection of raised intracranial pressure by ultrasound measurement of optic nerve sheath diameter in African children. Trop Med Int Health 2008;13:1400-4.  Back to cited text no. 7
Bhosale A, Shah VM, Shah PK. Accuracy of crescent sign on ocular ultrasound in diagnosing papilledema. World J Methodol 2017;7:108-11.  Back to cited text no. 8
Robba C, Santori G, Czosnyka M, Corradi F, Bragazzi N, Padayachy L, et al. Optic nerve sheath diameter measured sonographically as non-invasive estimator of intracranial pressure: A systematic review and meta-analysis. Intensive Care Med 2018;44:1284-94.  Back to cited text no. 9
Dixon A, Shetty A. Optic nerve sheath diameter; 2019. Available from: https://radiopaedia. org/articles/optic-nerve-sheath-diameter. [Last accessed on 2020 Sep 11].  Back to cited text no. 10
Al-Hassani A, Strandvik G, Abayazeed S, Ahmed K, El-Menyar A, Mahmood I, et al. Relationship of optic nerve sheath diameter and intracranial hypertension in patients with traumatic brain injury. J Emerg Trauma Shock 2020;13:183-90  Back to cited text no. 11
Mathews A, Cattamanchi S, Panneerselvam T, Trichur RV. Evaluation of bedside sonographic measurement of optic nerve sheath diameter for assessment of raised intracranial pressure in adult head trauma patients. J Emerg Trauma Shock 2020;13:190-5.  Back to cited text no. 12
  [Full text]  

Correspondence Address:
Dr. Vivek Chauhan
Department of Medicine, IGMC, Shimla, Himachal Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/JETS.JETS_151_20

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