A 44-year-old female presents to the emergency department after noticing swelling of her tongue and face, specifically the cheeks and periorbital area. She states the swelling began two weeks ago and has progressively worsened. She also complains of redness.
Myxedema is a term used to describe the appearance of nonpitting edema in patients with severe hypothyroidism. While the exact mechanism is not completely understood, this edema is thought to be secondary to increased deposition of dermal hyaluronic acid, a glycosaminoglycan that can grow up to 1000x its normal size when hydrated. Carotenemia is another possible manifestation of hypothyroidism and is secondary to impaired conversion of carotenoids to retinol in the setting of low levels of thyroid hormone. Additionally, patients may exhibit patchy alopecia, fatigue, cold intolerance, goiter, coarsening of the skin, and macroglossia.
The presentation of hypothyroidism is widely variable and may be subtle or atypical. Classically, hypothyroidism presents with pretibial myxedema, hyporeflexia, and cold intolerance. In some cases, facial edema may be the predominant feature, as seen in this patient.
Brittle, thinning hair on the scalp and eyebrows is a common feature. Thinning of the hair along the lateral eyebrows is called madarosis, also known as “Queen Anne’s Sign.”
In a patient with Grave’s disease, maintain a high index of suspicion for hypothyroidism, either as part of the natural history of the disease or as a sequela of treatment.
Succinylcholine is frequently used in the ED to facilitate intubation, but it may be avoided in some cases due to the risk of hyperkalemia. The underlying physiology of this effect appears to be directly related to its therapeutic mechanism of action. When succinylcholine binds to and activates acetylcholine receptors, it leads to an influx of sodium and calcium and and an efflux of potassium into the extracellular space [1]. Additionally, when these acetylcholine receptors are immature or denervated, it seems that these channels may stay open significantly longer, allowing for an increased amount of potassium to exit the cell, leading to an increased risk of hyperkalemia.
Evidence
Based on multiple studies that included patients with normal renal function, succinylcholine leads to a serum potassium increase of ~0.5 mEq/L [2-4]. This is likely clinically insignificant in most patients. In fact, an ED-based study found a variable response with serum potassium increasing in 46 cases, decreasing in 46 cases, and not changing in 8 cases [3]. It seems that even patients on chronic dialysis are not at increased risk of developing clinically-significant hyperkalemia from succinylcholine [5].
So, when should succinylcholine potentially be avoided specifically due to hyperkalemia concerns [6]?
Hyperkalemia with ECG changes present prior to succinylcholine administration
Denervating, crush, or burn injuries after 72 hours
In patients for whom succinylcholine is determined to be not an option, non-depolarizing muscular blocking agents (NMBAs), such as rocuronium, are still safe and do not lead to hyperkalemia.
Bottom Line
Succinylcholine-induced hyperkalemia is more likely to occur in patients with predisposing conditions
Development of hyperkalemia following succinylcholine is variable and not always predictable
If succinylcholine is not an option due to potential risk of hyperkalemia, NBMAs (i.e., rocuronium) are still safe and effective
Hovgaard HL, Juhl-Olsen P. Suxamethonium-induced hyperkalemia: a short review of causes and recommendations for clinical applications. Critical Care Research and Practice. 2021;2021:e6613118. doi: 10.1155/2021/6613118.
Magee DA, Gallagher EG. “Self-taming” of suxamethonium and serum potassium concentration. Br J Anaesth. 1984;56(9):977-980. doi: 10.1093/bja/56.9.977. PMID: 6466531.
Zink BJ, Snyder HS, Raccio-Robak N. Lack of a hyperkalemic response in emergency department patients receiving succinylcholine. Acad Emerg Med. 1995;2(11):974-978. doi: 10.1111/j.1553-2712.1995.tb03124.x. PMID: 8536123.
Raman SK, San WM. Fasciculations, myalgia and biochemical changes following succinylcholine with atracurium and lidocaine pretreatment. Can J Anaesth. 1997;44(5 Pt 1):498-502. doi: 10.1007/BF03011938. PMID: 9161744.
Thapa S, Brull SJ. Succinylcholine-induced hyperkalemia in patients with renal failure: an old question revisited. Anesth Analg. 2000;91(1):237-241. doi: 10.1097/00000539-200007000-00044 PMID: 10866919.
Martyn JAJ, Richtsfeld M. Succinylcholine-induced hyperkalemia in acquired pathologic states: etiologic factors and molecular mechanisms. Anesthesiology. 2006;104(1):158-169. doi: 10.1097/00000542-200601000-00022. PMID: 16394702.
Nitroglycerin (NTG) is an important intervention to consider for patients with Sympathetic Crashing Acute Pulmonary Edema (SCAPE) as it significantly reduces preload, and even modestly reduces afterload with high doses. For acute pulmonary edema in the ED, NTG is often administered as an IV infusion and/or sublingual tablet. Starting the infusion at ≥ 100 mcg/min produces rapid effects in many patients and can be titrated higher as tolerated, with doses reaching 400 mcg/min or greater. Combined with noninvasive positive pressure ventilation (NIPPV) and in some cases IV enalaprilat, patients often turn around quickly, from the precipice of intubation to comfortably lying in bed [1, 2]. But what does the literature say about starting with a high-dose NTG IV bolus followed by an infusion?
Evidence
A 2021 prospective, pilot study of 25 SCAPE patients proposed a clear and systematic protocol (below) for treating these critically ill patients with a combination of high-dose NTG bolus (600 – 1000 mcg over 2 mins) followed by an infusion (100 mcg/min) and NIPPV [3].There were no cases of hypotension after the bolus and 24 of the 25 patients were able to avoid intubation. Additionally, an earlier PharmERToxGuy post summarizes some of the previous studies evaluating the use of a high-dose NTG IV bolus for acute pulmonary edema.
It is important to note that some institutions may not allow IV push NTG or may limit the use of NTG boluses. Providers may then opt to implement dosing strategies such as bolusing from an IV infusion pump or initiating the infusion at a high rate for a short period (e.g., NTG 300 mcg/min for 2-3 minutes) before reducing the rate to a more traditional infusion rate (e.g., 100 mcg/min).
Bottom Line
A few small ED studies support the use of an initial IV NTG bolus followed by an infusion compared to the infusion alone [1, 2]
There is a low risk of hypotension following a single IV NTG bolus
Consider using the following protocol to identify which doses may be best for specific patients based on initial systolic blood pressure
Wang K, Samai K. Role of high-dose intravenous nitrates in hypertensive acute heart failure. Am J Emerg Med. 2020;38(1):132-137. doi: 10.1016/j.ajem.2019.06.046. PMID: 31327485.
Wilson SS, Kwiatkowski GM, Millis SR, Purakal JD, Mahajan AP, Levy PD. Use of nitroglycerin by bolus prevents intensive care unit admission in patients with acute hypertensive heart failure. Am J Emerg Med. 2017;35(1):126-131. doi: 10.1016/j.ajem.2016.10.038. PMID: 27825693.
Mathew R, Kumar A, Sahu A, Wali S, Aggarwal P. High-dose nitroglycerin bolus for sympathetic crashing acute pulmonary edema: a prospective observational pilot study. The Journal of Emergency Medicine. Published online June 2021:S0736467921004674. doi: 10.1016/j.jemermed.2021.05.011.
There are a few unique scenarios when beta-blockers may be indicated for patients in cardiac arrest. Use of esmolol for refractory ventricular fibrillation was summarized in a 2016 PharmERToxGuy post with an accompanying infographic. Another potential use for beta-blockers is in the rare case of a patient with inhalant-induced ventricular dysrhythmias. The term ‘sudden sniffing death’ refers to acute cardiotoxicity associated with inhaling hydrocarbons. Check out this ACMT Toxicology Visual Pearl for more information about the background and diagnosis of inhalant abuse.
It is thought that inhalants causes myocardial sensitization via changes in various cardiac channels (e.g., sodium channels, potassium channels, calcium channels, or gap junctions) leading to prolonged repolarization and conduction [1, 2]. Additionally, chronic inhalant use can lead to structural heart damage. When the above alterations are combined with a sudden increase in catecholamines (e.g., exercise, caught sniffing), a dysrhythmia can develop which is often fatal [2-4].
Evidence
There are no case reports to support the use beta-blockers to treat inhalant-induced dysrhythmias. However, the case reports below include patients that ingested various hydrocarbons who developed ventricular dysrhythmias and improved following the initiation of beta-blockers. As the adverse cardiac effects should be similar between inhaled and ingested hydrocarbons, we can potentially extrapolate this data to patients with inhalant-induced dysrhythmias.
Patients presenting to the ED with cardiopulmonary manifestations of inhalant use should have routine electrolytes and an ECG to assess cardiac status
A quiet environment is important to decrease stimulation and minimize catecholamine surges
For both stable and non-perfusing dysrhythmias, propranolol or esmolol are reasonable choices to counteract the catecholamine effects, in addition to standard care [5-10]
Consider avoiding epinephrine and other catecholamines unless necessary, as they may worsen the dysrhythmia
Gindre G, Le Gall S, Condat P, Bazin JE. [Late ventricular fibrillation after trichloroethylene poisoning]. Ann Fr Anesth Reanim. 1997;16(2):202–3. doi: 10.1016/s0750-7658(97)87204-8. PMID: 9686084.
Mortiz F, de La Chapelle A, Bauer F, Leroy JP, Goullé JP, Bonmarchand G. Esmolol in the treatment of severe arrhythmia after acute trichloroethylene poisoning. Intensive Care Med. 2000 Feb;26(2):256. doi: 10.1007/s001340050062. PMID: 10784325.
Shakeer SK, Kalapati B, Al Abri SA, Al Busaidi M. Chloral hydrate overdose survived after cardiac arrest with excellent response to intravenous β-blocker. Oman Med J. 2019 May;34(3):244–8. doi: 10.5001/omj.2019.46. PMID: 31110633.
Zahedi A, Grant MH, Wong DT. Successful treatment of chloral hydrate cardiac toxicity with propranolol. Am J Emerg Med. 1999 Sep;17(5):490–1. doi: 10.1016/s0735-6757(99)90256-5. PMID: 10496517.
Nordt SP, Rangan C, Hardmaslani M, Clark RF, Wendler C, Valente M. Pediatric chloral hydrate poisonings and death following outpatient procedural sedation. J Med Toxicol. 2014 Jun;10(2):219–22. doi: 10.1007/s13181-013-0358-z. PMID: 24532346.
Wong O, Lam T, Fung H. Two cases of chloral hydrate overdose. Hong Kong Journal of Emergency Medicine. 2009 Jul;16(3):161–7. doi: 10.1177/102490790901600307.
A patient presents to the Emergency Department after sustaining a twisting knee injury while skiing. She felt a pop and was unable to bear weight afterward secondary to pain and a feeling of instability. Shortly after the injury, she noted increased swelling and pain. On examination, she has a moderate effusion and a positive Lachman test. An x-ray was obtained and is shown above (Image 1. Case courtesy of Mikael Häggström, M.D. – Author info – Reusing images, CC0, via Wikimedia Commons).
Read this tutorial on the use of point of care ultrasonography (POCUS) for pediatric ocular ultrasonography for optic nerve evaluation. Then test your skills on the ALiEMU course page to receive your PEM POCUS badge worth 2 hours of ALiEMU course credit.
Madeline is a 15-year-old female presenting to the Emergency Department with chief complaint of a headache for 1 week. She has been struggling with headaches for more than a year. The headache has been intermittent and tends to develop close to the end of the day, but it does improve with sleep. She denies photophobia, but has been complaining of blurry vision over the last week for which she is scheduled to see an ophthalmologist. Her medications include ibuprofen as needed for the headache and a daily medication for her acne.
Vital Signs
Vital Sign
Finding
Temperature
97°F
Heart rate
78 bpm
Blood pressure
130/85
Respiratory rate
14
Oxygen saturation (room air)
100%
Weight
200 lbs (90.1 kg)
Exam
Overall she is well appearing. She has a normal cardiac, respiratory, abdominal, and neurological examination including the cranial nerves.
On ocular examination, she has normal extra-ocular movements and a pupillary examination.
Visual acuity: Right eye 20/30, left eye 20/25
No visual field deficits
You attempt to evaluate her optic discs with an ophthalmoscope. Although not confident, you believe she has blurring of the optic disc margins bilaterally.
Given your examination findings, you request an ophthalmology evaluation and consider head imaging. While waiting, you decide to perform an ocular point of care ultrasound (POCUS) examination.
Why perform an ocular POCUS?
Ocular POCUS can be performed for various complaints, and it can provide valuable information. This especially is true in cases where the physical examination is difficult to perform such as from lack of patient cooperation, sensitivity to light, or pain. In resource-limited settings and when access to advanced diagnostic imaging or an ophthalmologist could be delayed or unavailable, ocular POCUS can be easily performed and provide information within minutes.
Indications to performing ocular POCUS include:
Visual changes
Acute loss of vision
Ocular trauma
Non-traumatic eye pain
Evaluation for increased intracranial pressure (ICP)
IMPORTANT NOTE: Ocular POCUS should not be performed when there is a concern for globe rupture to avoid applying pressure on the eye and exacerbating loss of intraocular contents.
Figure 1: Hockey stick linear transducer that can be used for ocular point of care ultrasonography
Figure 2. Linear transducer to use for ocular point of care ultrasonography
Step-By-Step Technique
The examination can be performed with the patient in the supine position or with the head of the bed slightly elevated
A high frequency linear transducer (Figures 1 & 2) should be used, preferably with a smaller footprint
A copious amount of gel should be applied to a closed eye
Different types of gel could be used such as the regular water-soluble ultrasound gel, sterile gel/surgical lube, and commercially available ocular-specific ultrasound gel. All these are safe, easy to clean, and do not irritate the eye.
Pro Tip: A tegaderm placed over a closed eye could be used to keep the gel from going into the eye. A tegaderm placed over a closed eye could be used to keep the gel from going into the eye depending on the patient’s preference.
Ultrasound Setup: Ideally use the ocular preset. The ocular setting lowers both mechanical and thermal indices, thus decreasing the amount of ocular exposure to the energy released from the transducer. Set the depth at 4-5 cm. This will allow imaging of the globe and the orbit behind the eyeball.
Pro Tip: If your POCUS machine does not have an ocular preset, a musculoskeletal or small parts preset could be used after turning down the dynamic range and mechanical index. Figure 3 is an example of how this could be done on a Mindray TE7 ultrasound machine.
Figure 3: To change the mechanical index (highlighted in the left upper corner), press on image, then slide the A.power down. Note as you are reducing the A.power, the mechanical index decreases. A mechanical index around 26% is sufficient.
Provider Positioning: Anchoring is important when performing an ocular examination to avoid applying pressure on the eyeball. Place 2 or 3 fingers on the patient’s forehead, nasal bridge, or temple (Figure 4, left). Please note: Applying high pressure to the eye can induce the oculocardiac reflex leading to bradycardia. It can also stimulate nausea and vomiting.
Ultrasound Views: The ocular POCUS exam can be performed in transverse and sagittal orientations (Figure 5).
Transverse: place the transducer on the closed eyelids with the marker towards the patient’s right. Fan the probe until you identify the optic nerve.
Sagittal: with the transducer in transverse, turn it 90 degrees until the marker is pointing to the forehead. Tilt Fan the probe until you identify the optic nerve.
Figure 5: Transducer positioning while performing ocular POCUS in the sagittal (left) and transverse (right) orientation
Pro Tip: If the optic nerve cannot be seen, ask the patient to move the eye from one side to another. The optic nerve will move in the opposite direction (opposite to the patient gaze).
Normal Anatomy
Figure 6: A transverse ocular POCUS showing the hypoechoic eyelid anterior, the anechoic anterior chamber, hyperechoic iris, the hypoechoic lens with hyperechoic anterior and posterior edges, anechoic posterior chamber, and a hyperechoic retina. The optic nerve is appreciated posterior to the retina as a hypoechoic structure that may run vertically or at an angle.
Video 1: Normal ocular POCUS with a view of a straight optic nerve
Video 2: Another ocular POCUS showing a normal optic nerve and disc
Assessment of the Optic Disc
The optic disc is where the optic nerve enters the eyeball. On POCUS, it normally appears smooth and in-line with the retina. Sometimes a small elevation is noted at the optic disc. This is called Optic Disc Elevation (ODE). It can be measured from the base of the optic disc to its peak at the widest area. It normally measures < 1 mm (figure 7). If the ODE is > 1 mm, this indicates papilledema and increased ICP. Of note, normal ranges are still an active area of study, see table in Ocular POCUS: Facts and Literature Review section for more information.
Figure 7: Look at the optic disc. Is it elevated? When measured, it was 0.08 cm (0.8 mm).
Assessment of the optic nerve sheath diameter (ONSD)
The optic nerve is covered with the optic nerve sheath that is made up of the 3 layers of meninges surrounding the brain (dura mater, arachnoid mater, and pia mater). Pressure in the subarachnoid space is transmitted to the optic nerve sheath. ONSD (which is the hyperechoic membrane covering the hypoechoic optic nerve) can be measured 3 mm behind the retina (Figures 8 & 9 below). This measurement should done from the outer wall of the optic nerve sheath (hyperechoic sheath) to the outer wall of the sheath on the other side.
Do not include the shadow outside the ONSD in the measurement.
Identify the trajectory of the optic nerve because this measurement has to be done perpendicular to the nerve’s axis.
Although definitive ONSD normal ranges are still an active area of research, a rough guide for a normal ONSD measurement is:
Infants less than 1 year: ONSD <4 mm
Children older than 1 year: ONSD <4.5 mm
Figure 8: Identification of the optic nerve, sheath, and disc
Figure 9: Measuring the ONSD 0.3 cm (3 mm) behind retina results in an ONSD of 0.385 cm (3.85 mm)
Use color doppler to identify the central retinal vessels that run in the middle of the optic nerve. This will help identify the axis/direction of the optic nerve. However, care should be taken to limited duration of color doppler use (Figure 10).
Pro Tip: ONSD normative values are not well established in pediatrics. Multiple studies attempted to set normal cutoffs for ONSD in various age groups. While measurement more than 5 mm in adults is considered abnormal, a value of 4 mm for infants and 4.5 mm in older children is used as the cut off [1]. The are different cutoffs that are used in the literature with variable sensitivity and specificity. See literature review section. ONSD is also highly operator dependent. An inappropriate technique in measuring the ONSD can lead to under- or over-estimation of the diameter.
Ocular POCUS: Abnormal Ultrasound Findings
Optic Disc Elevation (ODE)
When ODE is >1 mm, it suggests papilledema, which is concerning for an increased ICP. The following figures and videos below illustrate abnormal ODE measurements. Note that normal ODE ranges are an active area of study.
Optic Nerve Sheath Diameter (ONSD)
Assessment of the optic nerve can provide information about intracranial pressure. Increased ICP is suggested when you see an enlarged ONSD.
Figure 11: Optic disc elevation can be seen as bulging of the hyperechoic optic disc into the posterior chamber, measured as 1.56 mm (normal is >1 mm elevation)
Video 2: Ocular ultrasound with bulging optic disc, concerning for papilledema
Figure 12: Ocular ultrasound label showing the elevated optic disc from Video 2
Video 3: Ocular POCUS showing elevated ODE and abnormal ONSD measurements for a 6-year-old patient
Figure 13: Labeled measurement of the optic disc elevation (ODE) from Video 3.
Figure 14: The optic nerve sheath diameter (ONSD) is 4.5 mm in Video 3, as measured 3 mm posterior to the retina. This is at the upper limit of normal for the age range.
Pseudopapilledema is a mimicker
Pro Tip: Pseudopapilledema (anomalous elevation of one or both optic discs without edema of the optic nerve) is a mimicker of papilledema and can be caused by a number of conditions including:
Optic nerve head drusen: Calcified deposits in the optic disc appear hyperechoic with posterior shadowing, and cause swelling (Video 4, Figure 15)
Congenital anomalies
Vitreopapillary traction
Systemic disease
In these mimic cases, the POCUS ODE is typically <1 mm, whileas true papilledema is ≥1 mm. If the findings are equivocal, providers should perform additional evaluation for papilledema and elevated ICP.
Video 4: Optic disc drusen
Figure 15: Optic disc drusen with hyperechoic calcium deposits of the optic disc with posterior shadowing. The ODE measurement is <1 mm.
Ocular POCUS: Facts and Literature Review
Ocular POCUS has been used in the Emergency Department for detection of various ocular conditions, including increased ICP. The American Academy of Pediatrics (AAP) supported its use for ocular evaluation in its policy statement [2].
Optic Disc Elevation (ODE)
ODE has been reported as a method for detection of increased ICP with decent accuracy. There has been multiple attempts to assess the quantitative measurement of ODE and its correlation with increased ICP (table 1). This is an area of ongoing research with early studies limited by small sample sizes.
Study
Sensitivity
Specificity
Comments
Teismann et al 2013 [3]
At 0.6 mm cut off: 82% (95% CI 48-98%)
At 1 mm cut off: 73% (95% CI 39-94%)
At 0.6 mm cut off: 76% (95% CI 50-93%)
At 1 mm cut off: 100% (95% CI 81-100%)
Sample size: 14 adults
These measurements were compared to ophthalmology-performed fundus exam. Only 6 of 14 patients had papilledema.
Tessaro et al 2021 [4]
At 0.66 mm cut off (for mean of ODE of both eyes): 96% (95% CI 79–100%)
93% (95% CI 79–100%)
Sample size: 40 children (mean age 11.4 years)
26/40 patients had increased ICP.
Table 1: Literature about optic disc elevation measurements using ultrasonography
Optic Nerve Sheath Diameter (ONSD)
Normal values for ONSD have been established in adults [5]. It is still a controversial topic in children. The current standard is that an ONSD >4 mm in infants and 4.5 mm in children older than 1 year is considered abnormal, based on pediatric study of 102 healthy children [1]. There have been multiple studies to assess the sensitivity and specificity of this exam (table 2).
Study
Abnormal ONSD if
Sensitivity
Specificity
Comments
Blaivas et al 2003 [5]
>5 mm
100%
95%
Sample size: 34 adults
This is an adult study comparing ONSD on POCUS with CT results.
Le et al 2009 [6]
>4 mm for infants
>4.5 mm for children >1 year old
83% (95% CI 60-94%)
38% (95% CI 23-54%)
Sample size: 64 children
24/64 patients had confirmed ICP based on CT, MRI, or direct ICP monitoring.
Marchese et al 2018 [7]
>4.5 mm
90% (95% CI 67–98%)
57% (95% CI 43–70%)
Sample size: 76 children
20/76 patients had concern for optic nerve swelling on ophthalmology exam. The test characteristics of ONSD changed with increasing or decreasing cutoffs or adding ODE as another marker for increased ICP.
Table 2: Studies assessing correlation of optic nerve sheath diameter (ONSD) measurements with increased intracranial pressure (ICP)
Case Resolution
You perform an ocular POCUS exam with a linear probe. The following image was obtained. What do you see?
Figure 16. Ocular ultrasound of patient case
ED Course
This patient’s POCUS showed optic disc swelling with optic disc elevation and an enlarged optic nerve sheath diameter suggesting elevated ICP. The brain MRI was normal without signs of hydrocephalus. Ophthalmology evaluation confirmed the presence of papilledema. After consulting with neurology, an ultrasound-assisted lumbar puncture (LP) was performed. The patient’s opening pressure was 35 mm H2O. CSF was removed until a goal pressure of 25 mm H2O was achieved. The patient was diagnosed with idiopathic intracranial hypertension (formerly known as pseudotumor cerebri). The patient symptoms were resolved after the LP. She was admitted for further evaluation and management.
Hospital Course
The patient was evaluated by neurology while on the inpatient unit. She was started on acetazolamide and discharged home. After multiple follow-up visits at the neurology clinic, her symptoms continue to be well-controlled.
Ballantyne J, Hollman AS, Hamilton R, et al. Transorbital optic nerve sheath ultrasonography in normal children. Clin Radiol. 1999 Nov;54(11):740-2. PMID: 10580764.
Marin JR, Lewiss RE; American Academy of Pediatrics, Committee on Pediatric Emergency Medicine; Society for Academic Emergency Medicine, Academy of Emergency Ultrasound; American College of Emergency Physicians, Pediatric Emergency Medicine Committee; World Interactive Network Focused on Critical Ultrasound. Point-of-care ultrasonography by pediatric emergency medicine physicians. Pediatrics. 2015 Apr;135(4):e1113-22. PMID: 25825532.
Teismann N, Lenaghan P, Nolan R, Stein J, Green A. Point-of-care ocular ultrasound to detect optic disc swelling. Acad Emerg Med. 2013 Sep;20(9):920-5. PMID: 24050798.
Tessaro MO, Friedman N, Al-Sani F, Gauthey M, Maguire B, Davis A. Pediatric point-of-care ultrasound of optic disc elevation for increased intracranial pressure: A pilot study. Am J Emerg Med. 2021 May 21;49:18-23. PMID: 34051397.
Blaivas M, Theodoro D, Sierzenski PR. Elevated intracranial pressure detected by bedside emergency ultrasonography of the optic nerve sheath. Acad Emerg Med. 2003 Apr;10(4):376-81. PMID: 12670853.
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 Jun;53(6):785-91. PMID: 19167786.
Marchese RF, Mistry RD, Binenbaum G, et al. Identification of Optic Nerve Swelling Using Point-of-Care Ocular Ultrasound in Children. Pediatr Emerg Care. 2018 Aug;34(8):531-536. PMID: 28146012.
