Here are some resources for hyperglycemia based on our session today. First here are RMC’s DKA protocols for adults and pediatric patients.

• DKA Protocol_2016.06.11
• Peds DKA guidelines final 2013

Then some videos (old and new) about DKA and HHS.

2013 DKA and HHS

These video review diabetic ketoacidosis and hyperglycemic hyperosmolar states. The second one has some formulas that you should know exist.

Pediatric DKA

The management of DKA in children has some important differences, namely worrying about cerebral edema.

Of note, the PECARN network released an article in NEJM June 14, 2018 comparing fast and slow IV administration of 0.45% and 0.9% NS to determine who gets neurologic deficits. There were no differences between the groups.

1: Kuppermann N, Ghetti S, Schunk JE, Stoner MJ, Rewers A, McManemy JK, Myers SR, Nigrovic LE, Garro A, Brown KM, Quayle KS, Trainor JL, Tzimenatos L, Bennett JE, DePiero AD, Kwok MY, Perry CS 3rd, Olsen CS, Casper TC, Dean JM, Glaser NS; PECARN DKA FLUID Study Group. Clinical Trial of Fluid Infusion Rates for Pediatric Diabetic Ketoacidosis. N Engl J Med. 2018 Jun 14;378(24):2275-2287. doi: 10.1056/NEJMoa1716816. PubMed PMID: 29897851.

Whenever the Neurology team comes down and starts asking for special MRI scans with T2-this and gadolinium that, my eyes usually glaze over. So here’s a very brief guide to MRI’s. Very brief.

General Principles

The MRI works by applying a magnetic field to the body. This magnetic field aligns the protons in water nuclei. Next, external radio frequency energy is applied which displaces the protons from that alignment. When this RF energy is removed, the energy emitted is measured.

There are two different ways to apply this RF energy, each with different time constants. Each differ based on how often the pulses are applied (TR) or the time between the RF pulse and reading the emitted energy (TE).

• T1: longitudinal, short TE and TR times, and
• T2: transverse, longer TE and TR times.
• T1 can be used using gadolinium (a non-toxic paramagnetic contrast agent) which changes the signal intensities in T1. This makes vascular structures very bright and is good for looking at the breakdown of the blood-brain barrier (tumors, abscesses, MS, among others).
• FLAIR is a kind of T2 that uses longer times. T2 FLAIR is good for differentiating between CSF and other abnormalities.
• Diffusion weighted imaging (DWI) detects the random movement of water protons in the space it has available to it. Normally, extra cellular water is able to move around freely. In ischemic tissue, diffusion becomes limited as the NA/K pump shuts down and water gets trapped in the smaller intracellular space.

Weighting	Which tissue appears brighter
T1: T1-weighted MRI	Tissue with short T1 relaxation time appears brighter (hyperintense). Grey matter is bright, CSF is dark. This is good for looking at anatomy.
T2: T2-weighted MRI	Tissue with long T2 relaxation time appears brighter (hyperintense). Edema lights up. Air will be black.
T1C: T1-weighted MRI after administration of contrast media	Many tumors show signal enhancement after administration of contrast agent. So contrast is good for looking at any structural abnormality.
FLAIR: fluid-attenuated inversion-recovery MRI	Bright signal of the CSF (cerebrospinal fluid) is suppressed which allows a better detection of small hyperintense lesions. This is good for looking at pathology in the white matter.
DWI: Diffusion weighted imaging	Bright signal in ischemic tissue, good for looking for acute stroke.

And there you have it. I’ll find some good open source pictures to include, as well.

At last month’s mortality and morbidity conference, we discussed a case of Posterior Reversible Encephalopathy Syndrome (PRES). Our consultant, a neuro-intensivist, told us that PRES is not always posterior, not always reversible nor always presenting with encephalopathy. Thanks whoever named that syndrome.

The presentation is extremely variable. Typically presenting with:

• headache,
• altered mental status,
• visual changes,
• hypertension or
• seizures.

And as our case demonstrated many (or all) of these can be initially absent. Most resolve (though can take weeks) though some do herniate and die. In the references, there is an article that lists three cases presenting with varying severity. Given this, PRES is likely more common than we think.

Risk factors for PRES include HTN, kidney disease, autoimmune disease, malignancy, transplant, cytotoxic meds, RAS, sepsis, pre-eclampsia, Takyasu, post-partum hemorrhage, Sheehan syndrome and MODS.

It is also associated with hemorrhage (20%), most are punctate though almost 10% of the bleeds can be pretty big.

Pathophysiology

Endothelial cell dysfunction leads to edema of the surrounding tissue. The posterior cerebrum is most vulnerable due to poor sympathetic innervation of its vasculature.

The symptoms seem to progress until it becomes obvious, hence many are missed on initial presentation. Even if diagnosed earlier, I don’t know what we can do other than remove the offending agent, lower the BP, and treat any seizures.

Imaging

MRI is the way to diagnose it. This will show increased T2 and T2 FLAIR signal intensity usually posterior, but remember PRES can present anywhere.

Treatment

Treatment is to lower the BP, treat seizure and remove any causative agent. Do not use NTG to lower BP as it can increase cerebral edema worsening things.

References

1. Image taken from https://en.m.wikipedia.org/wiki/Posterior_reversible_encephalopathy_syndrome
2. http://casemed.case.edu/clerkships/neurology/Web%20Neurorad/MRI%20Basics.htm
3. Thompson, R. J., Sharp, B., Pothof, J., & Hamedani, A. (2015). Posterior reversible encephalopathy syndrome in the emergency department: case series and literature review. The Western Journal of Emergency Medicine, 16(1), 5–10. http://doi.org/10.5811/westjem.2014.12.24126

Here are some great videos on how to use bougies.

Intubation with bougies

Scott Weingart… yes, yes, but his video is good.

Shows a preloaded bougie, which is what we should probably be doing.

Has some great trouble shooting techniques

Bougie cric

Darren Braude’s video.

A different view of the whole thing.

I like this one because it shows the technique we’ll more likely be using.

Crazy bougie cric in real life

Ruben Strayer of EMUpdates posted a great video on how to do a cricothyrotomy. The only things that I would change are

1. I would likely be soiling myself a lot more out of sheer panic
2. I’d have everything ready (syringe and bougie)
3. I’d pass the bougie in before removing the scalpel, just paranoid of losing that entrance
4. I would have just cut the dude’s jaw wires instead of his neck

Great video of a procedure we do not do often. The more we see it, the less freaked out we’ll be by it.

He actually has another video of the same. How many cameras does this guy have in the resusc bay?

The other day, Tom and I had a patient with the symptom of continuous vertigo. This is to be distinguished from someone with episodic triggered vertigo, such as when turning their head to the right, which we associate with benign paroxysmal positional vertigo (BPPV). The differential for continuous vertigo includes vestibular neuritis (a relatively benign diagnosis, the “Bells Palsy of Cranial Nerve 8”) and posterior circulation stroke (a potentially lethal disease if missed).

And as deus ex machina, Johnathan Edlow published an article on just this subject.

He believes the old teaching is failing us. We were taught to first ask “dizziness means different things to different people” to distinguish lightheadedness from ataxia from vertigo. If it was was to differentiate central from peripheral by using a constellation of symptoms: sudden or insidious onset, vomiting or not, severity of vertigo. The problem is, patients cannot make the distinction between vertigo and lightheadedness reliably and those distinguishing symptoms are all very insensitive.

So Edlow presents a different approach: timing and triggers.

• Acute Vertiginous Syndrome (AVS): vertiginous symptoms that lasts days, is continuous and may be accompanied by nausea, vomiting and change with motion. This is not BPPV.
• • Benign: vestibular neuritis, labyrinthitis
  • Serious: posterior circulation stroke, multiple sclerosis, cerebellum hemorrhage
• Triggered Episodic Vestibular Syndromes (t-EVS): lasts a short time, exacerbated by a specific trigger, such as moving the head or standing up.
• • Benign: BPPV
  • Serious: hypovolemia (hemorrhage, sepsis), central paroxysmal positional vertigo (CPPV)
• Spontaneous Episodic Vestibular Syndromes (s-EVS): episodes last minutes to hours without a particular trigger
• • Benign: vestibular migraines, Ménière’s disease
  • Serious: TIA
• Chronic Vestibular Syndromes (CVS): vertigo that lasts weeks to months
• • Benign: medication side effects, anxiety
  • Serious: posterior fossa mass

Our patient suffered from AVS. The HINTS exam has been shown to be even more sensitive the MRI in distinguishing between vestibular neuritis and a posterior circulation stroke.

The Anatomy

Pictured here is an actual photograph from a meticulous dissection. The thing that matters is that the cochlea (responsible for hearing) and vestibular apparatus (responsible for balance) are supplied by the vestibular and cochlear nerve, which come from the vestibulo-cochlear nerve. Both are supplied by the anterior inferior cerebellar artery, part of the posterior circulation. Occlusion of this artery can lead to balance and hearing changes as well as edematous cerebellar strokes that herniate. Hence it’s important to be able to distinguish the cause of acute vertiginous symptoms.

Inflammation of the vestibular nerve leads to vestibular neuritis. Inflammation of the vestibulo-cochlear nerve leads to labyrinthitis.

The Five Questions You Need to Ask in AVS

There are five questions you need to ask in order to distinguish between this central and peripheral cause.

1. Is there central nystagmus?
2. Is there skew deviation?
3. Is the head impulse test negative in a patient with nystagmus?
4. Are there any CNS signs on exam?
5. Any gait or truncal ataxia?

If you answer yes to any of these questions, evaluate for a central cause. If all are no, it’s likely vestibular neuritis. These questions will take us through the HINTS exam, but we don’t perform the exam in the order of the letters H-I-N-T-S, instead it’s N – TS – HI. But that doesn’t spell anything.

1. Is there central nystagmus?

First we should talk about nystagmus, the “n” in HINTS. These are the quick saccade movements that occur in patients with vestibular issues. There is a fast followed by slow movement and the nystagmus is named for the direction of the fast component. No nystagmus is considered normal.

Now have the patient look to the left and right. It may be necessary to hold a piece of paper to the side so the patient isn’t looking at anything in particular (which can extinguish nystagmus).

• Here you can see that when the patient is looking to the left (top drawing), there is a fast component to the right followed by slow to the left.
• When the patient looks to the right (bottom drawing), there is a fast component to the right followed by slow to the left.

This is unidirectional nystagmus. Contrast this with bi-directional nystagmus.

• Here you can see that when the patient looks to the left, there’s a fast to the right followed by slow to the left.
• When the patient looks to the right, there’s a fast to the left followed by a slow to the right.

The fast and slow components change direction when the patient looks in different directions.

Type of nystagmus	What’s it mean?
No nystagmus	normal state… though you can sometimes see this with a cerebellar stroke. Great.
Spontaneous horizontal nystagmus	not diagnostic
Gaze evoked horizontal nystagmus	not diagnostic, though probably BPPV
Direction changing horizontal nystagmus	Central cause
Vertical nystagmus	Central cause
Torsional nystagmus	Central cause

Nystagmus if the first thing to look for.

2. Is there skew deviation?

The next question to ask is if the eyes deviate upward and downward when you cover and uncover it. You are looking for small deviations so look first at one eye, cover and uncover both. Then look at the other eye, cover and uncover both.

Tell the patient to focus on your nose.

1. Cover one of the patient’s eyes
2. Uncover it and look for an upward deviation. It may be as small as 1 mm.
3. Cover the other eye. The patient is still looking ahead.
4. Uncover that eye and that eye may deviate downward 1 mm.

3. Is there head impulse in a patient with nystagmus?

Tell the patient to relax their head and focus on your nose. Then gently rotate the head left and right about 10-15° then quickly bring them back to center.

Normal is no saccade. This is what you would expect in a patient without nystagmus, so if the patient demonstrates no nystagmus in the first step, you do not progress further and get to this step.

If there is a saccade in a patient with vertigo, this represents a peripheral lesion.

Lack of vertigo in a patient with vertigo represents a central problem. So a “normal finding in a patient without vertigo” is the same as an “abnormal finding in a patient with vertigo.”

4. Are there any CNS signs on exam?

Ask if any of these are present.

• Abnormal neurologic exam → central cause
• Abnormal hearing exam → central or peripheral
• Anioscoria → central cause
• Ptosis → lateral medullary infarct
• Hoarseness → lateral medullary infarct
• Loss of facial pain and temperature sensation → lateral medullary infarct
• Abnormal finger-to-nose or heel-to-shin → cerebellar problem

5. Any gait or truncal ataxia?

• Cannot sit up without holding the railings → truncal ataxia → cerebellar or brainstem problem
• Cannot walk without ataxia → gait ataxia → cerebellar or brainstem problem

So what do you do if you suspect a central cause?

Do not order a CT scan. It gives you false reassurance and you’re more likely to send home a posterior stroke than if you hadn’t gotten the CT in the first place.

An MRI with diffusion weighted imaging (which is normally good for strokes) can miss strokes as well. The HINTS exam is said to be better than MRI in the first 48 hours.

Studies have not been done proving that ER docs can do this exam reliably, but it’s not outside of our skill set.

Documentation

So here’s how I may document my exam for patients with an acute vertiginous syndrome.

1. Is there central vertigo?
	*** No Nystagmus → not vestibular neuritis
	*** Spontaneous horizontal nystagums → non-diagnostic
	*** Gaze Evoked horizontal nystagmus → non-diagnostic
	*** Direction Changing nystagmus → possible central cause
2. Skew deviation 
	*** exists suggesting a central cause
	*** does not exist, potentially not a central cause
3. Head impulse test shows
	*** no saccade in a patient without vertigo
	*** saccade in patient with vertigo, possible peripheral cause
	*** no saccade in a patient with vertigo, possible central problem
4. Neurologic testing shows:
	*** normal neuro exam
	*** normal hearing exam
	*** no aniosocoria
	*** no ptosis
	*** no hoarse voice
	*** no facial numbness or temp insensitivity
	*** finger-to-nose and heel-to-shin are normal
5. *** No gait or truncal ataxia