Here is a potential airway technique that may help with visualization: hold the laryngoscope in the left hand (the usual) but the right hand, instead of being at your side, is behind the patient’s head. You then move it around until you get the best view. Then you have an assistant hold the head in that spot.


A hospital in Southern California started doing that. The technique deserves some exploration. The work of Richard Levitan reminds us that the airway is most patent in the sniffing position. Extension does not really help but true sniffing position does. Sometimes you think you have enough and you need more.


I have not seen this technique studied but it probably deserves some attention.



-Consider external cephalic manipulation as an analogy to “external laryngeal manipulation” as a way of fine tuning the visualization during a tough intubation



A patient presents with severe sore throat. You wonder about epiglottitis. You know that using a mirror to look at the epiglottis is a great way to check this but are not confident in your skills. What do you need?


Dental mirror – they are cheap, have your ED stock them


Light – can use a headlamp, the kind that are sold in outdoor stores. Get one with a spot beam rather than a flood light. Nice to have regular AAA batteries instead of the medical ones with cords that are always getting lost or damaged


Relaxed patient – explain to them what you are doing and rehearse it once first


Anatomy – have them lean forward, chin out


View – wrap gauze around their tongue. Don’t pull it out but hold it so they don’t have to sustain muscle contraction to keep the tongue out


No gag – not sure topical anesthetics really work. Try to avoid hitting their pharynx with the mirror until you are ready to lift the uvula and look. Have the patient fix vision in the distance. Have them say “eeeeeee.” Have them do slow panting style shallow breathing.


No fog – hydrogen peroxide or hot water will help prevent fogging


You look and it is hard to see. That reminds us the final thing you need – practice!



-Indirect laryngoscopy is a complex hand-eye skill that you can learn

-Get the right supplies and start doing this now. It may really help you one day.

Deep Space Infection of the Neck? Check Range of Motion

A young man presents with a severe sore throat. He was here yesterday and received antibiotics. Today he feels worse. You look in the throat expecting a peritonsillar abscess but the throat looks completely normal, not even erythema.


Now what?


Amidst the busy emergency department practice, sometimes we need a reason to take a second, closer look. Always trust your gut. In this case the patient had severe pain but no erythema. The concerning finding was not the severe sore throat or the normal examination, but the incongruity of both. Is there something deeper going on? What else should you check?


Check range of motion. He can do it but has severe pain, not so much with flexion but definitely with extension. You order a CT scan and it shows a retropharyngeal abscess.


I would have hoped to a review of the physical findings on this condition but they appear to be very limited (odynophagia, trismus, stridor, muffled voice)


Take Home Points:

-Incongruity/anomalous findings get your attention

-Check range of motion for suspected deep space infection of the neck



A pediatric patient presents with upper respiratory symptoms. The student says there is acute otitis media. You look, and indeed there is some erythema of the tympanic membrane. But is this acute otitis media, and will the patient benefit from antibiotics?


Studies are limited by variable clinical definitions of acute otitis media (Chandler Clin Pediatr 2007) and interobserver variability (Margolis Is J Med Sci 1979). One article presents their training module as improving the accuracy of diagnosis by 5%, but that is only from 62% to 67%. The limitations in the diagnosis of acute otitis media are striking. (Kaleida Pediatrics 2009). Guidelines came out in 2005 but immediately received critical commentary (Hoover, Pellman Pediatrics 2005).


Using positive tympanocentesis culture as a gold standard, it becomes clear that bulging of the tympanic membrane is the most important indicator of bacterial acute otitis media (Schwatrz Clin Pediatr 1981). A yellow color was more common than red. In fact, in another study with culture as the gold standard, 15 patients had erythematous tympanic membranes as the only abnormality and not a single one grew bacteria on culture (Halsted Am J Dis Child 1968). This is not to say that color should be ignored, but to the beginner I would say this: Use the whole clinical context, and understand that distortion of anatomy is more important than color. If doubt remains, pneumatic otoscopy has some of the highest likelihood ratios of all the clinical signs.



-Bulging of the tympanic membrane is more predictive of culture-proven acute otitis media than erythema alone


You are seeing a patient with suspected vestibular neuritis. The resident is having trouble with the physical examination. Will localization help her comprehend the bedside findings?


We understand neurolgical disease by localizing it. We can often localize vertigo, though it is more difficult for 3 reasons:

– the signal is tonic (there is always a basal tone which can then go up or down)

– it is bilateral

– Its sensory representation is space, which is not just within the body but includes the external world.


To localize vertigo, one only needs to know 2 physiological principles:

1) A head turn activates the ipsilateral labyrinth and suppresses the contralateral labyrinth.

2) The vestibulo-ocular reflex (VOR) makes the eyes move opposite the head turn.


Now let’s localize this patient’s vertigo.


Attending: “What direction is the spinning?”

Patient: “It is spinning to the left”


Attending (to the resident): “Now turn your head to figure out what induces a perception of ‘spinning to the left.’ (resident turns head to the right). Correct. A right head turn does this. So the patient has a more active right ear than left ear. Thus, the left ear is the suppressed ear. Let’s confirm that at the bedside with physical findings.”


Attending: “If the left ear is pathological, where will we see nystagmus, on right or left gaze?”

Resident: “Well the mnemonic of eyes to the ice would say left? Wait, no, to the right?”

Attending: “Forget about the mnemonic right now and use the head turn again. The VOR makes the eyes move opposite the head turn. So the eyes want to go to the pathologic side. When they look away from that you get nystagmus as the eyes try to overcome the pull, and then fatigue. So where do you see nystagmus?”

Resident: “When the eyes look away from the pull. So you get right beating nystagmus on right gaze.”

Attending: “Exactly. Nystagmus is the conscious mind overcoming the pull. We use nystagmus in cold calorics to confirm consciousness.”

Resident: (after testing the patient) “But there is no nystagmus either side.”

Attending: Ah, but you just got another localizing finding.

Resident: The hard blinking?

Attending: Yes, that is gaze aversion. It tells you the same thing nystagmus tells you. The eye doesn’t want to look that way. You can even ask the patient which side is harder to look at. That picks up subtler deficits.

Resident: So the lesson here is that the VOR makes the ear want to go to the pathologic side.

Attending: Exactly. The fast phase of nystagmus and gaze aversion on the right mean that the eye wanted to go to the left. Now we can confirm left pathology through one more test.

Resident: Head impulse test?

Attending: Exactly (this is performed and is equivocal to the left, normal to the right)

Resident: So do we need to get an MRI?

Attending: No. The studies you are thinking of were done on a select population with severe deficits. The patients were so sick they needed to consult neuro. This patient has a very mild presentation and we would not expect a definitive catch-up saccade. Future studies will catch up with this concept.


Take home points:

-You will forget these rules, but do not forget that turning your head to one side activates that ear and inactivates the opposite ear

-The VOR pulls the ear to the less active (pathologic) side, so the eye has trouble looking opposite that (fast phase nystagmus, gaze aversion on looking away from pathologic side)

The world spins toward the pathologic side

Head impulse test is positive to the pathologic side


A patient presents with an upper respiratory illness and wants antibiotics. She points out that she always gets antibiotics, and that she always gets better, therefore the antibiotics must be needed. Is this bacterial sinusitis?


The preferred term today is acute rhinosinusitis, which reflects the fact that the mucosa of the nasal and sinus mucosa are continuous and both affected. Upper respiratory infection is common, happening 6 times a year in children and 2-3 times per year in adults. The cause is initially viral in most cases. Bacteria superinfection is rare, occurring in 2-10% of cases. Nonetheless, antibiotics are prescribed in 81% of patients.


Imaging, whether radiographic or CT, does not differentiate bacterial from viral illness. With an ordinary cold, 87% of patients have abnormalities on CT.


Recent IDSA guidelines emphasize knowledge of the natural history of acute viral rhinosinusitis as a means of diagnosing bacterial superinfection. Fever and constitutional symptoms abate within 24-48 hours. Clear mucus becoming thick is normal and expected after about 3-4 days. The illness has peaked by day 5-6 and is starting to get better, even if not fully resolved.


Traditional signs of bacterial infection were a list of major criteria, but essentially they were indicators that the sinuses were either full of purulence or plugged (anterior or posterior purulent drainage, sinus fullness or pain, hyposmia).


To keep it simple, indications for antibiotics would be if the illness is:

-severe (for 3-4 days)

-prolonged (more than 10 days – 61% of taps at this time show bacteria)




Take Home Points:

-Viral acute rhinosinusitis is by far the most common cause

-Imaging does not reliably differentiate bacterial from viral causes

-Antibiotics are indicated when there is inappropriate worsening, severity, or duration


References: Chow, IDSA Guidelines, Clin Infect Dis, 2012


The traditional teaching is that one must not diagnose benign paroxysmal positional vertigo (BPPV) unless geotropic nystagmus is seen on Dix-Hallpike maneuver. But in the emergency department, we commonly see patients with classic paroxysms of vertigo, classic positional triggers, and yet Dix-Hallpike is normal. What is the basis for the traditional view that requires for the diagnosis of BPPV a positive Dix-Hallpike maneuver?


A critically appraised review found that only one study has “tested the test,” finding a sensitivity of 79% and a specificity of 75% (Halker, Neurologist, 2008). Supporting this is the reporting in a review that repositioning maneuvers were effective in 50-97% of these patients (Alvarenga, Braz J Otorhinolaryngol 2011).


Remember of course that Epley is for posterior canal BPPV. So some of these patients with a history that says BPPV and no confirming tests will have a different canal affected. Go ahead and try Epley but if it does not work, consider testing for alternate canals, or, more simply, refer to otolaryngology.


Take home points:

-Use the Epley maneuver in BPPV without nystagmus

-Refer non-responders to the otolaryngologist for consideration of anterior or horizontal canal variants.


A patient presents with difficulty feeding for the past month.  Specifically, she states that she is “unable” to swallow.  How do we perform the bedside examination so as to take this presentation to the highest degree of resolution?


Swallowing can be divided into 2 processes: oropharyngeal and esophageal.


The oropharyngeal process moves the food bolus from the back of the tongue to the pharynx, where the pharynx squeezes it into the upper esophagus.  This event involves the soft palate closing of the nasopharynx, the epiglottis closing of the tracheal entrance, and the upper esophageal sphincter transiently relaxing to accommodate the food bolus.  This is a complex neurological event, and oropharyngeal dysphagia is usually caused by a neurological disease.  Telltale signs include nasal and tracheal aspiration, as well as inability to propel food out of the pharynx.


The esophageal process moves food from the upper esophageal sphincter (cricopharyngeus) to the lower esophageal sphincter.  Disruption can be anatomic (obstruction) or physiologic (motility). It presents with the feeling that food gets stuck in the esophagus. Patients feel these symptoms in the chest.


Dysphagia to solids only (such as chewy meats) signifies an anatomic obstruction. Gastroenterologists use marshmallows to bring this out, and call it a “viscous swallow.” Typical causes of anatomic obstruction include stricture, ring, or cancer.


Dysphagia to liquids and solids signifies a physiologic motility disorder. These can be localized to the lower esophageal sphincter, such as achalasia, or can be diffuse, such as diffuse esophageal spasm. Motility orders can also be secondary to inflammation, such as in gastroesophageal reflux disease.


By clarifying which part of the swallow process is disordered as well as noting whether liquids are affected helps considerably narrow the differential diagnosis of dysphagia.



-Inability to swallow or aspiration indicates oropharyngeal dysphagia, and is usually neurologic.

-Dysphagia to solids indicates obstruction.

-Dysphagia to liquids and solids indicates a motility disorder.


A young patient presents with nausea and spinning vertigo.  There are no focal neurologic deficits to suggest stroke, no stroke risk factors, no neck pain or neck trauma to suggest vertebral dissection.

And yet, the patient has severe gait instability, which can be an indicator of a stroke.  Is this alone a reason to order an MRI?

This is the exact situation where head impulse testing plays a role in the ED. The head impulse test is a test of peripheral labyrinth function.  The labyrinths sense head movement, and send a signal to the eyes to maintain visual gaze despite head movement.

Turn your head side to side while reading this text.  No problem right?  If you had vestibular neuritis you could not do it.  The head impulse test is a way of testing these vestibulo-ocular reflexes.


Face your patient, put your hand on each side of the patient’s head, have them look at your nose, and jerk the head 10 degrees to one side, very abruptly.  The normal person can maintain fixation on your nose.  The vestibular neuritis patient will break gaze, and you will see a catch-up saccade as they look back again at your nose.

An abnormal test is reassuring that this is a peripheral vertigo problem.  It is exactly in the SEVERE cases of vestibular neuritis that you are more likely to see a catch-up saccade.  It is not 100% specific, as rare patients with strokes will also have catch-up saccades.  But this is rare, and in the patient with a low prior probability of stroke, the head impulse test is probably sufficient to effectively rule out stroke.


A 40 year old female presents with nausea and dizziness, with 3 recent visits to the emergency department. Could this be benign paroxysmal positional vertigo (BPPV)?


You ask the patient whether it is episodic or continuous. “Continuous.” The resident accepts that and starts to ask the next question.


“Hang on” and you gesture that you want to explore that a bit more. Patients sometimes say continuous when they mean “I get episodes all day long” or “I continue to feel nausea after the episode.”


You rephrase the question. “During an episode, how long does it take for the vertigo to stop?” Answer: “A few seconds.”


The resident, curious why the patient used the term “continuous,” asks her and she explains that she has persistent nausea even when the vertigo stops.


Dix-Hallpike testing showed the classic vertical/torsional nystagmus and Epley canalith repositioning maneuver led to complete resolution of symptoms.


Take Home Points:

-Patients with BPPV sometimes mischaracterize their symptoms as continuous. Ask how long the spinning lasts.