Maisonneuve Fracture - A can’t miss diagnosis!

Author: Benjamin Lindquist, MD

This post was peer reviewed.
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Chief Resident
Stanford/Kaiser Emergency Medicine Residency

A 50 year-old male pedestrian presented to the emergency department by ambulance after having his left foot struck by a bicyclist while the foot was firmly planted on the ground. He complained of severe pain to his medial ankle but denied knee or hip pain. He had no other injuries. On examination, he had slight eversion at the ankle with significant tenderness over the medial malleolus. He also had tenderness over his proximal fibula. He had normal strength, sensation and pulses.

X-ray showed widening of the medial tibiotalar joint space (Image A) and a comminuted fracture of the proximal fibula (Image B). These findings are suggestive of a Maisonneuve fracture with syndesmotic ligament disruption. He was placed in a splint and referred to orthopedic surgery. Ten days later, he underwent operative fixation of his syndesmotic ligament injury.

In evaluating patients with ankle injury, it is imperative to assess for concomitant proximal fibular fractures. As in this case, it is common for patients to complain only of ankle pain and not pain around the proximal fibula. However, Maisonneuve fractures are often unstable and require surgical fixation, whereas isolated fibular fractures or deltoid ligament sprains are managed nonsurgically.

Image A: Anteroposterior view L ankle

Image B: Anteroposterior view L tibia-fibula

References:

Taweel NR, Raikin SM, Karanjia HN, Ahmad J. The proximal fibula should be examined in all patients with ankle injury: a case series of missed maisonneuve fractures. J Emerg Med. 2013;44(2):e251-5. PMID: 23079149

Five Things to Keep in Mind When Treating an Asthmatic

Image from Alan Levine

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Author: Puja Gopal, MD
Emergency Medicine Resident
University of Illinois at Chicago
AAEM/RSA Publications Committee Member

Asthmatic patients present along a broad spectrum of severity. There are those who present with mild wheezing, have complete resolution with a single neb treatment, and go home with a refill of their albuterol inhaler. And then there are those patients who present unable to speak or breathe and become increasingly agitated and altered. Though presentations of asthmatic patients may vary greatly, there are some key things you can keep in mind with the asthmatics you see.

1. Monitor the patient and the 5 key vital signs closely – temperature, pulse, respiratory rate, blood pressure and oxygen saturation. Heart rate above 120 and respiratory rate above 30 are concerning for a severe asthma exacerbation. Also note that a decreasing respiratory rate can be concerning for the inability to maintain respiratory effort and possible decompensation. An oxygen saturation <90% is hypoxemia and requires your attention. Monitoring your patient’s mental status is of utmost importance to ensure they don’t become agitated or altered – both of which can occur with hypoxia and/or hypercapnia.[1]
   

Pre- and Post-Intubation Issues and Solutions

Photo Credit: Borls Ott - Flickr

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Author: Andrew V. Bokarius, MD
Emergency Medicine Resident
University of Chicago




There are a number of issues that may come up prior to, during, and after successful intubation. Let’s take a look at a few common problems and possible solutions.


 Pre-intubation:

• Can’t mask ventilate:
• Turn head to the side, consider oral/nasal airway or LMA.2 

• Can’t intubate, patient has a Grade 4/Mallampati Class 4 view:
• Change position or equipment, i.e., ear to sternal notch, B.U.R.P. maneuver (backward-upward-rightward-pressure or modified cricoid pressure), change blades, or consider a bougie, Glidescope, or other fiberoptic device.[1]  

A Cannot Miss Cause of Bradycardia

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Author: Daniel Balk, MD
Emergency Medicine Resident
Drexel University College of Medicine

The Case:

The tech hands the physician this EKG:

It’s slow with a rate of 37, it’s irregular, it’s wide with a QRS of 130, it’s scary, and there is no previous EKG. The tech doesn’t know the patient’s story as “he speaks only Portuguese” and his chief complaint is hypoglycemia.

Glancing at the monitor as the physician rushes towards the room, the blood pressure is 138/71. This elderly Brazilian traveller (with a prior history of two cardiac stents, hypertension and diabetes) is discussing with his family whether his two days of diarrhea caused his sugar to be low all day despite foregoing his insulin. His blood glucose was 40 this morning; it’s 135 now after eating normally all day and skipping his long acting and mealtime insulin doses. The review of systems is entirely negative other than for diarrhea and hypoglycemia. Other than marked bradycardia, the exam is unremarkable.

Acute Aortic Syndrome

Photo Credit: Charlotte Astrid

Author: Nathan Haas, MD PGY-1
University of Michigan

Originally Published: Modern Resident, February/March 2015

The acute onset of severe, ripping chest pain radiating to the back quickly brings to mind the diagnosis of aortic dissection. However, dissection is just one potential etiology of Acute Aortic Syndrome (AAS) which includes the acute presentation of aortic dissection, penetrating atherosclerotic ulcer, intramural hematoma, aneurismal leak and traumatic transection. Overlap frequently exists between these processes, and the various etiologies within AAS in some ways represent more of a spectrum of disease than distinct entities.

Aortic dissection results from an intimal tear penetrating the aortic media, with progressive dissection of the media creating a false lumen. Contrarily, a penetrating atherosclerotic ulcer occurs at the site of a preexisting atherosclerotic plaque and is the result of intimal erosion through to the media. Intramural hematoma is defined as a blood collection in the media without the presence of an intimal flap and physiologically is driven by the rupture of vasa vasorum. Aneurismal leaks are related to the acute expansion of a preexisting aortic aneurism. Traumatic transection most frequently occurs secondary to a rapid deceleration injury and classically occurs immediately distal to the left subclavian artery at the ligamentum arteriosum.