Notes from the Scientific Assembly

No Comments
Weren’t able to make it to Boston for the ACEP Scientific Assembly? Not to worry, we took notes.

9:30 Trauma
Three Red Flags
1) blunt chest trauma with possible mediastinal injury?
    >Consider lowering the BP to reduce shearing force on the vessel wall.
    >Use nitroprusside and a beta blocker (esmolol drip prior to CT is good choice)
2) High speed MVC with possible shock?
    >Think pelvic fracture
    >3rd most common cause of death in MVC
    >most bleeding is venous (relatively slow)
3) injury to the head/neck.  Should you screen the carotid/vertebral artery for injury?
Yes, if:
    >LeFort II/III fracture
    >c-spine fracture
    >basilar skull fracture
    >DAI (diffuse axonal injury) with GCS <6
    >hanging mechanism
No, if:
    >simple shoulder harness sign alone
What’s at risk?
    >13% mortality rate with blunt carotid vascular injury
    >25% will have CVA if left untreated

11:00 What is Non-Invasive Monitoring Really Telling You?
Pulse oximetry (Sa02)
    >at 95% Sa02, Pa02 is between 60 and 160 mm Hg!
End tidal CO2 (EtC02)
    >reflects alveolar ventilation, pulmonary perfusion, and CO2 production
    >underestimates PaCO2 by 4-5 mm Hg
    >may be unreliable in tachycardia, blood pressure abnormalities and critically ill
    >skin probe EtC02 is under development
    >decreased EtC02 correlates with decreased cardiac output
      ->PEA arrest? Guide to stopping CPR
CVP monitoring? How much does it help?
    >Not much
      ->some patients with a CVP of 16 still need fluids i.e. mechanical ventilation, chronic lung disease, pulmonary hypertension, tricuspid disease, heart failure give false positive CVP reading


Blood pressure varies?  What does it tell you?
    >If blood pressure varies >15-20% with respiration, patient needs hydration
Non-invasive cardiac output measurements
    >BP pulse wave form analysis
      ->changes in the DBP/SBP over time estimates aortic impedance, and estimate of cardiac output
    >Esophageal doppler estimates stroke volume.  This multiplied by HR is cardiac output   

2:00 Neuro
(In a Nutshell)

Fast exam
    >watch them walk
    >hear them talk
    >look in their eyes
      ->unilateral dilatation?  Think aneurysm (especially the post. inf. cerebral a.)
      ->unilateral constriction?  Think sympathetic chain disruption
      ->eyes are down and out or can’t adduct?  Think CN3 dysfunction
      ->eyes can’t abduct?  Think CN6 dysfunction
      ->bilateral adduction problems?  Think multiple sclerosis
      ->the patient tilts his head to resolve diplopia?  Think CN4 dysfunction

What is the level of the lesion?
>C5 = shoulder adduction
>C6 = wrist extension
>C7 = wrist flexion
>C8 = finger extension
>T1 = intrinsic finger muscles
>L1/2/3 = hip flexor
>L4 = foot inversion, patellar reflex
>L5 = toes up
>S1 = foot eversion, achilles reflex


Got nystagmus?  What does it mean?
    >peripheral nerve problem if:
      ->delayed appearance
      ->fatigues with repetition
      ->associated with intense vertigo
    >central nerve problem if:
      ->associated with severe tinnitus or hearing loss
      ->less intense vertigo

4:00 Overdoses
What can be dialyzed?
    >For sick, massive overdoses, virtually anything (even acetaminophen) can be dialyzed.
Do I hold off using gastric lavage if the overdose was more than an hour or two?
    >With massive overdoses, gastric decontamination may be effective long past the traditional “window” simply because there are that many more pills sitting in the gut.
QRS widening.  That must mean a TCA overdose
    >While most of us associate QRS widening with TCA overdoses, venlafaxine (Effexor) is becoming a more common etiology as TCAs are used less frequently. 
    >With an Effexor OD, if the QT is long consider magnesium.
Anything for a valproic acid ODs?
    >L-carnitine can be given to improve ammonia metabolism.
How about Seroquel?
    >Try lipid rescue for overdose of lipiophilic substances: it becomes a lipid sink for fat soluable drugs (such as Seroquel)

5:30 Updates in the Management of Acute Fibrillation
How to find the cause for AF in the “youngish”, healthy patients with new afib
    >the highest-yield tests are TSH and a TTE
Do I shoot for rate control or rhythm conversion?
    >For the long-term, rate control tends to win out over rhythm control. 
    >In the acute setting, trying to break afib w/RVR, magnesium wins over diltiazem in head-to-head trials!
The Ottawa protocol
    >know that it is an ED-based rhythm conversion method:
    >Patients have to be new-onset afib, meaning <48 hours
    >First, given procainamide 1g
    >If that fails, cardioversion is the next step
    >Overall, there is ~15% failure rate, including all of the bouncebacks
The problem is trying to determine the duration:
    >Silent afib is common, meaning the patient doesn’t always “feel” the arrhythmia
    >Even when an afib patient is in NSR, their atria aren’t contracting normally, so the clot risk is still present

7:00 Infections from Abroad: Unwanted Souvenirs
Where was the patient traveling?  The most important question to determining the pathogen
    >Time of travel, not so important.  Remember that the risk extends up to 1 YEAR for some of these diseases


Where did you travel?  What is the most likely pathogen?
North Africa:
    >water/food contamination most common (gastro, Hep A, typhoid, amebiasis), malaria not as common
Rest of Africa:
    >vector-borne illnesses most common, specifically malaria
East Asia:
    >diarrheal and respiratory illnesses most common, and TB risk is very high – 10% MDR in China! Malaria is not as common.
Southeast Asia:
    >similar to East Asia, but Dengue is also very common
Middle East:
    >Meningococcus is very prevalent
    >Rabies is much more common in the developing world, and is usually transmitted from dogs (unlike in the US, where bats/rodents much more common). Also, remember that the CDC changed the guidelines in June of this year from 5 shots to only 4.
    >TB, but remember that in diabetic patients TB presents atypically:
      ->Often large pleural effusions, lower extremity symptoms
      ->Any diabetic patient returning from the developing world with pneumonia MUST be ruled out for TB, even without upper lobe disease.  In the developing world, TB is thought to be a relatively common CAUSE of diabetes

Staff Notes
EPM contributors report on their most memorable ACEP moments

Amal Mattu: If the story is concerning and the risk factors are present, don’t rely too much on negative stress tests or negative coronary catheterizations — the plaque ruptures that can kill are often from arteries with moderate, not severe, stenosis.
The informatics session had a spirited debate on whether to quietly succumb to interoperable hospital-wide information systems or to fight for best-of-breed ED-only systems.

-Nicholas Genes, MD, PhD

Tom Scaletta, immediate past president of AAEM, met with both ACEP outgoing and incoming presidents who, “appreciate camaraderie with AAEM,” said Scaletta. “Made me feel great as past AAEM president”
I expected Paula Begala to generate more controversy with his speach. Instead, he seemed subdued. He was entertaining, with many amusing anecdotes, but I thought his speech lacked substantive content. Kind of like sitting at a bar and talking politics. Entertaining, but I was looking for more.

-WhiteCoat (via blog)

Aging Physician Taskforce: We need to prepare EPs for retirement just as much as we need to prepare residents for practice in the ED.

-Michael Carius, MD

Leave A Reply