Life in the eFAST Lane: Extended Focused Assessment with Sonography for Trauma (Part 1)

The Case: There are just too many eFAST cases to choose from. Which one to tell you…? Should I tell you about my first eFAST patient, the supposed-to-be-simple-but-really-wasn’t, on-coumadin guy who laid out his motorcycle? What about the lady from the rollover down a twenty foot embankment? Or the teenager from a horseback riding accident? Should I tell you about the night I hung out in resuscitation and did an eFAST on every patient that came through? A night in December I like to think of as Ultrasound Christmas. A night when a trauma alert rolled in and before I knew what was happening, the resident put the ultrasound probe in my hand and said “Go for it!” Needless to say it was AWESOME! Like do-a-secret-happy-dance-in-the-hallway-afterwards kind of awesome. I’m definitely still lovin’ the ultrasound elective, especially since I’ve become competent at eFASTs.

So what’s an eFAST you ask? It’s simple, really. It’s a systematic ultrasound scan to check for pneumothorax and free fluid (usually blood) in the abdomen and chest. It’s quick, easy, and incredibly useful. You don’t have to be a genius for this stuff. And it’s an ultrasound scan, so it means fewer patients being radiated by CT scans. Remember? Radiation bad. No radiation good. If you’re going to spend time in the ED, you should learn the eFAST. End of story. Plus if trauma’s your scene, you’ll get close to some wicked traumas. So now that you’re convinced… just how do you do an eFAST?

What’s eFAST All About?

The eFAST is a fast (pun intended) and easy way to check for blood in the chest and abdomen. eFAST is an acronym for extended Focused Abdominal Scan for Trauma. It’s an ultrasound exam designed for trauma patients that can be used at the bedside without interrupting ongoing care. Unstable patients with positive eFAST scans can then receive definitive care (get a chest tube, go to surgery, etc.) without the delay of waiting for a CT. The exam is a set of scans that quickly visualize free fluid (like blood) in the anatomical sites it most commonly collects, so the trick to quickly interpreting an eFAST exam is learning just where free fluid tends to collect. An eFAST looks at the right upper quadrant (RUQ), left upper quadrant (LUQ), pelvis, heart, and lungs. (Lungs are the extended part of the exam. Without the lung component it’s just called a FAST exam.) So that’s five ultrasound views, six if you’re picky about the whole 2 lungs thing, and you’ve completed an eFAST exam. It takes less than 5 minutes to complete, but more like 2 minutes as you approach ultrasound rock star status. Plus it’s more sensitive than x-ray for conditions like pneumo or hemothorax. Basically, eFASTs are a great ultrasound scan for rapidly identifying bleeding and other common injuries in the trauma patient.

The Patient: Who Gets an eFAST? 

  • Blunt and penetrating abdominal trauma
  • Blunt and penetrating chest trauma
  • Ectopic Pregnancies
  • Suspected abdominal or thoracic free fluid or active bleeding

How Do I perform an eFAST?

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It’s ALSO that time of year: Respiratory Syncytial Virus

Symptoms: Over 2 to 3 days development of wheezing, a so called “tight” wheezy cough, fever (usually low grade), cyanosis, tachypnea, retraction, fatigue.

Diagnosis:

Upon physical exam the above symptoms are noted, on auscultation inspiratory crackles and wheezing are usually present. Hydration status should be noted, as RSV is a diffuse small airway disease, leading to bronchiolitis.

Non-specific lab tests such as ABGs, CBC, and O2 sat., and age of child help determine candidates for admittance. Secretions can be analyzed using PCR but are expensive, a sophisticated virology lab is required in terms of antigen detection.

Imaging X-Ray is commonly ordered, revealing (nonspecific) hyperinflated lung fields, diffuse interstitial infiltrates, and in more advanced cases focal atelectasis.

DDx: Asthma, bronchitis, adenovirus, pneumonia, metapnuemovirus, influenza.

Treatment:  See part 2 coming soon!

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Anti-platelet therapy for stroke, what’s a ED Doc to do?

As a follow up to one of my esteemed colleague’s recent quick hit on the basics of strokes, I present some findings from time spent on the stroke unit these last few weeks.  Stroke is fairly popular here in the great state of Kentucky—we supremely enjoy our fried food, cigarettes, and lack of exercise (‘Merica!).  Therefore, stroke alerts are a fairly common occurrence in the ED and we keep our neurology friends busy (aka stroke team rounded for 10 hours a day).  But not everywhere is lucky enough to have an on call neurologist present for all stroke alerts.

So you’re the ED doc and they might have a stroke. Qu’est-ce que tu vas faire*!?!

Firstly, a head CT.  This is the first branch of the decision tree.  As previously mentioned, strokes are either hemorrhagic or ischemic, and the management of each is entirely different (ie do they get tPa or not). Without regards to whether to use tPa or not, this will focus on the ischemic subtype.

And within this subtype of ischemic stroke patients who cannot receive tPa, one comes to another branch in the decision tree.  Is the patient in atrial fibrillation (afib)?  Usually this can be evident from physical exam (ie irregularly irregular pulse) and telemetry, but an EKG can be confirmatory.  The management of an ischemic stroke in afib (aka cardioembolic ischemic stroke) differs greatly from one that isn’t (aka noncardioembolic ischemic stroke).  Cardioembolic strokes requires anticoagulants (eg warfarin) while a non-cardioembolic stroke only requires anti-platelets (eg aspirin).  Once again, the following will only focus on non-cardioembolic stroke and choice of anti-platelet.

*That’s French speak for ‘What ya gonna do’

Aspirin is dece*

There is some controversy in the stroke world as to the initial choice of anti-platelet for secondary prophylaxis of non-cardioembolic ischemic strokes.  One thing most everyone can agree on though is the utility of aspirin.  Aspirin within 48 hours has shown to decrease stroke reoccurrence and improve long term outcomes in multiple trials and meta-analyses 1,2,8.

*Dece= decent in Caucasian phrasin’

So what about the other fancy anti-platelets? 

There have been a multitude of trials that one is welcome to read by following the references below but I present my personal summary for secondary prophylaxis based on what I’ve read in the trials:

– Aspirin is more effective than placebo1,2

-Aggrenox (dipyramidole+aspirin) is better than placebo3

-Plavix is better than aspirin in composite vascular endpoint (you can decide for yourself whether that’s truly better for stroke or not)7

-Aggrenox may be better than aspirin3,5

-Plavix and Aggrenox are equivalent4

– ASA+ Plavix is equivalent to plavix alone but increases risks of bad side effects (eg bleeding)6

– Ticlopidine is better than placebo9

-Ticlopidine may be better than aspirin but with increased costs, lab f/u (i.e. biweekly CBC’s the first 3 months due to risk of neutropenia), and worse side effects may decrease the cost/benefit ratio10

Blah blah too many words—Break it down, C Belch

So a patient comes in with signs of stroke.  Their CT is negative for bleed and they’re outside of the tPa window.  They’re not in afib.  What are you gonna do?  My personal guidelines based on the evidence:

–          Aggrenox or Plavix monotherapy are good initial choices for non-cardioembolic ischemic strokes and better than aspirin alone

–          Do NOT use aspirin + Plavix dual therapy for these types of strokes due to the increased risks of bleeding. Leave that combo for cardiologists.

–          Aspirin and ticlopidine are also good initial choices.  But aspirin may be less effective than Aggrenox or Plavix monotherapy and ticlopidine has a poor side effect profile and increased costs

Public Service announcement:  As always, each patient is different and requires a personalized and evidence based approach to medication choices based on side effect profile and individual patient preference.  I also reference below the American College of Chest physician’s recommendations11 —they set forth their own guidelines based on the evidence which are very similar to what is proposed above.  And if all else fails, ask your friendly neighborhood pharmacist.

 

Sources:

  1. The International Stroke Trial (IST). Lancet. 1997 May 31; 349 (9065): 1569-81
  2. Chinese Acute Stroke Trial (CAST). Lancet 1997 Jun 7; 349 (9066): 1641-9
  3. European Stroke Prevention Study 2 (ESPS 2).  J Neurol Sci. 1996; 143(1-2): 1-13
  4. PRoFESS trial.  NEJM. 2008; 359 (12): 1238-1251
  5. European/Australasian Stroke Prevention in Reversible Ischemia Trial (ESPRIT).  Lancet. 2006; 367 (9534):  1665-1673
  6. MATCH trial.  Lancet. 2004. Jul 24-30; 364(9431):  331-7
  7. CAPRIE trial.  Lancet.  1996 Nov 16; 348(9038):  1329-39
  8. Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, MI, and stroke in high risk pts.  (Antithrombotic Trialists’ Collaboration).  BMJ.  2002 Jan 12; 324 (7329):  71-86
  9. Canadian American Ticlopidine Study (CATS).  Lancet.  1989 Jun 3; 1(8649):  1215-20
  10. A randomized trial comparing ticlopidine HCL w/ asa for prevention of stroke in high risk pts.  (TASS).  NEJM.  1989 Aug 24; 321 (8):  501-7
  11. Antithrombotic therapy and prevention of thrombosis, 9th ed: American College of Chest Physicians Evidence based clinical practice guidelines.  Feb 2012; 141 (2_suppl)

Compiled by: Chris Belcher

Miss anything? Forgot to include something important? Leave a comment and help us improve our knowledge base for medical students!

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IT’S THAT TIME OF YEAR: FLU QUICKHITS (PART 2)

Part two will cover the important basics about the flu treatment, chemoprophylaxis, high risk patient population w/ the flu management. This is a compilation of information provided by the CDC along with reference papers that have been clinically relevant as they have been referenced multiple times over the last few weeks during my rotation in the ED. 

flu2

Note that Tamiflu is now FDA approved for patients age 2-weeks and older (FDA NEWS RELEASE link)

 

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Pregnant women

Oseltamivir is preferred for treatment of pregnant women. Pregnant women are recommended to receive the same antiviral dosing as nonpregnant persons

  • Zanamivir might be preferred by some providers because of its limited systemic absorption; however, respiratory complications that might be associated with zanamivir because of its inhaled route of administration need to be considered, especially in women at risk for respiratory problems
  • Pregnant women are known to be at higher risk for complications from infection with seasonal influenza viruses and severe disease among pregnant women was reported during past pandemics
  • Oseltamivir, zanamivir, rimantadine, and amantadine are “Pregnancy Category C” medications, indicating that data from clinical studies are not adequate to assess the safety of these medications for pregnant women

Persons w/ impaired renal function

Oseltamivir: For patients with creatinine clearance of 10–30 mL per minute, a reduction of the treatment dosage of oseltamivir to 75 mg once daily and in the chemoprophylaxis dosage to 75 mg every other day is recommended

  • Serum concentrations of oseltamivir carboxylate, the active metabolite of oseltamivir, increase with declining renal function.

Person w/ Immunosuppression

  • oseltamivir was safe and well tolerated when used during the control of an influenza outbreak among hematopoietic stem cell transplant recipients living in a residential facility
  • Source: (retrospective study: Vu D, Peck AJ, Nichols WG, et al. Safety and tolerability of oseltamivir prophylaxis in hematopoietic stem cell transplant recipients: a retrospective casecontrol study. Clin Infect Dis 2007;45:187–93.)

flu4

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It’s that time of year: Flu QuickHits (part 1)

Part one (written by second year Nick Mancuso) will cover the important basics about the flu epidemic this season. Great summary!

The 2012/13 vaccine contains the typical triad against an H1N1, H3N2, and an influenza B variant.

  • A/California/7/2009 (H1N1)-like virus
  • A/Victoria/361/2011 (H3N2)-like virus
  • B/Wisconsin/1/2010-like virus.

Symptoms overlap with many URI’s, however the classics:

Abrupt onset, Chills, Varying fever temps, Myalgias, Frontal/retro-orbital headache, Sore throat, Nausea/Vomiting

Diagnosis

can be difficult because samples are sent to labs and take time to get results. A nasopharyngeal culture is taken. Most diagnosis is done at the bedside based on clinical criteria. Rapid tests are not accurate and results vary. (Check continue reading for more info about diagnostic tests!)

Treatment:

Read part 2!

For some cool data and graphs from the CDC continue reading…

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2012 in review

The WordPress.com stats helper monkeys prepared a 2012 annual report for this blog.

Here’s an excerpt:

600 people reached the top of Mt. Everest in 2012. This blog got about 3,800 views in 2012. If every person who reached the top of Mt. Everest viewed this blog, it would have taken 6 years to get that many views.

Click here to see the complete report.

Strokes: the quick and dirty

2 Major Types:

1) Ischemic: blood vessel supplying the brain is obstructed by a clot

  • Embolism
  • Thrombosis 

2) Hemorrhagic: blood vessel bursts, blood leaks throughout brain #1 Risk Factor: High blood Pressure Other Risk Factors:

  • Age
  • Sex: Male
  • Ethnicity: African Americans, Mexican Americans, Hawaiians, Asian Americans
  • Smoking
  • Fat, cholesterol-rich diet
  • Overweight
  • Pregnancy
  • Birth-control Pills
  • Smoking
  • Diabetes
  • Renal problems
  • Atrial Fibrillation

Signs of Stroke

  • Sudden, severe headache
  • High blood pressure
  • Problems with vision, reflexes, walking, movement, speaking, coherence
  • Vertigo
  • “Bruit” noise when listening to carotid arteries in neck with stethoscope

Treatment Options:

  • Ischemic: Blood thinners to reduce clots: warfarin, heparin, Coumadin
  • Hemorrhagic: surgery to remove blood in brain, repair damaged blood vessels

Academic life in emergency medicine NIH stroke scale PV card. Great resource:
http://academiclifeinem.blogspot.com/2010/02/paucis-verbis-card-nih-stroke-scale.html

Click continue reading for high yield quickhits on a few specific types of stroke and brain imaging examples Continue reading

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Beating a Dead Horse: Why Ocular Ultrasound Beats Papilledema for Detecting Increased Intracranial Pressure

Our earlier article on ocular ultrasound for measuring intracranial pressure was met with a common question. Primarily, why not just use papilledema as your initial assessment for intracranial pressure? This is what we are taught in medical school. Optic nerve disc swelling equals increased intracranial pressure (ICP). End of Story. Right? Not exactly…  While optic disc swelling can indicate increased ICP, it is an inferior measure of acutely elevated ICP. And here is why…

  • It’s an indirect measure.
  • It’s a late sign of increased ICP.
  • It’s more subjective.
  • It’s not a dynamic measurement.
  • It’s not always practical.

pap vs oc us 1

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Disseminated Intravascular Coagulation (DIC)

Pathophys of DIC. Source: Lippincotts

Pathophys of DIC. Source: Lippincotts

DIC is a pathological process where tissue factor or other thromboplastic substances from endothelial cell injury are released into circulation-Leads to paradoxical formation of 1) microthrombi leading to organ failure and 2) hemorrhaging.

 Associated Clinical Causes

-Sepsis
-Trauma (especially neurotrauma)
-Cancer
-Shock
-Major Surgery
-Immunologic (transfusion/transplant reaction)
-Obstetric complications

Diagnosis

Can be complicated by the underlying causes, lab tests indicating DIC:

– Platelets <100,000 or recent rapid large decrease in number
– Prolonged PT and aPTT
– Elevated D-Dimer (>.5ug/ml)
– Schistocytes in blood smear
– Fibrinogen -if obtainable <1g/L (only in ~28% of pts)

A scoring system has been developed (click continued reading)

DDx: DIC, Hemolytic Uremic Syndrome, Liver Disease, Thrombotic Thrombocytopenic Purpura, Heparin-induced thrombocytopenia, HELLP syndrome in pregnancy

Treatment

Treat the underlying cause, platelet and blood factor replacement to treat bleeding can be used but won’t correct DIC. Heparin used when fibrin deposition is excessive and no risk of hemorrhage present (no petechiae or bruising).

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Trigeminal Neuralgia

Trigeminal Neuralgia (Facial pain, tic douloureux)

  • Pain:  Paroxysmal stabbing pain affecting one or more divisions of the trigeminal nerve
  • rarely bilateral, and never on both sides at the same time
  • may last for days or weeks and patient may remain pain free for many months after pain subsides
  • Signs and symptoms:  usually no accompanying neurological problems, sometimes blunting of pinprick over affected region
  • Triggers: speaking, brushing teeth, washing face, eating, cold wind, touching a “trigger spot”
  • Mostly affects females and patients 50+ yrs of age

Investigation

  • CT or MR scan to exclude CPA lesion or demyelination

Acute Attack Treatment = Phenytoin 250 mg IV for relief for hours- 3 days

First line Agent =  Carbamazepine 100mg 1-2 times per day, with increase of 100-200mg every 3 days up to a maintenance dose of 400-800mg

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