Archive | February, 2014

acetaminophen overdose? remember: 150

28 Feb

If you can remember one number to get the ball rolling on an acetaminophen overdose….


remember: 150

150 mcg/mL is the 4 hr acetaminophen level of possible toxicity

150 mg/kg is the initial loading dose of IV N-acetylcysteine (NAC)


After that, you can look up the infusion doses, but here’s a nice chart from an EMN article.

Also, just to scare you: an article on IV NAC overdose.  

  • The quick lession: be VERY clear on your doses, and write the infusions out as mg/kg/hr.  


References: EMN article & picture; scary article

roc vs. sux?

27 Feb

quick review of some basics numbers for your common intubation paralytics, cribbed from a couple 2011 Annals articles/comments:


  • typical dose: 1.5 mg/kg
  • time of onset: 45 sec
  • duration of muscle relaxation: 6-10 min
  • risk profile: hyperkalemia, malignant hyperthermia (rare)


  • time of onset (at 1mg/kg dose): 60 sec
  • time of onset (at 1.2 mg/kg dose): 40 sec
  • duration of action: 25-60 min

References: article 1, article 2; picture

improvised atomizer/jet ventilator

24 Feb has a good summary of Awake and Fiberoptic intubation with some neat pictures of a disposable atomizer assembly.

I’ve also seen a Weingart video someplace where he puts the same setup together with a 14 g IV and uses it as an improvised jet ventilator, putting his hand on the open end of the T-piece not connected to the IV to deliver breaths, and letting go to allow for expiration (if anyone can find that link, please let me know, I’ve since lost that link).

check out the pics below from the post:


There you go.


References: crashingpatient post (with pictures).

good advice for the ED

21 Feb

something light for Friday: some good advice via Dr. Solomon in last December’s ACEP mag.  

the whole article’s worth a read, but here aresome of my favorites:



2. When you wonder why the patient is here for an apparently inconsequential problem, remember: We are in the reassurance business.


6. It is hard to make an asymptomatic patient feel better.


7. Schizophrenics are not immortal…


11. Do not order tests that will not influence patient management.


17. Abdominal pain in the elderly is a catastrophe until proven otherwise…


18. …You cannot assuage the patient’s worst fear if you don’t know what it is.


21. It is good to know guidelines…It is best to know the evidence.


Food for thought for your next shift.  Go forth.


References: Dr. Solomon’s ACEP article; picture

video review: emergent pericardiocentesis

20 Feb

Cribbed from this somewhat long but still useful NEJM procedure video (if you only watch 3 minutes, start at the 5:30 mark):


ultrasound guided (subxyphoid vs parasternal), ECG monitored (alligator clip to spinal needle), or blind approach (ballsy)

insert spinal needle through skin with stylet in place (avoids tissue biopsy), then take stylet out and advance with syringe attached

3-way stopcock between needle & syringe is handy for drainage assist

blind approach: subxyphoid, 45 degree angle, aim toward left shoulder

ECG-clip approach:

  • watch for ST elevations (this is too far–you’re touching the myocardium)
  • withdraw a bit until no ST elevations, then try to aspirate/reapproach



References: NEJM youtube video

Tranexamic Acid Use in Trauma

18 Feb


inhibits plasminogen activation thereby decreasing plasmin activity

Inhibits clot breakdown as opposed to new clot formation

-Excreted in urine

Half-life of 2 hours



1g loading dose over 10 minutes, followed by 1g over 8 hours


Data Behind its Use:

CRASH-2 Study

-looked at 20,211 trauma patients in 40 countries

-randomized double blinded placebo controlled multicenter study

-Primary outcome looked at was in hospital mortality

-Secondary outcomes included vascular occlusive events, transfusions, surgical interventions


Reduction in relative risk of all cause mortality (14.5% vs. 16%; p=0.0035) with a NNT of 67 trauma patients

Reduction in RR of death from bleeding of 15% (4.9% vs. 5.7%; p=0.0077)

-Benefits of TXA increased with administration within 3 hours and in hypotensive patients

-Death from head injury the same in both groups (previous studies showed not beneficial in SAH patients)

No significant difference in rate of vascular occlusive events (1.7% vs. 2.0%; p=0.084)


 Submitted by Joey Grover. 


Sources: Cap AP, Baer DG, Orman JA, Aden J, Ryan K, Blackbourne LH.  “Tranexamic Acid for Trauma Patients:  A Crticial Review of the Literature.” J Trauma.  2011;71:S9-S14.; CRASH-2 Trial Collaborators.  “Effect of Traneamic Acid on Death, Vascular Occlusive Events, and Blood Transfusion in Trauma Patients with Significant Haemorrhage (CRASH-2):  A Randomised Placebo-Controlled Trial.”  Lancet.   2010;376:23-32.; picture

Tetanus (quick review)

14 Feb

 -Caused from Clostridium tetani, a nonencapsulated anaerobic gram positive rod 

-Exist in either spore forming or vegetative state


-Once converted into vegetative form, it produces two exotoxins

1.  tetanolysin,  which helps spread the bacteria

2.  Tetanospasmin, responsible for clinical manifestations of tetanus


Effects of tetanospasmin:  

Acts on the motor end plates of skeletal muscle,

preventing the release of the inhibitory neurotransmitters glycine and GABA from presynaptic nerve terminals,

preventing normal inhibitory control of nervous system


-Overall features:  muscular rigidity, muscle contractions, autonomic nervous system instability

Incubation period is <24 hours to more than 1 month


-Types of Tetanus:

                1.  Generalized Tetanus

-Most common form (80% of cases)

Masseter muscle stiffness/pain (Lockjaw) most common complaint

-Shorter axon nerves affected first (facial muscles), with descending progression of the neck, trunk, extremities

-Transition of stiffness to rigidity leads to trismus and characteristic facial expression (risus sardonicus).

-Generally get dysphagia, arm flexing, wrist clenching, and lower extremity extension. 

-Autonomic disturbances include labile hypertension, hyperpyrexia, tachycardia, increased catecholamine release

                2.  Neonatal tetanus

-Frequently occur after unsterile treatment of umbilical cord stump with inadequately immunized mothers

-Generally present as weak, unable to suck, and irritable during 2nd week of life

                3.  Cephalic tetanus

                                -Generally occurs after head wounds

                                -Present with cranial nerve dysfunctions, traditionally cranial nerve 7

                4.  Local tetanus

                                -Rigidity of muscles near site of injury

                                -Resolves after weeks to months

-Diagnosed clinically



1.  Tetanus immunoglobulin– neutralizes circulating tetanospasmin.  Unknown dose needed but 3000 to 6000 units IM is recommended.  GIVE BEFORE WOUND DEBRIDEMENT .  Lasts in your system for 28 days so no need to repeat dosing

2.  Wound debridement- prevent further toxin production

3.  Metronidazole traditionally administered. 

4.  Muscle relaxants

5.  Autonomic dysfunction- Magnesium sulfate has been shown to decrease catecholamine release.  Labetalol can also be used.

6.   Active immunization- give them a TDAP


Submitted by Joey Grover.


Sources: Tintinalli’s Emergency Medicine:  7th Edition; Rosen’s Emergency Medicine:  7th Edition; picture