Winter is coming… Think CO toxicity!

Much has been written on the topic of Carbon Monoxide Toxicity. I will not reiterate that CO is a colorless, tasteless, odorless gas, nor will I restate that it is among the top killers of toxins worldwide. I may tell you, however, that whenever a carbon based material undergoes incomplete combustion, CO is generated. Another tidbit commonly discussed in this context is that dichloromethane (CH2Cl2) ingestion will lead to high serum CO concentrations from metabolic conversion in the liver. There have been countless laboratory, animal and human studies which elucidate aspects of the multifactorial pathophysiology of CO toxicity which show effects from displacement of oxygen, causing hypoxic injury, binding to cytochrome, myoglobin and other proteins causing disruption in cellular respiration or function, lipid peroxidation and inflammatory effects with oxygen free radical generation, etc. most commonly manifesting in neurological, neuropsychiatric and cardiac dysfunction1. I am going to cut to the chase, as this is a blog and not a stuffy scientific manuscript, and discuss the presentation, diagnosis, treatment and outcome of patients with CO exposure and toxicity. Be warned, there is much controversy, a lot of data- some of which is contradictory- and even more anecdotal case studies. There are also medical-legal overtones and regional differences in preferred treatment modalities.

CO 1
Figure 1: Electron Transport Chain and the Effect of CO.

Case: 54 yo woman presenting with headache, nausea and blurred vision for 7-10 days. She stated that her contractor hired to re-work a botched job on her boiler advised her to go the emergency department because the CO level in her house was “sky-high”. After seeing another physician and hours after leaving her house, she presented to the emergency department. The boiler was faulty for about 2 weeks. Her examination was normal. Her labs and ECG were normal. Her COHgb concentration was 4.

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The Cricothyrotomy Part 2: Pearls, Pitfalls, and Troubleshooting

a blog series on emergency medicine procedures

In the last post (the cricothyrotomy part 1) we focused on the basics of preparation and technique for the cricothyrotomy procedure. Here we focus on the pearls, pitfalls, and troubleshooting with a strong emphasis on anatomy.

As an aside…

Always consider alternatives to the cricothyrotomy, and especially, the “crash” cricothyrotomy

  • Try other non-invasive rescue maneuvers including the intubating LMA as Dr. Nestor mentioned last week

  • Review the difficult airway algorithms that were briefly acknowledged last week, and strive for expertise in airway decision-making

  • Do not hesitate to overhead anesthesia for assistance in any difficult airway

  • Avoid paralyzing patients with tenuous airways in appropriate situations, and consider awake (fiberoptic or other) intubation, or even awake cricothyrotomy with ketamine (and local anesthetic)



Why is this so important? First let’s explore some potential pitfalls….


PITFALL: You make your vertical incision OFF midline

  • You may not find the membrane
  • Complications: you may injure the following structures:
    • Cricothyroid muscles
    • Recurrent laryngeal nerves (uncommon)
    • Carotid artery / Internal Jugular vein (very rare)


PITFALL: You make a horizontal cut too SUPERIOR

  • Superior to cricothyroid membrane:
    • This is above the cords, and likely the location of your issue (i.e.: obstruction or other)
    • Complications: increased risk of vascular and nerve damage: superior laryngeal vessels and the internal branch of the superior laryngeal nerve

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The Cricothyrotomy Part 1: The Procedure

a blog series on emergency medicine procedures






  • Cannot intubate:
    • Multiple attempts with most experienced operator
    • Both conventional and rescue techniques attempted (1)
  • Cannot ventilate:
    • Cannot get chest rise with BVM, LMA, or other rescue devices between attempts
  • Cannot maintain O2 sat > 90%


  • Extreme facial or oropharynx deformity


  • Other airway options have not been considered
  • Pediatric patient (for open surgical method) (<10-12 years old, varies depending on expert opinion)
  • Tracheal transection, larynx or cricoid cartilage fracture, obstruction at or below the membrane


Watch this video to learn a simplified approach from Dr. Reuben Strayer.

From Dr. Reuben Strayer’s Advanced Airway Management for the Emergency Physician 



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Procedural Blog EXTRA: Reduction of TMJ Dislocation

9fabe73c-e43e-47b4-9027-a14138593117_zpsf54998b4a blog series on emergency medicine procedures


  • 14 year old female presented with inability to close her mouth after yawning.
  • Exam: uncomfortable with jaw open. Limited ROM of jaw bilaterally. Tenderness at TMJ with mandibular displacement bilaterally.

TMJ Dislocation

  • Mandibular condyle moves anteriorly along the articular eminence and becomes locked in place
  • Spasm of the surrounding muscles lead to trismus
  • Condyle cannot return to its normal position


From Roberts and Hedges’ Clinical Procedures in Emergency Medicine

Panorex of patient’s bilateral TMJ dislocation:


Facial CT 3-D reconstruction showing bilateral TMJ dislocation: 

tmj3 tmj4

Facial CT showing TMJ dislocation: 

tmj5 tmj6


  • Universal precautions (gloves!)
  • Gauze
  • Tongue blade
  • Suction
  • Forceps


  • Conscious sedation especially in children
  • Massage the masseter muscles in order to relax and fatigue them, which may facilitate manual reduction
  • Consider local anesthesia
    • TMJ space (see below) OR directly into the lateral pterygoid muscle (not discussed)
    • TMJ local anesthesia:
      • Clean the skin anterior to the ear
      • Insert the needle into the TMJ space at the palpable depression caused by the dislocated condyle
      • Direct the needle anteriorly and superiorly onto the inferior surface of the glenoid fossa
      • Inject ~2 mL of local anesthetic (we used lido 1% with epi)


Consider trying these methods first:

  • Gag technique: Elicit the gag reflex using a tongue blade or cotton swab. During the reflex, inhibition of the muscles of mouth closure permits the mandible to descend, which may free the condyle in some patients. Have suction handy in case of vomiting.
  • Syringe technique: Place a 5 or 10 mL syringe between the posterior upper and lower molars or gums on one of the affected sides. Have the patient gently bite down on the syringe while rolling it back and forth between the teeth until the dislocation on that side is reduced. The opposite side tends to reduce spontaneously. If this does not occur, place the syringe on the opposite side and try the same technique.
    • Note: this requires a high level of participation of the patient (i.e.: will not work in very young children)

If those fail…

  • “Classic Technique”/Intraoral reduction:

  • Have the patient sitting up, facing you, head against the back of the bed
  • Have your arms at the level of the mandible
  • Grasp the mandible with both hands
  • Rest your thumbs on the inside the mouth on the ridge of the mandible adjacent to the molars
  • Wrap thumbs in gauze (leave a trail of gauze outside of the mouth so that it can be easily removed)
  • Wrap your fingers around the outside of the jaw. You may place the thumbs on the occlusal surfaces of the teeth. If you do, keep your thumbs safe from being bitten by wrapping them in gauze
  • Have an assistant hold the head of the patient still.
  • Apply downward pressure to the mandible to free the condyles from the anterior aspect of the eminence, then guide the mandible posteriorly and superiorly back into the temporal fossae.


You are still having trouble with the reduction:

  • Rock the mandible back and forth to facilitate muscle fatigue
  • Have the patient open the mouth wider while attempting reduction, which will relax the masseter and temporalis muscles


Make a head-and-chin bandage after a successful reduction

  • Wrap gauze around the face so that the patient is unable to open their jaw widely while they are sedated/confused to avoid re-dislocation (see below)


Image from :

  • Other techniques: Wrist pivot, extraoral reduction, recumbent approach, posterior approach, and ipsilateral approach, which will not be discussed here.

After Discharge

  • Avoid extreme opening of the jaw for 3 weeks.
  • Support the lower jaw when yawning.
  • Soft diet, warm compress, NSAIDs, muscle relaxants.
  • Referral to ENT and/or oral surgery for possible future surgical fixation.

Thank you to Dr. Amir Yavari, Dr. Leslie Sowikowski, Dr. John Diune and the Samuels Sinclair Dental Center for their teaching and allowing us to use this footage. Thank you Dr. Gregory Lockhart, MD and Dr. Michael Prucha, MD for this interesting case. 



Faculty Reviewer: Gita Pensa

Resident Reviewer: Jonathan Ameli

Author: Chana Rich  


Please offer your own tips on TMJ dislocation reductions in the comments section!


Riviello, Ralph. Dislocation of the Mandible, Chapter 63, 1298-1341.e1 In: Roberts J, et al. Roberts & Hedges’ Clinical Procedures in Emergency Medicine. 6th Saunders; 2013.

Reyes Mendez, Donna. Reduction of temporomandibular joint (TMJ) dislocation. In: UpToDate, Post TW (Ed), UpToDate, Waltham, MA. (Accessed on November 17, 2015.)


Knee Dislocations: High risk, can’t miss!

By: Dr. Maddie Boyle


A 19-year-old male presents with left knee pain. He injured his knee yesterday while wrestling with friends and was seen in a local ED where his knee was reduced. He was discharged in a knee immobilizer and now returns with complaints of increasing pain and recurrent deformity after removing the immobilizer to shower.


Imaging demonstrates lateral tibiofemoral subluxation. He has a normal neurovascular exam, including strong distal pulses. Orthopedics is consulted and performs closed reduction of his knee. His ABI is subsequently measured at 0.92, and the knee is immobilized in 20° of flexion.


Image 1

Image 2


What would you do next?

(a) Call an emergency Vascular Surgery consult
(b) Admit for serial physical exams and ABI measurements
(c) Obtain a CTA of the lower extremity
(d) Discharge home in a knee immobilizer with outpatient Orthopedic follow-up
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ROCKSTARS: Ultrasound vs Chest X-ray in the Detection of Traumatic Pneumothorax

brownsound 2

Picture this…A 45 year old male is activated as a trauma after falling off 30 feet off scaffolding. He is flown from the scene and the report from the paramedics notes concern for spinal cord injury, as he has no sensation below the nipple line and flaccid extremities. On primary exam the resident notes diminished breath sounds on the right, however he asks the question to the rest of the trauma team: “are the decreased breath sounds from a pneumo/hemothorax or from a partially paralyzed/weakened diaphragm, in a patient with a high c-spine injury”. In a minute of clinical reasoning in an otherwise algorithmic setting, the resident challenges his clinical exam (inspection, palpation, auscultation) and places an ultrasound on the patient acquiring the following images:

Video: Lung point–the most specific sign for pneumothorax on thoracic ultrasound.

Lung Sliding

Image 1: M-mode of lung point showing both seashore and stratosphere

A chest tube is placed and the remainder of the trauma survey proceeds.

At our institution, we wait for a chest x-ray that shows no pneumothorax before sending a patient to the CT scanner. This is despite the studies that show the sensitivity of supine chest x-rays is 28 % to 75%.[i] This begs the question, would a bedside ultrasound be quicker and more sensitive to evaluate for a pneumothorax. A quick review of the literature says a definitive yes.

Three articles are at the core of the US for pneumothorax evidence. First in 2005, Blaivas et al published a paper that used EM attendings in a prospective single blinded trial to evaluate 176 patients for pneumothorax. They used 4 protocol views in each hemithorax (2nd intercostal mid clavicular, 4th intercostal ant. Axillary, 6th intercostal midaxillary and 6th intercostal post axillary) and evaluated only for lung sliding. No M-mode, no doppler. Their results were compared to the Trauma attending read of the supine CXR and the Radiologist’s view of the chest CT.

In this study: the sensitivity and specificity for thoracic US was :

Ultrasound (95% CI) CXR (95% CI)
Sensitivity 98.1% (89.9%-99.9%) 75.5% (61.7-86.2%)
Specificity 99.2% (95.6%-99.9%) 100% (97.1%-100%)

Wilkerson and Stone in 2009 published a meta-analysis of 4 trials including the Blaivas trial noted above. This meta-analysis looked at EM physicians as US operators in the analyses of pneumothorax or no pneumothorax in the setting of trauma. This study again found superior outcomes for thoracic ultrasound:

Ultrasound CXR
Sensitivity 86%-98% 28%-75%
Specificity 97%-100% 100%

Lastly in 2012, Hyacinthe et al. published a paper that aimed to assess the ability of thoracic ultrasound to detect, on arrival, the occurrence of common thoracic lesions in a cohort of chest trauma patients. This is likely the most relevant study as the methods consisted of a prospective observational cohort study where two separate EM physicians were used. First the physician taking care of the patient primarily used the Clinical Exam (Inspection, palpation, percussion and auscultation) and chest x-ray to determine the presence of pneumothorax. The physician performed their exam, looked at the supine chest x-ray then was asked to give the patient a score of how likely they are to have a thoracic lesion (0=no chance, 3=sure presence of lesion). A separate EM attending blinded to the initial exam and CXR then performed a thoracic ultrasound in both lung fields, including the upper, middle and lower parts of the anterior and lateral regions of both chest walls. Pneumothorax was defined as the absence of lung sliding or by the presence of lung point. The performing physician then, in a similar way, recorded their findings on a scale from 0-3. Results for this study included the sensitivity and specificity for each modality however, given the scales of probability entered by each physician, the more encompassing statistic is the area under the curve (AUC) for each modality.

Ultrasound CE+CXR
Sensitivity 53% 19%
Specificity 95% 100%
Area Under the Curve, mean (95% CI) 0.75 (0.67-0.83) 0.62 (0.54-0.70)

These articles make a strong case for the increased use of ultrasound in trauma. In the hands of an experienced user, a bilateral thoracic ultrasound takes 2-4 minutes, is arguably shorter than the time to call an x-ray tech, shoot the x-ray, develop the images and walk down the hall to view them, not to mention the test is overwhelmingly more sensitive.


[i] Gentry Wilkerson, R. and Stone, M. B. (2010), Sensitivity of Bedside Ultrasound and Supine Anteroposterior Chest Radiographs for the Identification of Pneumothorax After Blunt Trauma. Academic Emergency Medicine, 17: 11–17. doi: 10.1111/j.1553-2712.2009.00628.x

[ii]Blaivas, M., Lyon, M. and Duggal, S. (2005), A Prospective Comparison of Supine Chest Radiography and Bedside Ultrasound for the Diagnosis of Traumatic Pneumothorax. Academic Emergency Medicine, 12: 844–849. doi: 10.1197/j.aem.2005.05.005

[iii]Hyacinthe AC, Broux C, Francony G, et al. Diagnostic accuracy of ultrasonography in the acute assessment of common thoracic lesions after trauma.Chest. 2012;141(5):1177–83


CITW 9: The Racing Heart

Welcome back to another Clinical Image of the Week from the case files of the Brown EM Residency!

HPI: A 60 year old female presents with palpitations after walking on the beach with friends. She states she was sitting at her favorite clam shack, and felt the onset of a “rapid heart rate”. Thinking she was dehydrated, she drank some water, and her palpitations resolved after five minutes. After returning home, the palpitations recurred, and after 40 minutes she felt “really tired, really washed out”, but at no point had any chest pain, dyspnea, or lightheadedness. She looked “gray” to her husband, so he called 911.

Vitals: BP 160/110, HR 210, T 98.7 °F, RR 22, SpO2 99% on RA

Notable PE: Pale and anxious appearing. On auscultation, tachycardic without murmur, rub, or gallop. Regular rhythm. Intact and equal pulses throughout. Mild increased work of breathing. Lungs are clear bilaterally. No lower extremity edema.

The following EKG was obtained:

BeforeWhat’s the diagnosis?

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Procedural Blog EXTRA: Inferior Alveolar Nerve Block


A blog series on emergency medicine procedures

Video and idea proposed by the brilliant Dr. Michael Prucha

  • Dental pain control
Location of Numbing:
  • Ipsilateral teeth along the mandible, as well as the lower lip and chin (mental nerve is distal to inferior alveolar nerve)
  • 50/50 mixture: 1-2% lidocaine with epinephrine + 0.5% bupivacaine (lasts up to 6 hours)
  • Syringe with 25-27 g needle
  • Consider topical anesthesia on gauze or as viscous gel prior to injection
  • Patient seated upright, back of head against stretcher, mandible parallel to floor
  • Position yourself opposite side of target nerve
  • HAND #1: thumb in cheek (not in between the teeth…ouch!), palpate RETROMOLAR FOSSA and find CORONOID NOTCH (image A), visualize the PTERYGOMANDIBULAR TRIANGLE (image C)
  • HAND #2: syringe between first and second premolars on opposite side, enter space until mandibular bone is felt, pull back small amount (and check for aspiration of blood) (complication note: if no bone is felt, you increase your chances of injecting into the parotid gland, i.e.: facial nerve…a temporary facial nerve palsy may occur)
  • Inject (image B)
  • Patient may jump/jerk. BE PREPARED.
  • ~2ml or double amount if needed
  • Wait 3-5 minutes for anesthetic to work



Images from Roberts and Hedges’ Clinical Procedures in Emergency Medicine, 6th ed, 2013

Thank you to Dr. Fearon and the Samuels Sinclair Dental Center for allowing us to use this footage. 
Please offer your own tips on head and neck nerve blocks in the comments section!

Textbook References

Amsterdam JT, Kilgore KP. Regional Anesthesia of the Head and Neck. Chapter 30, 541-553.e1. In: Roberts J, et al. Roberts & Hedges’ Clinical Procedures in Emergency Medicine. 6th Saunders; 2013.

Jonathan Ameli MD

Infections bite! Antibiotic prophylaxis for mammalian bites

This is part of a recurring series examining landmark articles in Emergency Medicine, in the style of ALiEM’s 52 Articles.

Discussing:  Medeiros, I, and H Saconato. “Antibiotic prophylaxis for mammalian bites.”  Cochrane database of systematic reviews Online 2 (2001) : CD001738.

Main Points:

  1. The use of antibiotic prophylaxis for hand bites reduces infections
  1. There is weak evidence supporting the use of antibiotic prophylaxis after human bites to reduce infections (based on one study)


Mammalian bites account for up to 1% of all ED visits and administration of prophylactic antibiotics is based on studies with insufficient power to determine true efficacy. In order to gather enough cases to sufficiently power a study, The Cochrane Collaboration did a meta-analysis of randomized trials considering the value of antibiotic prophylaxis in human and other mammalian bites. The goal of this analysis was to determine if the use of antibiotics in mammalian bites is effective in preventing bite wound infection.

Eligible studies were searched and retrieved based on inclusion criteria (see details) by two reviewers. Relevant data to answer the study question were extracted, risk of bias was assessed for included studies, and subgroup analysis was performed based on intention to treat of the eight final studies chosen.

For dog bites, there was no statistically significant reduction in infection rate after prophylactic antibiotics (4% (10/225)) versus control (5.5% (13/238)). Only one trial analyzed human bites and the infection rate was significantly lower in the antibiotic group (0/33) versus the control group (47% (7/15)) (OR 0.02, 95% CI 0.00 to 0.33). The infection rates for hand bites were significantly reduced by antibiotic administration (2% vs. 28% in control group) (OR 0.10, 95% CI0.01 to 0.86, NNT=4, 95% CI 2 to 50). There appeared to be no significant difference in infection rate with antibiotic prophylaxis for cat bites, when separating out wound type (laceration vs. puncture), or for bites on body parts other than the hand.

Pitfalls of this meta-analysis:

  1. The antibiotics chosen for prophylaxis were not consistent across studies, and no more than two studies used the same antibiotic. In some studies, the antibiotic used was inappropriate for coverage of mixed anaerobes and aerobes, which is common in many mammalian infections.
  2. The predominance of included patients suffered dog bites (463/522) compared to cats (11/522) or humans (48/522), so the results are skewed heavily toward one species of bite.
  3. Only five studies reported LTFU and three of these had rates over ten percent. Four studies did not even include LTFU numbers, and an intention to treat analysis could not be performed in these. This may bias the results toward no effect since those who did not go on to have an infection would likely not return to the ED.
  4. Only 25% of the studies used double-blinded methods with a placebo of identical appearance.


This was a meta-analysis study, with the following inclusion criteria:

  1. Study type: RCTs or quasi-RCTs
  2. Participants: patients with mammalian bites (including humans) if they presented within 24 hours and had no clinical signs of infection.
  3. Interventions: use of antibiotics within 24 hours of injury compared to placebo/no-intervention.
  4. Outcomes measured: proven bacterial infection (clinical signs of infection plus positive culture), presumed infection (clinical signs of infection with negative culture) or absence of infection (no clinical signs).

Nine studies met all inclusion criteria but one study did not separate infection rates for each mammalian species.

Level of evidence:

ACEP Level I for Meta-analysis

Source article: Medeiros, I, and H Saconato. “Antibiotic prophylaxis for mammalian bites.” Cochrane database of systematic reviews Online 2 (2001) : CD001738.


The Neonate in Shock: When to think CARDIAC

Clinical Case:

2-week-old male with history of “funny breathing” since birth presents to ED with 1 day of decreased feeding, now with 30 second apneic and cyanotic episode at home tonight.

Sternal_retractions-3** Neonates in shock MAY show obvious signs/sx of end-organ dysfunction (similar to adults), but their presentation may be subtle and progress rapidly!**

 Signs/Symptoms of Shock in Neonate:

  • History
    • Poor feeding
    • Respiratory distress (tachypnea, cyanotic/apneic episode)
    • Altered mental status (irritability, difficulty awakening)
  • Physical Exam
    • Tachycardia
    • Tachypnea
    • Hypotension
    • Poor Perfusion: Decreased capillary refill, mottled skin

Differential Diagnosis:

Think of “THE MISFITS” to recall critical diagnoses in the neonate in shock:

T –       Trauma (accidental and non-accidental)
H –       Heart disease and Hypovolemia
E –       Endocrine (congenital adrenal hyperplasia, hypothyroid, etc)
M –      Metabolic
I –        Inborn errors of metabolism
S –       Sepsis
F –      Feeding problems, Formula mishaps (under- or over-dilution)
I –        Intestinal catastrophes (NEC, volvulus, etc)
T –       Toxins
S –       Seizures

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