Facial Edema

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This was an interesting presentation from a Peds shift.

15 y/o AAM with no significant medical history who presents with facial swelling. Patient noticed significant swelling to the left side of his face upon awakening in the morning. The swelling involved his entire left cheek, inferior lid of his left eye, upper lip and part of his right cheek. The patient denies any pain, tongue swelling, voice change, difficulty breathing or swallowing, fevers, recent ill symptoms (cough, congestion, vomiting, diarrhea), dysuria, hematuria, rectal bleeding, sore throat, ear complaints. He denies any new exposures including new medications, new soaps, detergents, animal exposures, environmental exposures, recent travel, insect bites.

PMH:none. PShx: had 4 wisdom teeth removal 1 month prior (finished antibiotics), no other recent surgeries or dental work. No EtOH, drugs. No current medications. No known allergies.

Vitals: 97.8, 90, 110/70, 18, 99 % on RA

Exam: HEENT- moderate swelling of the left buccal area, inferior lid of the left eye, upper lip. Mild swelling to the right buccal area. No erythema or palpable areas of fluctuance. No swelling surrounding the right eye. No conjunctival injection. No erythema within the ears, TMs normal. No mastoid tenderness. No lingual swelling, no erythema within the mouth or palpable areas of fluctuance. No signs of infection from previously removed wisdom teeth. No posterior oropharyngeal swelling or uvular deviation. No lymphadenopathy.

Heart- normal. Lungs- clear, no wheezing or stridor. Abdomen- normal. No CVA tenderness.

Treatment started with Benadryl for possible allergic reaction. Basic labs obtained and urine for possible nephrotic syndrome. WBC-17, otherwise normal. Urine with 200 protein, no RBC or WBC- nephrology consulted and recommended repeat POC labs as outpatient and follow-up in clinic, but no intervention at this time. Patient had mild improvement with Benadryl. Discharged home with Benadryl and steroids.

Patient re-presents 6 hours later (just came back for my shift the next day)

Facial swelling has worsened. Now involves bilateral buccal areas, bilateral lower eyelids and upper lip. No fevers, no difficulty breathing, no dysphagia. Patient had taken 1 repeat dose of Benadryl at home and had not started steroids yet. No other changes in HPI except patient mentions some bleeding from the inside of his upper lip. Upon exam, patient has some bleeding and purulent drainage from the gumline of his left central incisor. No palpable fluctuance, but able to express drainage with pressure to upper lip.

Labs obtained: WBC 17, CRP 1.6, ESR 41. UA- minimal protein. All other labs unremarkable. CT face with contrast obtained showing left central incisor periapical abscess with cortical erosion as well as extensive cellulitis of the midface. Also some concern for phlegmon within the paranasal sinus. ENT, OMFS, and finally pediatric dentistry consulted. Patient admitted for IV clindamycin, Unasyn for cellulitis and dentistry consult for possible root canal versus tooth extraction.

Bottom line: Odontogenic infections can cause orofacial infections and rarely but more importantly peripharyngeal space infections as well as jaw osteomyelitis. If concerned about deep facial infection, CT face is warranted. Treatment includes draining of pus from abscesses (either through I&D or needle aspiration) and culture as well as antibiotic therapy. Common regimens include a penicillin plus metronidazole, clindamycin, augmentin, or unasyn depending on disposition. Dentistry should be involved whether through consult or outpatient follow-up for root canal versus tooth extraction.

“Knot in my Throat”

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Recently had a patient while on a Peds EM shift with an interesting presentation. Not sure how many of us have had this case, so this should serve as a helpful reminder for management.

 

15yF with no significant PMHx presenting with a “knot in my throat.” Per patient report, she woke up the morning of presenting to the ED with a palpable knot. Unsure how long it had been present, but she happened to notice it that morning. Denies hx of fever, chills, changes in energy level, palpitations, shortness of breath, odonyphagia, dysphagia, changes in menstrual cycle, recent URI, changes in hair or nail quality nor irradiation to the neck. Mother was really concerned because 2 people in her family had either thyroid carcinoma or nodules removed. One was diagnosed in her 20s.

 

On physical exam:
General: AFVSS
HEENT: NCAT, EOMI, PERRLA, no evidence of exophthalmos
Neck: Supple, Trachea midline, R anterio-lateral neck mass – approx 1.5cm x 2cm. Firm to palpation and located anatomically near superior pole of R thyroid lobe. Moves with swallowing. No associated erythema or fluctuance. No cervical lymphadenopathy.
Lungs: CTAB,
CVS: RRR, no m/r/g. Pulses equal. No peripheral edema.

 

So you get labs: CBC,TSH, Free T4
All within normal limits

 

Beside USN revealed what appeared to a multicystic nodule in the R thyroid lobe where the patient’s palpable mass was located. So let’s get a formal USN.

 

Formal reveals that patient actually has multiple nodules. The largest being approx 3cm x 2cm x 2cm, and read as a colloid nodule.

Let’s recap:

We have a 15yF presenting with an asymptomatic thyroid nodule, who is euthyroid based on hx, physical exam, and labs. What’s next??

 

1. Discuss the case with a Pediatric Endocrinologist. Nothing acutely needs to be done; however, she should have outpatient followup with an endocrinologist to help keep surveillance of her nodules.

 

2. Add testing for Thyroid specific antibodies to rule out Hashimoto’s thyroiditis and other autoimmune inflammatory processes. Consider adding Anti thyroid peroxidase (Anti-TPO) and Anti-Thyroglobulin antibodies.

 

3. Ultrasound simply characterizes the mass that we’ve palpated. Yes, the nodule was read as a “colloid nodule,” which is fairly common regarding thyroid nodules; however, this needs to be confirmed by Cytopathology. Nuclear studies can be done but not recommended in isolation. Such studies can be helpful when determining whether a nodule is “hot” or “cold.” Simply speaking, is there increased thyroid uptake or not. CT and MRI imaging is not cost effective in the initial stages of evaluation.

 

4. Lastly, the best way to determine whether a nodule is benign or malignant, you have to sample the source via Fine Needle Aspiration Biopsy (FNAB). Await the cytopathology results and return to #1.

Cervical seatbelt sign and CTA

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Summary: No CTA for isolated cervical seatbelt sign.

Good blog post.
http://wueverydayebm.blogspot.com/2014/07/does-cervical-seatbelt-sign-mandate.html
Take Home:
CT-angiogram is not necessarily indicated based on the finding of a cervical seatbelt sign alone in the absence of significant hematoma, neurologic symptoms, or other traumatic injuries.

EAST Guideline:
https://www.east.org/education/practice-management-guidelines/blunt-cerebrovascular-injury
What patients are of high enough risk, so that diagnostic evaluation should be pursued for the screening and diagnosis of BCVI?
1. Patients presenting with any neurologic abnormality that is unexplained by a diagnosed injury should be evaluated for BCVI.
2. Blunt trauma patients presenting with epistaxis from a suspected arterial source after trauma should be evaluated for BCVI.
3. Asymptomatic patients with significant blunt head trauma as defined below are at significantly increased risk for BCVI and screening should be considered. Risk factors are as follows:
* Glasgow Coma Scale score ≤8;
* Petrous bone fracture;
* Diffuse axonal injury;
* Cervical spine fracture particularly those with (i) fracture of C1 to C3 and (ii) fracture through the foramen transversarium;
* Cervical spine fracture with subluxation or rotational component; and
* Lefort II or III facial fractures

From EAST Guideline:
An isolated cervical seat belt sign without other risk factors and normal physical examination has failed to be identified as an independent risk factor in two retrospective studies and should not be used as the sole criteria to stratify patients for screening.
References:
https://www.ncbi.nlm.nih.gov/pubmed/12013287
https://www.ncbi.nlm.nih.gov/pubmed/12013287

Alternate Screening Guidelines:

Screening Criteria for BCVI adapted from Biffl et al[10] (with permission)
Screening Criteria for BCVIInjury mechanism

  • Severe cervical hyperextension/rotation or hyperflexion, particularly if associated with
    • Displaced midface or complex mandibular fracture
    • Closed head injury consistent with diffuse axonal injury
  • Near hanging resulting in anoxic brain injury Physical signs
  • Seat belt abrasion or other soft tissue injury of the anterior neck resulting in significant swelling or altered mental status

Fracture in proximity to internal carotid or vertebral artery

  • Basilar skull fracture involving the carotid canal
  • Cervical vertebral body fracture
Denver Modification of Screening Criteria for BCVI adapted from Cothren et al[51] (with permission)
Denver Modification of Screening CriteriaSigns/symptoms of BCVI

  • Arterial hemorrhage
  • Cervical bruit
  • Expanding cervical hematoma
  • Focal neurological deficit
  • Neurologic examination incongruous with CAT scan findings
  • Ischemic stroke on secondary CAT scan

Risk factors for BCVI

  • High-energy transfer mechanism with
    • Lefort II or III fracture
    • Cervical spine fracture patterns: subluxation, fractures extending into the transverse foramen, fractures of C1-C3
    • Basilar skull fracture with carotid canal involvement
    • Diffuse axonal injury with GCS =6
    • Near hanging with anoxic brain injury

Decreased Survival with Intubation During Cardiac Arrest

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Quick Read on something I feel like comes up a lot with our cardiac arrest patients. They don’t typically need intubated, they need good CPR. Bag or put an LMA in and stop at that. While the numbers aren’t astounding, given the differences in such a large amount of patients think these make sense.

http://www.healio.com/cardiology/arrhythmia-disorders/news/online/%7B5396b1a2-0167-4a2d-885c-0e1bc527398e%7D/findings-do-not-support-early-tracheal-intubation-for-in-hospital-cardiac-arrest-in-adults

Top Ten UTI Myths

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Good 5-10 minute read on myths regarding UTI and asymptomatic bacteriuria. Hope you’ll take a look as this is a common problem in many EDs, not just ours with regards to over-diagnosis and over-treatment.
http://www.medscape.com/viewarticle/865175
Ross

Abandon the BVM?

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Excellent 1 pager from Dr Levitan in the new ACEP now newspaper.

I have been trying to get the residents to implement the nasal cannula, and to a lesser extent the LMA, for years. Pearl: nasal cannula plus mandible traction opens the nasopharynx and allows oxygen to diffuse to the alveoli (due to gradient made by hemoglobin absorbing oxygen). This is apnea oxygenation, increased safe apnea time. See the pure gold article by Levitan/Weingart, apparently 4th most read annals of EM article.

Add the cannula and mandible thrust to a properly positioned patient, ear to sternal notch or even well above sternal notch, and you will be amazed how long it takes to desat. OOPS (Oxygen On, Pull the mandible, Sit the patient up.

Read this brief article a few times and change how you practice.

Level 1 Rapid Infuser & Autotransfusion

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All,
Couple videos on what was covered today with Level 1 Infuser and Autotransfusion. They’re not bad, definitely get the overall setup at least. With the autotransfusion videos, there are a few small differences in their setup vs ours I think, but overall for your purposes is mostly the same. Hope this helps.
Ross

Level 1 Infuser
https://www.youtube.com/watch?v=9YIROsYE_Yo

Autotransfusion
https://www.youtube.com/watch?v=WmLs-43jaR4

How Evidence Based Are We?

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Here is a pretty comical article by Dr Ioannidis. If you do not know who this is stop now and read this.

This article was just published. It is written as a report to the father of evidence based medicine, Dr David Sackett. It takes a not terribly optimistic view of the current state of medical research. He calls out industry bias, ghost authorship, and many other flaws of our system. We are very lucky to have people like Dr Ioannidis ensuring integrity to the research process.

QTc

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Yesterday I had a 21 yo female come in by BLS crew, tachycardic with a GCS of 3, spontaneously breathing with equal and reactive pupils bilaterally at ~ 6mm, with vomitus around her airway.  She was found down at home after her significant other called EMS due to concern that she was going to attempt suicide.  Report received that she was found with multiple empty pill bottles nearby.  No response to Narcan either in the field or in Room 9.

Here is her ECG: Calculated QTc (automated) is 401 ms, rate is 143.   The accepted normal value for QTc is: below 450ms for men and below 460ms for women.  The 99th percentile of normal: 470ms (men) and 480 ms (women).

ecg_case_micu

Just how does the computer calculate this?

By using the Bazett formula: QTc = QT / sqrt( R-R interval in seconds)

This means of course that if our rate is 60 BPM, then our R-R interval would be 1000ms, (or 1 second), and thus our QTc = QT/sqrt(1); and therefore in this situation QTc equals QT.

In our particular case: the R to R interval is 10.5 boxes (thus 420 ms, or in seconds: 0.420).  The QT was autocalculated at 260 ms, and when using the Bazett equation, this gives us a QTc of 401 ms.

What if you cannot rely on the computer calculated QT (which certainly can be inaccurate)? Then calculate the QT yourself by finding the tangential intersection of the T wave downslope with the ECG baseline, and measuring the intersection distance from the start of the QRS.  See the diagram below:

qt_picture

Using this measurement principal, and (in our case) using the lead V2 where the p wave and T wave are 180 degrees out of phase, we obtain a QT ranging from 8-9 boxes (320-360 ms).  When using the Bazett, this gives us a calculated QTc of 493-555. Of course qualitatively we can tell the QTc seems long as it exceeds half the R-R interval, quantitatively this is an increased QTc of 38% from the auto calculated, and is certainly in the significantly prolonged QTc range.

Follow-up: TCAs and benzos positive on her drug screen.  She was started on a bicarb drip in the ED (placed 3 amps of bicarb in a bag of D5); pH 7.34, lactic acid 1.2.  She is supposedly on Flexeril (similar in structure to TCA and will light up as TCAs on the drug screen), treated the same, however appears to be less cardiogenic in toxicity:J Emerg Med 1995;13(6):781-5.  Pt is intubated and stable currently.

Click here for the EMCrit on TCAs (overview below):

  1. Bicarb drip:  Goals: QRS duration <100, hemodynamically stable, Na ~150, pH ~7.5.  Sodium and bicarb don’t rise significantly in severe toxicity, her repeat showed no change in either.
  2. Magnesium: may help, though risk of Torsades is low as long as the patient remains tachycardic.
  3. Lidocaine: even though lidocaine is another Na-Channel Blocker, it will antagonize the effects of the TCA-like medications.
  4. Watch the electrolytes (decreases expected in both K+ and Ca+):  Lytes and ABG Q1H; (My pt’s Ca+ dropped from 9.8->8.5 over 4 hours).
  5. Intubation: hyperventilate to ensure no hypercapnia (want alkalosis).  Sedate with versed or propofol to raise seizure threshold.
  6. ECMO: If everything else fails.

Can you give Vasopressors through a PIV?

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I looked back and couldn’t find a post about this topic in the last year or so but forgive me if it has already been posted. I have been following R.E.B.E.L. EM for a few months now  and I would recommend it to everyone who has the time and wants quick summaries on the latest EM literature.  They have short written summaries of papers including pros/cons of the study and what they feel are the most important take away points. It was founded by Salim Rezaie with Rob Rogers, Matt Astin and Anand Swaminatham serving as editors.

Occasionally they will have a “mythbuster” post looking at common myths in the ED and the most uptodate literature available on the topic. (their latest mythbust is on “safe” glucose levels before ED discharge but I digress)

 

Back in May they reviewed the safety of vasopressors through a PIV. The topic paper was titled “A systematic review of extravasation and local tissue injury from administration of vasopressors through peripheral intravenous catheters and central venous catheters”

What the review found was very interesting: of 318 events, 204 results in local tissue damage, 114 were only extravasation events and 7 events involved the use of a CVC (so clearly not completely safe). Interesting, of the 204 local tissue events 85.3% involved PIV distal to the antecubital fossa and 96.8% involved administration of >4hrs.

REBEL EM’s take away points were:

In critically ill patients, with hemodynamic instability, vasopressor infusion through a proximal PIV (antecubital fossa or external jugular vein), for <4hours of duration is unlikely to result in tissue injury and will reduce the time it takes to achieve hemodynamic stability.

What I feel like this means for us is simple: If you have a crashing, hypotensive patient who needs a pressor without a CVC but good proximal PIVs, start the pressor immediately, stabilize the patient as best you can, then take the time to properly place a CVC.

Continue to monitor the PIV until it can be switch to the CVC and stop the pressor immediately if there is any suspicion for local extravasation. I am sure this will make some people nervous but I think this is better then placing a “crash line” that is less then sterile which will expose an already ill patient to infection or other complications secondary to a hastily placed CVC.

I highly recommend read their review and how they came to this conclusion along with their other posts. I have included the link to this study at the bottom.

http://rebelem.com/mythbuster-administration-of-vasopressors-through-peripheral-intravenous-access/