Last week we had an ENT sim, lead by our always helpful ENT colleagues, focusing on 4 ENT emergencies we should all be familiar with:

1. Epistaxis
2. Auricular hematoma
3. Peritonsillar abscess
4. Cricothyrotomy

Epistaxis

While about 60% of the population will experience epistaxis, less than 10% will seek medical attention.

When it comes to epistaxis, it is important to fist understand the anatomy. The majority of nosebleeds will be anterior bleeds, meaning bleeding from the anterior portion of the septum, in a watershed area called Little’s area or Keisselbach’s plexus, supplied by branches of the ethmoidal artery, sphenopalatine artery and superior labial branch of the facial artery.

The first thing you want to ask yourself when it comes to epistaxis is: is this a life-threatening bleed? Usually, in the absence of trauma or recent surgery (le Forte procedures, etc.), the answer is no. When you have determined that the epistaxis is not life threatening, you can take a stepwise approach to controlling the bleeding.

First you want to start with the basics: holding pressure. This may seem straightforward, but you need to make sure to educate your patients on the proper way to hold pressure. Have your patient first blow their nose, to remove any clot burden. You can then use Afrin (oxymetazoline, a vasoconstrictor) spray in the nare. Then firm pressure must be applied with the alae held tightly against the septum. A good trick is to tell the patient “hold your nose as if there were a bad smell in the room”. Pressure must be constant for at least 10-15 minutes.

Some common mistakes:

• Holding pressure over the nasal bones (no pressure is actually applied against the septum)
• Letting up pressure every couple minutes to “see if it stopped”

If bleeding is persistent, you can try to control the bleeding with chemical cautery, silver nitrate. You must first ensure that you have a good view of the source of the bleeding using a nasal speculum and adequate lighting. After the septum has been anesthetized with 4% lidocaine or lidocaine with epi, you should apply the tip of the silver nitrate stick to a small area surrounding the source of the bleeding, beginning at the periphery and working your way towards the center of the bleeding. You should take caution to avoid cauterizing large areas and remove excess silver nitrate with a cotton swab when finished. You should never cauterize both sides of the septum as you are putting the patient at risk for tissue necrosis, septum ulceration and perforation.

If cautery is unsuccessful or if you cannot visualize the source of the bleeding, you can use nasal packing to tamponade the bleeding. At Rush, we have two types of nasal packing, the rhino rocket (nasal tampon) and the rapid rhino (nasal balloon catheter). As before, when using either of these, you should make sure the patient blows their nose and the nare is pre-treated with a vsoconstrictor (afrin).

The Rhino Rocket is a nasal tampon that is easy to use and effective. The rhino rocket is inserted by sliding the tampon along the floor of the nasal cavity until the entire tampon lies within the nasal cavity. The tampon will then absorb any moisture or bleeding and expand to cause tamponade.

The Rapid Rhino is a nasal balloon catheter coated in a carboxymethylated cellulose mesh. This catheter must be soaked in sterile water (NOT saline) for 30 seconds prior to insertion, making it slick and easier to insert. The balloon must then be inflated with 20cc of air, NOT water or saline as they can cause too much pressure on the tissues and lead to tissue necrosis.

If bleeding stops with with of these forms of nasal packing and the patient is stable with normal vitals, they can be safely discharged with close ENT follow up within 24-48 hours and strict return precautions if bleeding recurs. If nasal packing is prolonged (>72 hours), patients are at increased risk of complications, including necrosis, toxic shock syndrome, sinus infections and dislodgement.

It a patient has a posterior bleed or a life threatening bleed, you can try to tamponade the bleeding with a device such as the Epistat, with both anterior and posterior balloons. This device should be inserted similarly to the other devices mentiones abo

ve. The posterior balloon should be inflated first, with 5-10cc of air, and then pulled forward until snug. The anterior balloon should then be inflated with 30cc of air. If an epistat is not available, similar results can be achieved using a foley catheter.

Any posterior or life threatening bleeding should have an emergent ENT consult and any patients with posterior packing should be placed in the ICU for monitoring due to the risk of recurrent bleeding resulting in significant blood loss, apnea and hypoxia. There is a postulated nasopulmonary reflex causing changes in pulmonary function secondary to posterior nasal packing, although evidence on this is somewhat controversial.

Auricular hematomas

 An auricular hematoma is a collection of blood between the cartilage and pericondrium of the outer ear, usually caused by blunt trauma. Hematoma formation in this tight space disrupts the blood supply to the cartilage and can lead to necrosis and infection of the cartilage, followed by fibrosis and scarring of the ear leading to cosmetic deformity known as cauliflower ear.

To prevent this complication, auricular hematomas must be drained promptly and the perichondrial layer must be re-apposed to the cartialage to restore blood flow to the cartilage. To do this, the following steps must be taken:

1. Clean the ear with antiseptic
2. Apply local anesthetic or perform an auricular block
3. Incise the hematoma along the curvature of the auricle (for best cosmetic purposes) and completely evaluacte the hematoma and any clots that may have formed
4. Irrigate the pocket copiously with sterile saline
5. Suture the incision closed with a boster on either side of the auricle to reduce the dead space and prevent reaccumulation of blood or fluid. It is important that the bolster is tight enough to hold the tissues together without being too tight and causing additional pressure on the cartilage.

Typically, a dental roll can be used as a bolster (see our sim models). If no dental rolls are available, xeroform gauze is a good alternative. Patients should have follow up with ENT or a plastic surgeon 24-48 hours after drainage of auricular hematomas and patients are generally discharged on a 7-10 day course of antibiotics against staph aureus and pseudomoanas. Bolsters are typically removed after 7 days.

Peritonsillar abscess

A peritonsillar abscess (PTA) is a collection of pus located between the capsule of the palatine tonsil and pharyngeal muscles. This generally occurs in the superior pole of the tonsil and is usually preceded by tonsillitis or pharyngitis that progresses from cellulitis to abscess formation. PTA is the most common deep neck infection in children and adolescents.

Patients usually present with sore throat, fever, “hot potato” or muffled voice, and trismus. On exam you will see an extremely swollen tonsil/posterior soft palate with fluctuance and deviation of the uvula to the opposite side. Bilateral PTAs are rare. Intraoral or submandibular ultrasonography can be used to confirm PTA with good sensitivity (89-100%), however this is user dependent and often can not be used to guide your needle for aspiration given limited intraoral space, especially in a patient with trismus.

If a PTA is large enough to cause impending airway compromise or the patient has significant comorbidities or is immunocompromised, etc, it is good to get ENT involved early for prompt surgical intervention. If the patient is stable, you can attempt aspiration or incision and drainage in the ED.

The following steps should be taken for aspiration or drainage of the PTA:

• Apply anesthetic: topical anesthetic spray, along with 1-2mL of lidocaine with epi into the anterior tonsillar pillar
• If aspirating:
  • Cut the distal tip off the needle sheath of an 18 gauge needle to expose only 1cm of the needle to avoid inserting your needle too deep (carotid injury is always a concern, although rare)
  • Aspirate with 18 gauge needle (good rule is to start superior, may need to do additional aspiration inferiorly)
• If incising and draining:
  • Use an 11 or 15 blade scalpel
  • You can similarly cut the distal tip of the blade sheath to avoid incising too deep (do not penetrate more than 1cm)
  • Make a horizontal and a vertical incision to allow adequate space for drainage of pus

Some helpful tips:

• Have the patient hold the suction themselves and apply as needed
• You can use a laryngoscope in place of a tongue blade, that gives the added benefit of an additional light source

Once the PTA is adequately aspirated or drained, the patient should be placed on antibiotics. PTAs are usually polymicrobial, and you should cover for streptococcus species, anaerobes, Eikenella and H. influenza. First line is generally Augmentin 875mg po BID x 7-10d. If pt is requiring admission for IV antibiotics, you can start with Unasyn. Steroids may additionally be given to decrease he duration and severity of pain, generally methylprednisolone 125mg IV x 1 or dexamethasone 10mg PO/IM x1.

Patients with stable vitals and no concern for airway compromise can be safely discharged from the ER. If it is a first time PTA in an otherwise healthy patient, you can have them follow up with ENT only as needed. If your patient has a recurrent PTA, recurrent tonsillitis or other complicating factor, encourage prompt follow up with ENT.

Crichothyrotomy

For our last ENT emergency sim station, we practiced cricothyrotomies. We all know the indication for an emergency cricothyrotomy: can’t intubate, can’t ventilate. Instead of boring you with the details of the procedure, here is a link to a video of the procedure taught by Scott Weingart:

https://vimeo.com/123573243

It is important to note that needle cricothyrotomies (transtracheal ventilation using a 14 gauge needle) are preferred in children less than 10 years of age due to the difference in their airway anatomy. This is due to the fact that the airway of a child is funnel-shaped, with the narrowest part at the cricoid ring rather than at the vocal cords. This increases the risk for developing subglottic stenosis following a cricothyrotomy.

Big thanks to Dr Schiebler who came to conference to drop radiologic-knowledge bombs on us. This lecture was loaded with tons of information; here are some of the big take-aways!

Gimme a differential diagnosis for this CXR:

See the little white spots everywhere? That should make you think Miliary Tuberculosis (milliary like millet seeds) , histoplasmosis, or thyroid cancer.

This one was Miliary TB, how do you know? Look for other signs of hematogenously spread TB like: Pott’s disease, tubercular chorioretinitis, skin lesions, pulmonary cavitary nodules.** I’d google image all of these to get a better idea of the variety of presentations. 25% of the world has tuberculosis, it is spread by droplets and even as the spit dries the little guys can keep living. By these little guys I mean these:

Changing course; here is the brain:

Refresher course, if I say this is a FLAIR MRI scan, you perk up and know that this means the CSF if dark (like a T1) but abnormalities are bright (like a T2.) This particular finding is called the “parenthesis sign.” See em? This is pathognomonic for Infectious Encephalitis. Now we don’t get a lot of infectious encephalitis around these here parts seeing as Chicago is cold enough that the wind feels like it wants to steal your kidneys BUT these are common elsewhere and may be increasingly more American as we warm up the globe with pollution. If you see parenthesis sign think possible Malaria, dengue, eastern equine, West Nile, etc.

Lastly, this image of the LAD is pertinent for calcifications.

Calcifications may or may not be normal depending on age, sex and race. If you are an old white dude you have a 50% likelihood of having calcifications, go you! So use the MESA calculator to see if your patient should have calcifications in general or if this is an unexpected finding. To quote Dr. Schiebler, calcium deposits are “the single most important predictor of future cardiac deaths.” How? Well it can be a marker for a lipid plaque (not visible on CT.) Lipid plaques are way scarier than calcium because they can get mad and shoot off from the wall and clot the artery AT ANY TIME.  Women are way more likely to have lipid plaques than calcium so if you see calcium on a woman, especially one with a low MESA calculated score -then they are likely to have lipid plaques as well and should undergo further work up.

Again – Big thanks to our radiology friends who do this for us and big thanks again for helping us learn some image magic!

This week’s 5-minute Journal Article discussion covered

“Validation of a Clinical Prediction Rule for the Differentiation Between Septic Arthritis and Transient Synovitis of the Hip in Children” by Kocher et al.

Why is it important to differentiate between septic arthritis and transient synovitis in pediatric patients? Because both diseases can present similarly with acute onset of pain, fever, limp or inability to bear weight and patients holding their hip in the flexed, abducted, externally rotated (FABER) position. The difference is transient synovitis is exactly that, transient, while septic arthritis can lead to permanent joint damage and disability if not treated aggressively with surgical intervention and IV antibiotics.

This study’s goal was to validate the four independent predictors of septic arthritis of the hip in children that Kocher described in his original study, published in 1999 in the Journal of Bone and Joint Surgery, when tested in a new population. The four independent predictors, known as the “Kocher criteria” are:

1. Fever with temp >38.5C in the past week
2. Inability to bear weight
3. Serum WBC > 12,000 cells/mm3
4. ESR >40mm/hr

According to Kocher’s orginal study, if all 4 of these variables were present, the predicted probability of septic arthritis was as high as 99.6%.

This validation study ultimately enrolled 213 patients with acutely irritable hip at Boston Children’s hospital, a large tertiary care children’s hospital, between the years of 1997 and 2002. Of the 213 patients, 24 were diagnosed with true septic arthritis (joint fluid with >50,000 wbcs + positive cultures), 27 with presumed septic arthritis (joint fluid with >50,000 wbcs with negative cultures) and 103 with transient synovitis (< 50,000 wbcs in joint fluid, negative cultures, resolution of symptoms without antibiotics and no further disease progression), and 59 were excluded for various reasons.

The diagnostic performance of the prediction rule was analyzed using a Receiver Operating Characteristic Curve and compared to the original study. The area under the curve for the original study was 0.96, whereas the area under the curve for the validation study was 0.86. The authors argued that this diminished performance was expected in this new population as most clinical prediction rules are optimized towards the original study population. However, an area under the curve of 0.86 still shows very good diagnostic performance for a predictive test and because of this, many EM physicians and orthopedic surgeons still use the “Kocher criteria” for septic arthritis today.

•••

Interestingly, the Kocher criteria does not include CRP as at the time of the study, Boston Children’s Hospital could only test CRP weekly so only about 40% of the participants of the validation study had a documented CRP. Today, it is common to use CRP in addition to serum WBC and ESR when working up a patient for septic arthritis.

I have to say that scuba injuries are not my strong suit. However, in doing this blog post, I have to say it’s not the worst thing to read about. For instance, you get a lot of random information like for some reason depth is measured in fathoms (which is just 2 yards, and seems completely unnecessary to have this). Also since a lot of these disorders were discovered in the 1800s, they have awesome nicknames like the bends, rapture of the deep, the chokes, and all the squeezes including face squeeze and ear squeeze.

For this blog post, I wanted to keep it simple and have it be a quick rundown of the things we need to know when looking at diving injuries as well as when our friends inevitably ask about if it’s okay for them to go diving. And as always, end on some fun history.

Descent Injuries

These are the more commonly seen injuries with diving. They occur from increasing pressure as the person dives deeper. Water is obviously far denser than air so submerging up to 30 feet can increase pressure significantly. For instance, a person would only need to dive to 33 feet to double atmospheric pressure, whereas a person would need to climb 18,000 feet from sea level to decrease atmospheric pressure 50%.

These injuries are all associated with barotrauma from the increasing pressure and include Middle Ear Barotrauma (most common disorder), Barosinusitis (2nd most common disorder), Facial Barotrauma (Face Squeeze), Inner Ear Barotruama, and External Ear Barotrauma.

The good news about these injuries is they are easily avoided with certain maneuvers that are taught to all divers. The maneuvers equalize pressures during descent preventing associated barotrauma. Furthermore, if these injuries do occur, they are often self-limited or treated in regular fashion (e.g. a perforated eardrum is still a perforated eardrum, no matter the cause)

Ascent Injuries

These are the more serious conditions. These are the ones we associate with hyperbaric chambers. The literature likes to subdivide these into Decompression Sickness (DCS)–which can be further divided into Type I (MSK, skin, and lymphatics), Type II (neurologic)–and into Arterial Gas Embolus (AGE). However, there is a movement to lump these all together into “Decompression Illness,” which I think is fitting because they have the same etiology and same treatment.

The main thing to know about the above is that “Decompression Illness” occurs from nitrogen bubbles forming while a diver ascends. The nitrogen bubbles can deposit in any part of the body leading to joint pain, rash, lymphatic obstruction (edema), CNS (neurologic symptoms), or lead to embolus that can go to any tissue. Initial treatment is with 100% O2. The O2 displaces nitrogen gas in the lungs which increases the gradient allowing for the removal of nitrogen at higher rates. In addition, no matter the presentation, these pts should be sent for recompression therapy. The faster they can get to a hyperbaric chamber, the better their outcomes. However, no matter the timing, they should be transferred to a hyperbaric facility as there is evidence of improved mortality and morbidity at up to 24 hrs.

Pulmonary barotrauma can also occur during ascent. This is usually prevented by continuously breathing during ascent. For instance, if a diver took a full breath at 33 feet and held the breath during ascent, the lungs would need to double in size to accommodate the expansion of air. Although the lungs show great compliance, this could result in the rupture of alveoli and lead to pneumothorax, pneumomediastinum, subcutaneous emphysema, and/or alveolar hemorrhage. The great thing about this, though, is that it starts with the same treatment as above–with 100% FiO2. Furthermore, these pneumothoraces are often small and do not require a chest tube. (Of note, however, if a pt had concomitant DCS, then a chest tube should be placed prior to recompression therapy as could potentially lead to tension pneumothorax).

Differentiating These Disorders

Some of the above disorders can have similar presentations. For instance, ear barotrauma can lead to nausea, vomiting, vertigo, ataxia as can DCS with neurologic symptoms. However, these can be easily differentiated by the timing (e.g. ascent vs. descent) of the symptoms as well as the diving logs. All scuba divers are expected to keep a diving log (which includes duration and depth of diving). Based on these logs, you should be able to calculate the risk for DCS that a diver would have.

Differentiating pulmonary DCS from arterial gas embolus could also be difficult. However, arterial gas embolus is often more acute, occurring within 10 minutes of ascent, while DCS often has sporadic and progressive course, occurring >10 minutes after ascent. However, I would also argue that this really does not matter as you will still treat with 100% FiO2 and transfer to hyperbaric facility despite the etiology.

Who Can’t Dive

I mainly included this section because I think we were all curious as to whether Dr. Heinrich could dive. Also as doctors, we should be able to impress all our friends and family with answers to any medical question they could ever have.

1. It is recommended that pts with recent sinusitis or URI abstain from diving for 2 weeks after resolution of symptoms. This is due to increased risk of ear and sinus barotrauma as they cannot equalize pressures adequately during descent. My roommate actually went diving with sinusitis (he didn’t want to delay his certification for his trip), and he ended up perforating his eardrum. It was the first time I saw nystagmus, and he ralphed everywhere–it was great. He had to get certified at another time.
2. I felt like this goes without saying, but pregnant pts should also avoid scuba diving. This is actually due to the increased risk of the fetus developing DCS as the majority of fetal circulation bypasses the pulmonary bed (where nitrogen bubbles are expired). Scuba diving and pregnancy has been associated with low birth weight, prematurity, congenital malformation, and spontaneous abortions
3. And then there is COPD and asthma… I read a few different guidelines on this, but Rosen’s has a nice section that combines all these recommendations. Essentially, asthma is only contraindicated if in active flare (which was defined as requiring rescue inhaler within previous 48 hrs). It was also advised to abstain from diving if asthma was cold-, exercise-, or emotion-induced as diving involves all of these. The reason for these recommendations is that asthmatics were at a 2-fold increased risk of pulmonary barotrauma (e.g. pneumothorax) than the general population.

Medical History

Paul Bert (1833-1866) is credited for the discovery of oxygen toxicity (known as “the Paul Bert Effect”) as well as the implication of nitrogen in Decompression Syndrome. He was given the nickname “The Father of Aviation Medicine” as he worked on much of the physical effects seen on climbers and “balloonists” during that time. He also became interested in diving science after reading about Dr. Alphonse Gal’s first-hand experience of diving disorders. He not only helped to discover the cause of decompression sickness, but also posited that it could be prevented with slower ascents and treated with 100% FiO2 and recompression chambers.

References
Rosen’s Emergency Medicine : Concepts and Clinical Practice. St. Louis :Mosby, 2002. Print.

Dive-Tech, Mark Powell. Dive-Tech: Decompression Theory – Paul Bert and John Scott Haldane, www.dive-tech.co.uk/bert and haldane.htm.

EKG

Last week’s 5-minute EKG discussion was lead by our APD, Dr. Scott Heinrich.

You get handed this EKG from a patient in triage with chest pain. Should you activate the cath lab?

…

The answer: No

This EKG is showing left ventricular hypertrophy (LVH) with repolarization abnormality, also known as LVH with strain. This can be easily confused for ischemia, so how do we differentiate between the two?

First and foremost, you must meet criteria for left ventricular hypertrophy. While the gold standard for diagnosing LVH is through echo, there are several different EKG criteria we can use to diagnose LVH, including:

• S wave depth in V1 + tallest R wave height in V5 or V6 > 35 mm (Sokolov Lyon Criteria)
• R wave in aVL and S wave in V3 > 20mm (female) or >28mm (male) (Cornell Criteria)
• R in aVL > 11mm
• And several other criteria, although these are the most common

In LVH, the myocardium becomes thickened, which causes the electricity to move more slowly through the heart. This slowed conduction causes widening of the QRS and repolarization abnormalities. This will appear on EKG as increased R wave peak time of >50ms in leads V5 or V6 and ST depressions with T wave inversions in lateral (left-sided) leads. It is important to note that in LVH with strain, T wave inversions are often asymmetric, in contrast to the symmetric t wave inversions often seen in ischemia.

Ex: Deep, symmetric inverted t waves in Wellen’s (type B)

In summary, in LVH with strain you will see:

• Lateral leads (I, aVL, V5 – V6) with increased R wave amplitude, time to peak R wave at least 50ms, and ST depressions with asymmetric inverted t waves
• Inferior and anterior/septal leads with deep S waves and ST elevations in V1-V3 (discordant to deep S)

Lastly, here are some tips from EKG guru Amal Mattu that may help to differentiate between LVH with strain and ischemia:

• If voltage criteria for LVH is not met, assume ischemia
• Asymmetric T wave inversions favor LVH with strain (although this is NOT always the case, you can have asymmetric TWI in ischemia)
• Horizontal ST elevations and depressions should be concerning for ischemia

Resources:

1. Life In the Fast Lane – LVH
2. Amal Mattu ECG weekly – LVH with strain

Goal of This Blog

Pacemakers are becoming increasingly common as our population ages, and are seen more and more in the emergency department. The goal of this post is to summarize common pacemaker settings, the 5-letter nomenclature of pacemakers, indications for pacemaker placement, pacemaker components, common pacemaker complications (majority of blog), and lastly the management of pacemakers in the ED (including applying a magnet).  …And as always, the blog ends with some medical history

Background

• Modern pacemakers essentially have two functions:  1) To sense and 2) To pace.
• Sensing:  pacemakers can either sense the atria or ventricle (or both) for intrinsic cardiac function.
• Pacing:  If the pacemaker does not sense an adequate atrial or ventricular depolarization for a selected time interval, then the pacemaker will “fire”, thus, providing the needed electrical stimulus to cause cardiac depolarization
  • If the pacemaker does sense an adequate atrial or ventricular depolarization, then it will allow the intrinsic heart to function without interruption (in short, the pacemaker will inhibit itself)

• VVI implies that the ventricle is being paced and sensed. Furthermore, the pacemaker will inhibit itself in response to intrinsic ventricular depolarization
• VVI is more commonly used in elderly/inactive patients
• A CXR that shows only a single lead in the right ventricle often implies VVI mode. (However, it can also be seen in multiple lead pacemakers as well)
• If the pacemaker is firing, the EKG will show a pacer spike prior to the QRS complex which will result in the appearance of a LBBB (formation of RBBB signifies lead displacement)
• It is also possible to see the appearance of “fusion beats” which occur when intrinsic ventricular depolarization begins at the same time as the pacemaker discharge. This is often seen in intermittent heart block, when the pacemaker is intermittently firing.

  

  Each beat is preceded by a pacer spike. The complexes marked “P” have normal paced LBBB morphology. The complexes marked “F” have varying QRS morphology as the intrinsic and paced ventricular depolarization occur together

DDD

• I think this description of DDD from Canadiem.org explains it the best: “[DDD] is the wonderkid of pacemakers. It can pace and sense both the atria and ventricle. So if you have a normal P and QRS it just sits back and relaxes. If your P is normal but your QRS is lazy it will kick in to pace the ventricle. If your P is slow but always followed by a normal QRS it will pace the atria but not the ventricle. Finally, if both the atria and ventricle are slow it will pace them both consecutively.”
• CXR will show an atrial lead and a ventricular lead
• The EKG may have a variable appearance depending on the intrinsic underlying cardiac function as noted above. For instance:
  • The EKG can appear “normal”—atria and ventricles are depolarizing on their own
  • There can be an atrial pacer spike with a normal narrow QRS that follows as seen in sick sinus syndrome (implies abnormal SA node with intact AV circuitry)

    

    Atrial Pacer Spike Followed By Normal Narrow Intrinsic QRS Complex

  • There can be normal intrinsic P Waves with a paced wide QRS as seen in complete heart block (implies normal SA node but abnormal AV circuitry)

    

    Normal Intrinsic P Wave Followed By Paced QRS Complex

  • Or there can be dual pacing of the atria and ventricle with corresponding pacer spikes to each

    

    Atria and Ventricle Pacer Spikes

  • Also of note, the above issues can be intermittent so an EKG can show complexes with intrinsic function as well as paced complexes

    

    – 1st Circle: Atrial paced – 2nd Circle: normal P and QRS – 3rd Circle: both atrial and ventricle Paced – 4th Circle: normal intrinsic P with paced QRS

VOO/DOO

• The vast major of pacemakers are set to VVI or DDD. If a magnet is applied, it will revert the pacemaker to its default settings. VVI typically becomes VOO, while DDD becomes DOO.
• These are called Fixed-Rate Settings
• VOO:  results in a paced ventricular depolarization at a constant rate (often near 70 bpm) regardless of the patient’s own heart rate or rhythm. Therefore, it will compete with the intrinsic function of the heart. Due to this, fusion beats are not uncommon. Also, if pacer spikes occur during the refractory period, then it will not produce a QRS
  • There is a small risk that the pacer spike can fall during the “Vulnerable period” resulting in Ventricular Fibrillation
• DOO:  same concept as VOO except it will pace an atrial as well as ventricular beat. Again it does so at a fixed-rate despite the patient’s own heart rate or rhythm.

Overview of 5 Letter Code System

• Letter 1:  chamber paced:  (A)—atria, (V)—ventricle, or (D)—both chambers
• Letter 2:  chamber sensed:  (A)—atria, (V)—ventricle, or (D)—both chambers
• Letter 3:  response to pacemaker sensing: (I)—inhibited, (D)—both chambers inhibited. (T)—triggered (however, no longer seen in modern pacemakers)
• Letter 4:  refers to rate modulation. This indicates method pacemaker uses to modulate rate in response to physiologic demand (e.g. increasing heart rate during exercise, etc.)
• Letter 5 (added in 2002):  indicates the presence of multi-site pacing in each chamber

Pacemaker EKG

• The pacing spikes may be difficult to see in all leads. There are many reasons for this, but the type of pacemaker greatly affects this
  • Epicardially placed leads result in smaller pacing spikes than endocardially placed leads
  • Bipolar leads produce smaller pacer spikes than unipolar pacer spikes
• Intrinsic QRS complexes are typically narrow while paced QRS complexes are wide with LBBB morphology.

Pacemaker Indications

• Sinus node dysfunction (most common cause)
• 3rd degree or advanced 2nd degree (Mobitz type II) AV Block
• Symptomatic bradycardia
• Atrial fibrillation with slow ventricular response

Components of the Pacemaker 

• Pulse Generator (lithium battery)
• Electronic circuitry
• Leads
  • Number of Leads
    • Single lead–endocardial lead positioned in contact with right ventricle
    • Dual Lead–endocardial lead positioned in contact with right atrium and right ventricle
  • Type of Lead
    • Unipolar Configuration:  not compatible with ICD systems and is prone to oversensing of depolarization. Since is of small diameter, less prone to fractures. Consists of negative electrode within the heart and positive electrode within the pulse generator. Due to the distance between the two electrodes, unipolar leads are relatively more prone to oversensing as “outside electrical impulses” can be mistaken for cardiac electrical impulses
      • Pacer spikes are larger  (>20 mm in amplitude on EKG) due to distance between electrodes
    • Bipolar Configuration:  compatible with ICD systems but are larger and relatively more prone to lead fractures. Oversensing is rarely a problem (as the electrodes are closer together so that outside potentials do not get confused as depolarizations). Consists of positive (proximal) electrodes separated by 1 cm negative (distal) electrode both located within the heart.
      • Pacer spikes are smaller (<5 mm amplitude on EKG)

Common Pacemaker Complications

Background of Pacemaker Complications

—  The vast majority of pacemaker complications occur soon after its placement, often within weeks to months. Most often these issues are discovered on routine postoperative pacemaker interrogations.
—  Furthermore, the symptoms that suggest pacemaker malfunctions are often similar to the symptoms that prompted the placement of the pacemaker in the first place (e.g. syncope, pre-syncope, orthostatic hypotension, lightheadedness, dyspnea, or palpitations)
—  There are several ways to divide pacemaker problems, and they differ within resources. Below is a combination of a few of the methods, and I think it helps organize the differential. They are discussed in more detail in a corresponding order as below

1. Pacemaker Box Complications

• Pocket Infection (2%)
• Bacteremia (1%)
  • 20-25% of pts have positive blood cultures. Staph aureus and Staph epidermidis are identified in ~60-70% of cases
• Endocarditis as a complication of the above should also be considered as infections like to spread contiguously
• Tx:
  • Vancomycin until culture results
  • Often requires replacement of pacemaker system after appropriate control of infection via antibiotics

• May mimic presentation of wound or pocket infection
• Tx:  Needle aspiration of the pocket. This should be done under fluoroscopy by cardiothoracic team to minimize risk of damaging the pulse generator

• Presents as pain, swelling, venous engorgement of the ipsilateral arm (most commonly left). Pain in the ipsilateral arm should prompt the consideration of thrombophlebitis. The incidence of venous obstruction seen on imaging ranges from 30-50%. However, due to the creation of collateral vessels, only ~0.5-3.5% of pts develop above symptoms
• Tx:  anticoagulation

Pacemaker Syndrome

• This occurs from the loss of AV synchrony and the presence of ventriculoatrial conduction. This is most commonly seen in VVI pacing with intact sinus node function, which results in the atria contracting against a closed tricuspid and mitral valve. This “contractile asynchrony” results in backloading of atrial contents and loss of atrial “kick”
• This results in symptoms similar to CHF:  syncope/presyncope, orthostatic hypotension, exercise intolerance, generalized weakness, palpitations, chest fullness, uncomfortable pulsations in the neck or abdomen, cough, RUQ pain (hepatic congestion).
• Pt may present shortly after pacemaker placement complaining that initial symptoms that prompted pacemaker are now worse
• Of note, this is a diagnosis of exclusion. Full work-up including pacemaker interrogation should be performed prior to making this diagnosis.
• Tx:  ~20% of pts reports symptoms suggestive of pacemaker syndrome. In most instances, symptoms are mild and patients adapt to them. However, 6% of patients may experience severe symptoms. If symptoms are severe, pacemaker settings can be adjusted. If necessary, pacemaker can be replaced with a dual chamber pacemaker which creates better atria and ventricular synchrony as supplies both P and QRS depolarizations.

 2.  Is the Rate Too Fast

Tachycardia in the setting of a pacemaker can be normal physiology vs. atrial arrhythmias. However, it can also be from a “malfunctioning pacemaker,” which should be of consideration. Of note, this tachycardia will not exceed the upper heart rate limit set in the pacemaker settings.

• The pacemaker should adapt to physiologic needs, therefore, normal causes of tachycardia (infection, hypovolemia, PE) should be considered.

• Atrial Flutter, Afib with RVR, SVT can cause tachycardia as the P waves will be sensed by the pacemaker leading to tachycardia

Pacemaker-Mediated Tachycardia (PMT)

• This is a type of reentry tachycardia—ventricular depolarization (e.g. PVCs) conducts retrograde into the atria leading the atrial lead to detect activity as incoming P wave resulting in ventricular depolarization (“vicious cycle” develops). Note, that since the pacemaker has a set upper rate limit, the heart rate will not exceed this upper limit.
• Tx:  block AV to stop reentry tachycardia (adenosine, BB, CCB). Can always apply magnet if unstable. Vagal maneuvers
  • It can also spontaneously self resolve
  • Most modern pacemakers have a feature that will help recognize this issue and self-terminate the loop. It is called the “PMT Function”–it works by prolonging the refractory interval between V and A

    

    Pacemaker-Mediated Tachycardia

Sensor-Induced Tachycardia

• Pacemaker is designed to respond to physiologic stress by increasing heart rate (i.e. during exercise, hypercapnia, tachypnea)
• The pacemaker can react to stimuli not intended to increase heart rate (vibrations, electrocautery during surgery, intense muscle contractions) causing pacemaker to fire at higher rates. Again, this should not exceed the upper heart rate limit set by the pacemaker.
• Tx:  apply a magnet or decrease upper limit of pacemaker

3.  Is the Rate Too Slow (aka Output Failure)

Failure to capture can be divided into two broad categories. The first category is that the pacemaker is malfunctioning completely, and therefore, there will be no pacer spikes present at all. The second category is that the interface between the lead electrode and the endocardium has changed. This produces an EKG where the pacer spikes are present, however, they are not reaching the needed threshold to result in P or QRS depolarization.

• No pacer spikes often implies a hardware problem (lead disconnection from pulse generator, lead fracture, battery depletion, or a severely displaced lead)
• Of note, lead fractures are relatively uncommon nowadays due to the durability of the lead coating. If it does occur, it is often at predictable locations (e.g. site of attachment to pulse generator or at abrupt angulations).
• Severe lead displacement can also result in lack of pacer spikes. It is discussed below as the lead is more commonly displaced only a few millimeters resulting in failure to capture. It can also result in intermittent capture and pacing if it is “floating” in the pulmonary vasculature as discussed below.

• Exit Block
  • Exit Block typically results in presence of pacer spikes but no resultant P or QRS depolarization. This is caused from injury or process that affects the endocardium at site of pacer electrode.
  • Most often this is from an MI that causes injury at this electrode site causing scarring that prohibits conduction of the pacer spike
  • It can also be caused by systemic electrolyte abnormalities (e.g. hyperkalemia) that suppress endocardium reaction to the pacer spike
  • Rarely, it can be caused by drugs that suppress cardiac activity (e.g. Class III anti-arrhythmic drugs such as amiodarone)
• Displaced Lead
  • This is the most common cause of failure to capture. It most often occurs within the first month of pacemaker insertion.
  • Micro-dislodgment:  describes small displacement of the lead that is too small to be seen on CXR. However, the small displacement reduces the lead’s contact with the endocardium resulting in an increased threshold for capture (results in presence of pacer spikes but no resultant P/QRS waves).
  • Macro-Dislogment:  describes larger displacement that can be seen on CXR. This can result in two possibilities
    • Most commonly this results in catheter tip “floating” in pulmonary outflow tract, which allows for intermittent contact with the endocardium. Therefore, will see the presence of intermittent paced complexes as well as loss of some pacer spikes. This leads to a dynamic and changing QRS morphology on EKG
    • If very severe dislodgment, then will see complete lack of pacer spikes as discussed above.

This occurs from inappropriate sensing (oversensing or undersensing).
Remember that oversensing=less pacing spikes. Undersensing=more pacing spikes

• Undersensing
  • Undersensing occurs when the pacemaker fails to detect spontaneous intrinsic depolarizations. This results in asynchronous pacing. Atrial or ventricular pacing spikes arise regardless of P waves or QRS complex

    

  • As you can see, the pacemaker is not appropriately sensing the underlying rhythm, therefore, it is firing in attempt to pace the strip. However, since the pacer spikes are occurring during refractory period, it is not resulting in a paced complex
    • Pacer spikes within QRS and T waves are indicative of undersensing
  • Undersensing can be complete or intermittent so it is possible to see some paced complexes depending on when the pacer spike appears in the EKG rhythm
  • Undersensing can result from a change in pacemaker settings (e.g. the sensitivity threshold is increased so that a larger amplitude is needed to result in sensing by the pacemaker)
  • More commonly it results from right ventricular infarction or progressive fibrosis that accompanies several of the cardiomyopathies—these changes in the endocardium result in a decrease in the intracardiac amplitude which may not be sensed by the pacemaker
    • Note that we also discussed these as causes of failure to capture. Damage to the endocardium can cause both a sensing and capturing issue, and it is possible for these to occur concurrently.
•  Oversensing
  • These are events that cause the pacemaker to think the heart has intrinsic depolarizations when it really does not. Therefore, the pacemaker does not fire when it should.
  • This is rare. It is caused by the pacemaker detecting “electrical activity” that is non-cardiac in origin. This may lead to intermittent/irregular pacing or a complete absence of pacemaker function
  • Myopotentials from the pectoralis major can cause this.
  • More common in unipolar lead system
  • Can also be caused by Large T waves that are confused for QRS complexes

4.  Uncommon Problems But Fun to Talk About

• More of a historical footnote that occurred in older generation pacemakers resulting from low battery voltage
• Pacemaker delivers runs of pacing spikes in excess of 2000 bpm. On EKG, it looks similar to VFib

• Dysfunction of pacemaker resulting from patient manipulation of the pulse generator (accidentally or purposely). Can result in diaphragmatic or brachial plexus pacing (e.g. arm twitching)
• This is a specific form of displaced lead

• Although discussed as an etiology above. This should be relatively rare with the newer lithium batteries as they are not prone to sudden power failure. Instead, they should have issues with gradual battery depletion which should cause a low battery alarm over months to years before complete depletion.

 5.  STEMI in Paced Rhythm 

• Sgarbossa criteria was initially developed from the GUSTO-1 trial. Less than 0.1% of these patients had a ventricular paced rhythm.
• The best evidence I could find was a retrospective study in 2010 that examined 57 patients (not a great sample size) with ventricular paced rhythms who were formally diagnosed with MI
  • Essentially, it did not find great utility in using the Sgarbossa criteria.
  • It did find
    • discordant STE >5 mm to be the most useful criteria (specificity 99%, sensitivity 10%)
    • No pts had concordant STE >1 mm
    • STD >1 mm in leads V1-V3 (specificity 81%, sensitivity 19%)
• Takeaway:  Sgarbossa’s criteria may be able to point you towards MI, however, it by no means rules it out. Therefore, if you are worried for MI based on history and/or have an EKG that is dynamic or changed from previous EKGs (pacemaker patients should have several), then it is likely a good idea to involve cardiology early

Pacemaker Management In The Emergency Department

Labs and Imaging

• Luckily, the work-up for pacemaker related symptoms is the same for any patient with palpitations, chest pain, or SOB (CBC, BMP, +/- Magnesium, CXR, troponin, EKG). However, it should also always include pacemaker interrogation as well.
• CXR
  • requires AP and lateral views to determine correct location of pacer wires
  • Although there are algorithms to determine correct position based on these views alone, it is much easier to compare to lead placement on previous CXRs
  • Requires over penetration of CXR if want to see model of pacemaker

• Applying Magnet Video
• Magnet is useful in any unstable tachycardic patients with pacemaker
• Magnet causes closure of a “reed switch” within the pacemaker circuitry which converts the pacemaker to an asynchronous or fixed rate-rate pacing mode (VOO or DOO depending on the type of pacemaker discussed above).
  • VOO:  ventricle is paced.
  • DOO:  both the atria and ventricle are paced.
  • Once the magnet is removed, the reed switch will revert back causing the pacemaker to resume its regular programmed settings. If PMT, then should stop the tachycardia as magnet eliminates the reentry tachycardia.
• Note that if there is a co-associated ICD, the magnet will also deactivate the ICD, as long as the magnet is in place

• No changes

• Apply pacer pads in anterior-posterior orientation, often at least 8 cm away from the device so that its circuitry is not augmented.

• CXR should be performed post-arrest (as in all patients). Although rare, special consideration should be taken to note if the pacing leads were displaced during chest compression.
• Immediate return of pacing (capture) may not occur after resuscitation and/or defibrillation–this is a result of global ischemia and increased pacing threshold (Exit Block), and often not an indication of pacemaker malfunction. This may require temporary transcutaneous pacing if capture or pacing cannot be resumed.

Main Takeaways

• Know the settings of VVI and DDD as these are the most common
• Pts often carry a pacemaker card which should list the reason the pacemaker was placed as well as the pacer settings
• The vast majority of pacemaker complications occur within the first few weeks or months of pacemaker implantation
• Pacemaker complications/malfunctions can fall into several categories including
  • Pacemaker Box Complications (infection, hematoma, thrombophlebitis, pacemaker syndrome)
  • Rate is Too Fast (Normal response, Atrial Arrhythmias, Pacemaker-Mediated Tachycardia, Sensor-Induced Tachycardia)
  • Rate is Too Slow (failure to capture, failure to pace)
  • Uncommon problems (Twiddler’s syndrome, Runaway Pacemaker, Battery Depletion)
  • STEMI in paced rhythm:  Sgarbossa can point you in the right direction; however, does not rule out. A changed or dynamic EKG in the right history is concerning.

History of Implanted Pacemakers

Bonus Pacemaker History–How did we find out that we could externally pace the heart? It’s crazy.

                      Catharina Serafin Along Side The First Paced Rhythm

Resources

1. RebelEM (Link)
2. CanadiEM (Link 1, Link 2)
3. LITFL (Link 1, Link 2)
4. Aquilina O. A brief history of cardiac pacing. Images in Paediatric Cardiology. 2006;8(2):17-81. (Link)
5. Rosen’s (Marx, J. A., & Rosen, P. (2014). Rosen’s emergency medicine: Concepts and clinical practice (8th ed.). Philadelphia, PA: Elsevier/Saunders.)

Part of our new conference schedule is doing a quick 5 minute summary on a journal article of interest, EKG from the past week, and Xray. The idea being that by the end of the year, we will have roughly covered 40 journals, EKGs, and Xray Topics.

5-Minute Journal

Today’s 5 minute journal was performed by the great resident, Dr. Bill McDowell, who absolutely crushed it.

I think this is a great article to review as we see abscesses frequently, and it somewhat becomes humdrum in the ED. Abscesses are also fraught with debate on who should receive antibiotics vs. I+D alone. The main takeaways from this article are below.

Abscess Background
— Historically, I+D by itself has an approximate 84% cure rate
— Many small previous studies showed no difference in cure rates of I+D alone vs. I+D with antibiotics
— One prior large study (Talan et al, 2016) found superior cure rates with Bactrim/I+D vs. placebo/I+D (80.5% vs. 73.6% cure rate).

Article Summary
—  Clinical Question:  Do antibiotics with anti-MRSA activity improve cure rates for abscesses when given following I+D?
—  Study Type:  Multicenter, prospective, randomized, double-blind, placebo-controlled clinical trial (superiority design)
—  Study Groups:  10-day courses of Clindamycin vs. Bactrim vs. Placebo (following standard I+D)
—  Inclusion Criteria:  single abscess <5cm diameter, age>6 months, 1 day of 2 or more symptoms (erythema, swelling/induration, local warmth, purulent drainage, tenderness)
—  Exclusion Criteria:  BMI>40, immunocompromised (including diabetes, chronic renal failure), immunosuppresive therapy, SIRS criteria present, Temp>38.5C, human/animal bite, site requiring specialist (genitalia, perirectal, hand), anti-staphylococcus antibiotic in past 14 days, requires admission, resident of long-term care facility, major surgery in past 12 months
— Primary Outcome Being Tested:  Clinical Cure. “Lack of Clinical cure” was defined as:  continued signs/symptoms, occurrence of skin infection at new body site, reoccurrence at original site, inability to take entire course of antibiotic secondary to adverse side effects, hospitalization related to infection, or unplanned surgical treatment of infection
— Study Population:  786 patients (36% peds). 343 patients fully adherent to antibiotic 10-day course. Average surrounding area of erythema 27.4 cm²  (~5×5 cm)
— Results:
—  Cure rates:  clindamycin: 83.1%, Bactrim: 81.7%, Placebo: 68.9%
(Statistical significance for antibiotics vs. placebo). No statistical
signifance between bactrim vs. clindamycin
—  Most failures due to new lesion at other site or use of rescue
medication- especially in placebo group
—  Rates of Diarrhea:  Clindamycin 21.9%, Bactrim 11.1%, Placebo 12.5%
—  Study population had large surrounding erythema suggesting large
percentage of co-associated cellulitis

Conclusions/Takeaways
—  Antibiotics have a clinically significant higher cure rate compared to placebo. However, this study population had a relatively large surrounding area of erythema, which makes it unclear whether the antibiotics were treating the abscess itself or the co-associated cellulitis. Furthermore, it appears the advantage of antibiotic use in these patients was in preventing occurrence of an abscess at a separate site, which suggests the antibiotics main function was in clearing MRSA recidivism in this patient population vs. the actual treatment of the original skin infection.
—  Although there was no statistical difference in cure rates between Bactrim and Clindamycin, it does appear to be advantageous to prescribe Bactrim vs. Clindamycin as was associated with fewer side effects–mainly rates of diarrhea (Clinda 21.9% vs. Bactrim 11.1%)
—  Abscess treatment has evolved greatly over the last decade with several studies performed during this time. RebelEM provides a great summary of this research (RebelEM Abscesses). I also love this review because it refers to some amazing work by our own RUSH staff including Dr. Gottlieb and Dr. Hallock as well as our always consulted pharm team including Josh DeMott and Gary Peska (Annals of EM Link)

5-Minute EKG

The 5-minute EKG was presented by our fan-favorite attending, Dr. Patwari. See EKG below (Answer to follow)

As always, it is important to approach an EKG in a systematic way including rate, rhythm, axis, intervals, and segments. However, the big takeaway from this EKG is that it is a Regular Narrow-Complex Tachycardia with HR roughly 150. Now we just need to decide which type of Regular Narrow-Complex Tachycardia. This should lead us to a differential including Sinus Tachycardia, SVT (AVNRT vs. AVRT), and Atrial Flutter. You could also consider Atrial Ectopic Tachycardia (more commonly seen in peds), however, it is a rarer diagnosis compared to above.

Drumroll… This is Atrial Flutter. Clues to this are the saw-tooth appearance caused by the flutter waves, HR of roughly 150, and P waves that march out at a rate of roughly 300.

Atrial Flutter Basics
— Type of supraventricular tachycardia caused by re-entry circuit within the right atrium
— Since it originates from the atria, the heart rate will resemble the atrial rate, most often ~300 bpm (though there can be variability person-to-person with average range 250-350)
— The AV node acts as the electrical gateway between the atria and ventricle, and has long refractory period allowing it to “block” excessive depolarizations from the atria
— This most often leads to a 2:1 AV ratio block meaning for every two P waves produced, a QRS will form (as seen above) which often produces a ventricular rate (QRS) of HR roughly 150.
— If there is a higher-degree block (e.g. from medications or underlying heart disease), you can see a 3:1 or 4:1 block, which corresponds to the number of P waves prior to the QRS. This also gives a much better “saw-tooth” appearance which we remember from our Med School rhythm strips  seen in FirstAid (as below)

— If we confused the first EKG with SVT, and gave adenosine (AV nodal blocking agent), we would see the continuation of flutter waves, but no QRS depolarizations due to the AV nodal blocking properties of adenosine (seen in EKG below). The good news is that adenosine only lasts 10-15 seconds, and ventricular contractions will continue thereafter. The same is true for vagal maneuvers which may transiently unmask the flutter waves (though more commonly will cause no changes)

Pitfalls of Diagnosing Atrial Flutter
— The rate isn’t always exactly 150. If the rate is slower (e.g. HR 125-140, it can resemble Sinus Tachycardia. Therefore, in any regular narrow-complex tachycardia with HR 130-170, it is important to consider atrial flutter. Also Atrial flutter patients are often stable, and therefore, there is time to work up the EKG
— If the rate is faster (e.g HR 160-175), it can resemble SVT as P waves become buried in the frequent QRS complexes. Of note, SVT typically presents with HR 170-250. You can attempt vagal maneuvers to either convert to NSR or cause unmasking of flutter waves. Adenosine can also unmask the underlying flutter.

Treatment of Atrial Flutter
— Treatment options to be discussed in more detail in a following conference. But briefly, the options include cardioversion, rate-control and +/- anticoagulation. Treatment is very similar to Atrial Fibrillation. Of note, atrial flutter is very sensitive to cardioversion often only requiring 50-100 J.

5-Minute Xray

This week’s radiology review focused on Pelvic Ring Fractures. Again, it’s only a 5-minute review so we dedicated it to the AP view. However, in a detailed work-up, additional views (including inlet/outlet and CT) will be obtained.

Quick Review of AP Pelvic Xray

Classifying Pelvic Ring Fractures
— As is anything in Emergency Medicine, start with the basics. Is the pt hemodynamically stable or unstable? The pelvis is notorious for being able to hide blood. Also it is important to do a thorough secondary survey as these injuries are associated with high energy blunt trauma, and secondary injuries can be missed. For instance, pelvic ring fractures were associated with chest injury in 63% of cases, long bone fractures in 50% of cases, head and abdominal injury in 40% of cases, and spine fractures in 25% of cases (Orthobullets).
— Is the fracture stable vs. unstable? There are two classification systems that can be used (Tile Classification vs. Young-Burgess Classification) with the end goal of determining the stability and severity of the fracture. The Young-Burgess is used more commonly (reviewed below) and divides fractures by mechanism (Lateral Compression, Anteroposterior compression, and Vertical Shear)

1. Lateral Compression Fracture (LC)
   — Often seen in T-bone MVC or pedestrian hit from side
   — Typically, Rami Fracture with ipsilateral iliac fracture.
   — Most common Pelvic Ring Fracture.
   
2. Anteroposterior Compression (APC)
   — Often from head-on-collision MVC
   — Symphysis widening. >2.5 cm is a more unstable fracture that often requires fixation surgery. May also have associated SI joint diastasis as well as disruption of SI ligaments
   — These are the patients that present with hypotension. This is due to the mechanism that causes the iliac wings to be forced outward allowing for increased pelvic volume
   
3. Vertical Shear
   — Results from vertically oriented force. Most often fall from great height (e.g. fall from building onto legs)
   

Young Burgess Classification System
And as promised… For all the people that really want to get in the weeds, The Young Burgess Classification System. I love that vertical shear is not further divided by severity as it implies badness.

Fun Medical History

I really enjoy medical history, and it’s my goal to share at least a small piece of medical history at the end of each post. I actually learned this piece of trivia from Dr. Somy Thottathil. This past week we celebrated the 47th anniversary of the first CT scan ever. It took place on October 1, 1971, in Wimbledon, London. It was performed by the scientist Sir Godfrey Hounsfield (yep, of Hounsfield unit fame)–pictured below. It was only designed for brain imaging, and in this first Head CT, revealed a brain tumor in a 41-year-old female. In another 4 years, the first whole-body CT scanner was developed.

Additional fun fact–the development of this first CT scanner is partially owed to the Beatles. Hounsfield was part of the EMI company, which was the same company that owned The Beatles’ music. The profits from their music helped to fund this research.

Here are some resources for hyperglycemia based on our session today. First here are RMC’s DKA protocols for adults and pediatric patients.

• DKA Protocol_2016.06.11
• Peds DKA guidelines final 2013

Then some videos (old and new) about DKA and HHS.

2013 DKA and HHS

Pediatric DKA

Of note, the PECARN network released an article in NEJM June 14, 2018 comparing fast and slow IV administration of 0.45% and 0.9% NS to determine who gets neurologic deficits. There were no differences between the groups.

1: Kuppermann N, Ghetti S, Schunk JE, Stoner MJ, Rewers A, McManemy JK, Myers SR, Nigrovic LE, Garro A, Brown KM, Quayle KS, Trainor JL, Tzimenatos L, Bennett JE, DePiero AD, Kwok MY, Perry CS 3rd, Olsen CS, Casper TC, Dean JM, Glaser NS; PECARN DKA FLUID Study Group. Clinical Trial of Fluid Infusion Rates for Pediatric Diabetic Ketoacidosis. N Engl J Med. 2018 Jun 14;378(24):2275-2287. doi: 10.1056/NEJMoa1716816. PubMed PMID: 29897851.