EMS is called to the home of a 62-year-old female who complains of shortness of breath and epigastric discomfort.

On their arrival, they find the patient sitting on a chair in her living room, holding her hand to her chest while she talks with first responders. She is not pale, but appears diaphoretic, anxious, and has mildly laboured respirations.

A brief medical history is obtained while gathering a set of vitals and applying the ECG electrodes.

Onset:              “It woke me up from my sleep”
Provocation:   “Nothing makes it better or worse”
Quality:            “Like heartburn, but worse”
Radiation:        None
Severity:           Rated 8 out of 10
Time:                “About ninety minutes ago”

Pulse:              74/min, strong and regular at the wrist
RR:                  20/min, clear air entry on auscultation
NIBP:              152/88
SpO2:              92% on room air
BGL:                7.4mmol/L (133 mg/dl)
Temp:             36.2C (97.2F)
PMHx :           Hypertension, asthma, dyslipidemia

A 12-lead ECG is acquired.

At this point, the attending paramedic was highly suspicious that an acute coronary event was taking place, and proceeded to treat with Aspirin, SL Nitroglycerin, and serial 12-leads while initiating transport.

The following ECG was acquired with V4 moved to the position of V4R, and V5 & V6 moved to the position of V8 & V9, respectively.

The transporting paramedic recognized the posterior STEMI and transmitted the ECG to a consulting physician. Based on these findings, and considering the significant distance to a PCI-capable facility, the decision was made to administer Plavix and IV thrombolytics (TNK).

About 20 minutes post-TNK, it was noted that the patient’s heart rate had decreased to the low 40’s, while her chest discomfort simultaneously improved.

The following 12-lead was acquired.

Despite the precipitous drop in blood pressure and heart rate, the patient appeared healthier now than she had at any point previously during the encounter.

Does this ECG represent improvement, or a decline in clinical condition?

Posterior STEMI

The diagnosis of a truly isolated posterior STEMI appears to be a relatively uncommon occurrence, presenting in about 3% of myocardial infarctions ¹, however it’s highly likely that underdiagnosis has played a role in these underwhelming stats. This may be due to a misconception by many practitioners that ST Depression (STD) in leads V1-V3 represents anterior ischemia, despite the fact that myocardial ischemia does not localize on the 12-lead ECG.

This misinterpretation, combined with arbitrary millimeter criteria, often result in delayed cath lab activation, or a diagnosis of UA/NSTEMI in patients who are in fact suffering acute posterior STEMI.

There are several key criteria on the 12-lead ECG that, when observed in a patient suffering from a suspected acute coronary syndrome, should lead you to make the diagnosis of posterior STEMI. They include:

• Horizontal ST depression in V1-V3 with upright T-waves
• Early R-wave progression in the precordial leads
• ≥ 0.5mm ST Elevation (STE) in one or more posterior leads (V7-V9)*

* Due to the anatomical structures located between the posterior leads and the heart, there’s an increased amount of electrical impedance, which results in the appearance of much smaller QRS complexes in the posterior leads. This is why half of a millimeter of STE is significant in these leads!

However, these low-voltage leads can make ST-segment elevation difficult to appreciate, which has the potential to confuse the diagnosis. As a result, some experts suggest that the diagnosis of posterior STEMI can and should be made using the other two criteria alone.

Prehospital Thrombolytics

Over the last ten years, the use of thrombolytics in the prehospital arena has increased significantly around the world, especially in rural and remote communities.

While primary-PCI within 120 minutes of first-medical contact (FMC) remains the ideal pathway for patients with acute STEMI, a combined pharmaco-invasive approach has been suggested to be comparably effective in reducing morbidity/mortality in patients presenting with acute STEMI in regions that cannot provide primary-PCI.

In these cases, patients are treated with intravenous fibrinolytics, usually following ECG transmission, expert consultation, and careful screening processes. Following this, the patient is promptly arranged transport to a PCI center where rescue catheterization or follow-up angiogram can be completed.²

With the goal being to minimize infarction size and myocardial necrosis, many services have implemented protocols that allow for EMS administration of fibrinolytics. This has been shown to significantly reduce the time-to-treatment when compared to services which transport to the closest facility prior to the administration of fibrinolytics.³

When paramedics are given the appropriate level of training and equipment, prehospital fibrinolysis can be an effective and efficient means of reducing total ischemic time, and efforts should be made to lobby for this intervention in regions which cannot meet the 2-hour PCI window.

Reperfusion Arrhythmias

Between 80-90% of STEMI patients who receive either PCI or thrombolytics will experience some form of reperfusion-related arrhythmias within the first 48 hours of treatment.

With the expanding utilization of thrombolytics for acute STEMI, the occurrence of these “reperfusion rhythms” has become increasingly common in prehospital and ED settings alike. These rhythms most commonly occur when oxygenated blood begins flowing through previously occluded coronary arteries, and while it’s uncertain what degree of coronary artery patency they represent, it’s generally accepted that these arrhythmias represent some degree of myocardial reperfusion.⁴

Slower reperfusion arrhythmias such as sinus bradycardia and ventricular escape rhythms are thought to be resultant of increased vagal tone in the recently ischemic myocardial tissue; a phenomenon known as the Bezold-Jarisch Reflex, which is most commonly seen in inferior or posterior MI’s.⁵

These slow rhythms often occur alongside periods of frank hypotension, however these incidents are most often self-limiting and well tolerated, and may in fact occur at a time when the patient reports finally feeling better! Consequently, aggressive interventions to increase the heart rate are rarely required, and can usually be limited to postural changes or the administration of atropine, or very rarely transcutaneous pacing. ⁷

Faster reperfusion arrhythmias may include frequent premature ventricular complexes, accelerated idioventricular rhythm, or nonsustained runs of ventricular tachycardia. These “irritable” rhythms  are thought to originate from the zone of ischemia, which surrounds the zone of infarction, where “overactive” calcium channels are believed to play a significant role. The arrhythmia may be occurring as a result of an ectopic foci, or serving as an escape rhythm when the sinus node is depressed (perhaps due to the vagal response mentioned above).

Recent research suggests that the presence of these arrhythmias may predict a larger area of infarction, or possibly incomplete or poor reperfusion (TIMI flow grade <3). Management of these patients should be aimed primarily at continuous cardiac monitoring and hemodynamic support to maximize myocardial perfusion, with use of antiarrhythmic drugs to be considered further down the treatment algorithm.

References

1. Oraii S, Maleki M, Abbas Tavakolian A, et al. “Prevalence and outcome of ST-segment elevation in posterior electrocardiographic leads during acute myocardial infarction.” J Electrocardiol 1999;32: 275-8 http://www.ncbi.nlm.nih.gov/pubmed/10465571
2. Danchin N, Durand E, Blanchard D, “Pre-hospital thrombolysis in perspective.” European Heart Journal. DOI: http://dx.doi.org/10.1093/eurheartj/ehn462 2835-2842 First published online: 23 October 2008
3. McCaul M, Lourens A, Kredo. “Pre-hospital versus in-hospital thrombolysis for ST-elevation myocardial infarction.” Cochrane Database Syst Rev. 2014 Sep 10;9:CD010191. doi: 10.1002/14651858.CD010191.pub2 http://www.ncbi.nlm.nih.gov/pubmed/25208209
4. Ersan Tatli, Güray Alicik, Ali Buturak, Mustafa Yilmaztepe, and Meryem Aktoz, “Arrhythmias following Revascularization Procedures in the Course of Acute Myocardial Infarction: Are They Indicators of Reperfusion or Ongoing Ischemia?,” The Scientific World Journal, vol. 2013, Article ID 160380, 7 pages, 2013. doi:10.1155/2013/160380 http://www.hindawi.com/journals/tswj/2013/160380/cta/
5. Koren G, Weiss AT, Ben-David Y, Hasin Y, Luria MH, Gotsman MS. “Bradycardia and hypotension following reperfusion with streptokinase (Bezold-Jarisch reflex): a sign of coronary thrombolysis and myocardial salvage.” http://www.hindawi.com/journals/tswj/2013/160380/cta/
6. Gulumser Heper, Mehmet Emin Korkmaz, Ayhan Kilic, “Reperfusion Arrhythmias: Are They Only a Marker of Epicardial Reperfusion or Continuing Myocardial Ischemia After Acute Myocardial Infarction?” ANGIOLOGY 2008 vol. 58 no. 6 663-670  doi: 10.1177/0003319707308891  http://ang.sagepub.com/content/58/6/663
7. Esente P, Giambartolomei A, Gensini GG, Dator C. “Coronary reperfusion and Bezold-Jarisch reflex (bradycardia and hypotension)”, Am J Cardiol. 1983 Aug;52(3):221-4. http://www.ncbi.nlm.nih.gov/pubmed/6869265

Unfortunately not every patient that suffers a STEMI makes a complete recovery, even if treated with primary PCI. Patients that present late into their infarct have a higher risk of developing a complication.

Here are two cases that illustrate the spectrum of mechanical complications that can occur in the aftermath of an infarct.

Case 1

A 53 year old lady with hypertension and hypercholesterolaemia called an ambulance about 8 hours after the onset of her chest pain.

Vital signs are assessed.

BP: 100/60
HR: 96bpm

The pre-hospital ECG traces obtained by the paramedics are shown:

Both ECGs show clear inferior ST elevation with prominent Q waves. There is reciprocal change anterolaterally but importantly for an inferior MI, heart rate is normal. The ECGs are 50 minutes apart and the changes appear to be slightly worse on her second ECG, but not drastically.

She was still in pain on arrival at the interventional centre and transferred immediately to the cath lab. Her left system showed moderate disease in the circumflex artery. However, as expected, the acute problem was her right coronary artery, which was occluded.

Below you can see the guide catheter engaged with the blocked right coronary artery and no flow is getting past the clot.

A thin angioplasty wire is passed through the thrombus and to the distal vessel. The thrombus was more resistant (i.e. mature) than most acute infarcts, which fit with the 8 hour history of pain.

You can see even passing a 0.014” diameter wire restores some flow. The wire tip is in the posterior descending artery. Reperfusion is often when patients destabilise and indeed the patient’s heart rate dropped to 20bpm and blood pressure to 60mmHg but she responded quickly to atropine and fluid. In the proximal vessel, a filling defect can be seen which is a sizeable thrombus.

A 3.5mm wide and 38mm long drug-eluting stent was placed without complication in her RCA, producing a nice angiographic result. However, the long period of coronary occlusion may well have caused significant myocardial injury. She was kept under close observation.

A satisfying sight for any healthcare professional is seeing a patient’s ST elevation resolve after opening their artery. However, her post procedure ECGs revealed persistent ST elevation.

You can see the evolution of her infarct as the deeply inverted inferolateral T waves revert but her STs remain elevated and develop a more mature ‘rounded’ appearance.

She returned to the ward but deteriorated. Inferior STEMIs carry a more favourable prognosis than anterior (as LV function is normally not as dramatically affected), so clinical instability post procedure should be a concern. On examination she was pain-free but breathless:

RR 24
SO2 92% 2L O2
HR: 80bpm
Chest auscultation: crackles bibasally
Heart sounds: loud pansystolic murmur

A bedside echocardiogram was performed.

A parasternal long axis view reveals the posterior mitral valve leaflet is tethered. The basal posterolateral wall is hypokinetic.

A close up of the valve with colour Doppler demonstrates mitral regurgitation.

An apical 4-chamber (zoomed in) shows the mitral regurgitation is significant.

This parasternal short axis view gives the clearest demonstration of the problem. A regional wall motion abnormality is clearly seen affected the infero-septum and inferior wall. The rest of the left ventricle is contracting well.

Her chest radiograph confirmed the clinical suspicion of pulmonary oedema and she was treated with diuresis. She responded well.

Why did the patient develop pulmonary oedema?

The papillary muscles are very strong muscles connected to the mitral valve to prevent it inverting during ventricular systole. There are two papillary muscles in the left ventricle, each connected to a mitral valve leaflet.

The anterolateral papillary muscle is connected to the anterior mitral valve leaflet and receives a blood supply from both the left anterior descending artery (via a diagonal) and the circumflex artery (via an obtuse marginal). However the posteromedial papillary muscle only has one blood supply, which is the posterior descending artery, a branch of the right coronary artery in 90% of people.

Therefore one can appreciate why mitral valve problems are more common following an inferior STEMI. In this case an almost akinetic segment, which included the posteromedial papillary muscle, caused the posterior mitral valve leaflet to become fixed, causing mitral regurgitation. Even though overall left ventricular function was only mildly impaired on the echocardiogram, the regurgitant pressure into the lungs can precipitate pulmonary oedema.

In more severe cases, the papillary muscle may rupture completely causing a ‘flail leaflet’ and catastrophic mitral regurgitation. It is often fatal. This complication typically occurs 2-7 days following a myocardial infarction, so if a patient suddenly deteriorates in the days after an MI, check for a murmur and organise an urgent echocardiogram. They can develop cardiogenic shock within minutes.

Case 2

An 80 year old man suffered a severe episode of chest pain but did not seek medical attention until about 2 weeks later, by which time he’d become progressively more breathless. His primary care doctor heard a loud, previously undocumented murmur and referred him into hospital.

On examination, in addition to the murmur, he had signs of right sided heart failure with an elevated JVP and peripheral oedema. His ECG revealed inferior Q waves.

Parasternal long axis view: The septum is moving in an unusual jerky fashion and something can be seen in the RV. Despite left ventricular function appearing reasonable, the aortic valve is not opening much suggesting cardiac output is low.

Parasternal short axis: There is a large ventriculo-septal defect in the infero-septal LV. The right ventricle is severely impaired.

Apical 4 chamber:

The LV function is hyperdynamic. The infero-basal septum is tethered near the mitral and tricuspid valves but highly mobile, creating a large VSD. The right ventricular free wall appears to bulge out and the RV is almost akinetic.

Apical 4 chamber colour Doppler:

There is free flow between LV and RV.

Apical 2 chamber. This view demonstrates the bulging from the RV also appears to involve the LV. This is a sealed perforation with aneurysm formation.

In this remarkable loop, the echo probe moves and one can clearly appreciate the defect in the septum, along with the thin membranes sealing the perforation.

What happened?

In addition to problems with the mitral valve, ventricular perforation and ventriculoseptal defects (VSDs) are the two other catastrophic mechanical complications of an MI. LV wall rupture typically occurs in the first 5 days, but some can be as late as a fortnight later. In this case, it is unclear when the complication occurred.

Complete free wall rupture rapidly leads to tamponade and death, but a sub-acute perforation refers to one that has been sealed with thrombus or the pericardium. This remains very high risk for subsequent complete rupture. Somewhat paradoxically the risk of developing any mechanical complication is not proportional to the size of the infarct and small infarcts can pose a large risk.

This patient suffered both a large VSD and a sealed perforation of the inferobasal free wall.

Management

These patients may present in cardiogenic shock and should be managed accordingly. Treatment might include diuresis, vasopressors, inotropes, intra-aortic balloon pump or mechanical cardiac support. The only definitive treatment is invasive, but these patients are exceedingly high risk and optimal timing can be very hard to judge. Most patients will be considered for early surgery but percutaneous closure of VSDs is increasing, to avoid the risk of a general anaesthetic.

Summary

• There are three mechanical complications of acute myocardial infarction: acute mitral regurgitation, VSD and LV rupture
• They typically occur 2-7 days following an MI
• Have a high index of suspicion if a patient presents following an MI with a sudden deterioration
• Symptoms and signs include breathlessness, right-sided heart failure and a new harsh pansystolic murmur
• Urgent echocardiography is indicated and diagnostic in most cases
• Treatment is supportive and surgical

References:
Mechanical complications of acute myocardial infarction, accessed 26^th February 2016. Available at: http://www.uptodate.com/contents/mechanical-complications-of-acute-myocardial-infarction

“Today, the vogue seems to be an irresistible urge to call VT supraventricular with aberration…” Marriott

A middle-aged male with a complex arrhythmia history contacts EMS after several hours of palpitations.

He has an implantable cardioverter defibrillator (ICD) but denies feeling any activations. He also denies any significant symptoms of dyspnea or discomfort.

Medications: Flecainide, Mexilentine

Vital signs are assessed.

• RR: 18
• HR: 136
• NIBP: 136/91
• SpO2: 99% on room air

The cardiac monitor is attached.

A 12-lead ECG is obtained.

The treating paramedics believed the rhythm was supraventricular tachycardia (SVT) with aberrancy. The patient was transported to the Emergency Department.

Another 12-lead ECG was obtained on arrival.

In the Emergency Department one physician thought the tachycardia might represent atrial fibrillation or SVT with aberrancy. Another wondered if the ECG showed Wolff-Parkinson-White syndrome.

However, a far more likely explanation is ventricular tachycardia (VT).

As Dr. Marriott observed, many clinicians are unable to resist the siren song of aberrant supraventricular tachycardia or atrial fibrillation.

Let’s look at some of the myths and cognitive biases we frequently encounter in the interpretation of wide complex tachycardias.

“I didn’t see an extreme right axis deviation.”

It is true that an extreme right axis deviation (right superior axis) in the frontal plane — “no man’s land” — is strongly supportive of VT. However, the absence of such an axis does not support a supraventricular origin.

If the focus of the VT is in the basal portion of the LV, or the RVOT, an inferior axis (as seen in our patient) will be found.

“The heart rate was too slow to be VT.”

Ventricular rhythms can present with any rate! When the rate exceeds 110-120 bpm we call it VT, while a rate of 50-110 bpm is called accelerated idioventricular rhythm.

Is VT with a rate of 130 unusual? Hardly! One study examined patients who had episodes of VT after ICD placement. Over 30% of the patients had episodes of VT at rates between 101 and 148 bpm. A more recent study found a similar rate of VT episodes at rates between 130 and 186 bpm.

“The rate seemed a little irregular so I thought maybe AF.”

Certainly, gross irregularity should prompt the clinician to consider AF with aberrant conduction! But the rhythm strip and the 12-lead look quite regular here. Having said that, VT can be irregular for brief periods, usually during the initiation or “wind up” phase.

“The patient didn’t have any symptoms even though it had been going on for hours.”

Ventricular tachycardia can be remarkably well tolerated. This patient, in particular, had a normal ejection fraction, no history of MI, and did not have any concurrent illness or intoxication during the episode.

“The ICD didn’t go off, so it probably wasn’t VT.”

Most ICDs are programmed to shock at a particular rate limit — not based on QRS morphology. Modern devices are also capable of anti-tachycardia pacing (ATP) which is not felt by the patient. It turned out that this patient had a “trigger” rate of 182 bpm.

Conclusion

The most important criterion for ventricular tachycardia is “wide and fast”.

In some circumstances it may be possible to distinguish between VT and SVT with aberrancy.

However, the reasons listed above are not sufficient to do so.

A 55 year old man is brought in by EMS for altered mental status.

It is the middle of February and he was found sleeping outside. He smells of alcohol, is moaning on the gurney, and responds to painful stimuli.

Vital signs are assessed.

• RR: 13
• HR: 38
• BP: 110/90
• Temp: Cold to touch
• SpO2: Unable to obtain reading

A 12-lead ECG is obtained due to bradycardia and altered mental status.

At this point the patient’s temperature was found to be 24°C / 75°F by bladder temperature monitoring.

Osborn waves typically have a positive deflection in all leads except aVR and V1. They are known by a number of other names such as the camel-hump sign, late delta waves, hypothermic waves, or prominent J-waves.

In a patient who was found outside in February, they can safely be presumed to represent hypothermia.

The physiologic cause of Osborn waves is not well understood. Since the 1920s many hypothesis have been proposed including anoxia, injury current, acidosis, delayed ventricular depolarization and early ventricular repolarization.

While the treatment of the patient with prominent Osborn waves is based on the precipitating cause, the presence of Osborn waves is related to an increased incidence of ventricular fibrillation.

The patient was aggressively resuscitated with both internal and external warming with warm intravenous fluids and forced heated air blankets.

A repeat 12-lead ECG was performed 2 hours later.

The patient’s temperature is now 32°C / 89°F.

As the internal temperature improved the patient’s heart rate began to rise and the Osborn waves became less prominent. However, the artifact is worse due to increased shivering.

Rewarming was continued and a third ECG was performed, 3 hours after initial presentation.

Core temperature at this point was 33°C / 91°F.

Discussion

Osborn waves consist of a positive deflection at the J-point in all leads except for aVR and V1 where the deflection is negative.

Prominent J-waves can be seen in hypothermia, hypercalcemia, neurovascular accident, vasospastic angina, and Le syndrome d’Haïssaguerre (idiopathic ventricular fibrillation or as a normal variant).

While the true physiologic cause of Osborn waves is not known their presence can indicate a progression to ventricular fibrillation.

Osborn waves that are secondary to hypothermia should improve with patient warming.

Hypothermia also causes bradycardia, prolonged PR, QRS and QTc intervals, ventricular ectopy and atrial fibrillation.

Shivering may contribute to poor 12-lead ECG data quality but usually disappears below a threshold temperature.

Resources
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1501063
http://lifeinthefastlane.com/ecg-library/basics/hypothermia
http://hqmeded-ecg.blogspot.com/2011/11/osborn-waves-and-hypothermia.html

Diabetic emergencies constitute a substantial percentage of ‘9-1-1’ calls and emergency department visits, with occurrences expected to rise as the percentage of the population diagnosed with diabetes mellitus (DM) increases.¹ Severe hypoglycemia, or “diabetic shock”, is generally thought to be a true medical emergency, and treatment has been made widely available for prehospital professionals to provide to patients who are  suffering from dangerously low blood glucose levels (BGL).

Traditionally, hypoglycemia which produces unconsciousness warrants obtaining vascular access and administering highly concentrated dextrose-containing solutions intravenously in order to swiftly restore patients to a euglycemic state, but there’s a lack of consensus about just how fast those solutions should be given, or how concentrated that solution should be. A preliminary search of the various treatment algorithms used around North America, the UK, and Australia will turn up two primary methods of dextrose administration (or variations of them). They include:

• Give highly concentrated Dextrose-containing solutions (50% Dextrose in water, or D50W) in an IVP bolus, titrated to effect, with doses ranging from 0.25g/kg to 0.5g/kg (up to 50g) and given over a short period of time.²
• Or, give a diluted dextrose-containing solution (typically 10% Dextrose in water, or D10W), titrated to effect and infused over a longer period of time (typically 5 to 15 minutes).³

The former appears to be more prevalent amongst North American providers, while the latter is more commonly utilized in the UK and Australia.

Does one method work faster than the other?

It’s fair to think that the administration of push-dose 50% Dextrose should result in a quicker resolution of hypoglycemia when we’re comparing to an infusion of D10W, but a study published in the Emergency Medicine Journal in 2005 suggests otherwise.⁴ The authors compared the time from administration of treatment to the return of normal consciousness (as defined by a Glascow Coma Score of 15) following the administration of incremental doses of 50 ml of D10W (5 grams) vs 10ml aliquots of D50W (5 grams), repeated as necessary. Both groups had almost the exact same time to recovery, averaging about eight minutes each,  despite the fact that the D10W group only required a median dose of 10 grams, while the D50W group received a median dose of 25 grams.

Will administering less dextrose result in rebound hypoglycemia?

An article submitted by Kiefer et al, published in Prehospital and Disaster Medicine in 2014, looked at the feasibility, safety, and efficacy of 10% Dextrose for prehospital treatment of hypoglycemia.⁵ They utilized 100 ml infusions of D10W (10 grams), and over an 18-week period they treated 164 patients, and only 29 of them (18%) required a second dose, and only one required a third dose. They found no reports of adverse events related to the use of D10W, and their analysis of the data suggested that there was “little or no short-term decay in blood glucose values after D10 administration.” Additionally, an article published in 2015 by Arnold et al in the Journal of Intensive Care Medicine demonstrated that the implementation of a careful, titratable approach to the management of hypoglycemia for critically ill patients resulted in less glycemic variability following treatment.⁶

What are the risks of over-correcting hypoglycemia?

While the data suggests that D10W use is unlikely to result in undertreatment, there’s significant data which shows that the routine use of 50% Dextrose results in an unpredictable over-correction of blood glucose levels. This isn’t new information, as a study published in 1986 looked at the rise in blood glucose levels in both diabetic and non-diabetic patients patients who received a standard bolus of 25 g D50W.⁷ They found that blood glucose levels rose anywhere between 2.06 mmol/L to 20.56 mmol/L, which equates to a range of 37 to 370 mg/dl.  A massive and sudden jump in glucose levels can have many deleterious side effects, including hyperglycemia, glycosuria, hyperosmolar syndrome, and increased morbidity/mortality for patients with concomitant sepsis, MI, or CVA.

Looking beyond some of the more obvious adverse effects of over-correcting hypoglycemia, “The Rollercoaster Effect” is a commonly described short-term side effect brought about following the prehospital administration of D50W, especially in brittle diabetics, or those who have difficulty in controlling their own blood sugars. The wide range of blood glucose levels experienced over a short span of time can precede weeks of glycemic variability, which can make insulin management remarkably more difficult, and often leads to repeated periods of hypo/hyperglycemia. This leads to increased EMS activation and emergency room visits over the coming days, and exposes the patient to more risk of short-term and long-term complications. Perhaps not surprisingly, some samples of patients report having much less incidence of this roller coaster effect after they’ve been treated by EMS personnel who utilized 10% Dextrose infusions, compared to times that they’ve been treated with push-dose D50W for management of their hypoglycemia.

Summary

Emergency medicine has come a long ways since the days of blindly giving every unconscious patient D50W (see: “the coma cocktail”). Use of 10% Dextrose appears to be safe, effective, and efficient for the emergent management of clinically significant hypoglycemia. Protocols and guidelines which recommend the use of D10W instead of D50W are becoming common practice worldwide, and expert opinion supports the implementation of this practice for prehospital providers. Benefits include cost efficiency, reduced glycemic variability, and a decreased risk of side effects including nausea, vomiting, and venous irritation or phlebitis.

For more on this topic, here are a few posts from various sources:

• Should EMS Still Use 50% Dextrose – Rogue Medic
• Is D50 Too Much of a Good Thing? A reappraisal of the safety of 50% dextrose administration in patients with hypoglycemia – JEMS
• D50 vs D10 for Severe Hypoglycemia in the Emergency Department – Academic Life in Emergency Medicine

References

1. American Diabetes Association. (2014). National diabetes statistic report. Retrieved from http://www.diabetes.org/diabetes-basics/statistics/
2. Canadian Diabetes Association Clinical Practice Guidelines Expert Committee. (2013). Hypoglycemia: Clinical practise guidelines. Canadian Journal of Diabetes, 37(1), S69-S71. Retrieved from http://guidelines.diabetes.ca/app_themes/cdacpg/resources/cpg_2013_full_en.pdf
3. Walden, E., stanisstreet, D., Jones, C., & Graveling, A. (2013). The hospital management of hypoglycaemia in adults with diabetes mellitus. Joint British Diabetes Society Guidelines. 1-31. Retrieved from http://orangejuicepr.co.uk/wp-content/uploads/2013/09/Hypo-guidelines.pdf
4. Moore, C., & Woollard, M. (2005). Dextrose 10% or 50% in the treatment of hypoglycaemia out of hospital? A randomised controlled trial. Emergency Medical Journal, 22, 512-515. doi:10.1136/emj.2004.020693
5. Kiefer, M. V., Hern, H. G., Alter, H. J., & Barger, J. B. (2014). Dextrose 10% in the treatment of out-of-hospital hypoglycemia. Prehospital and Disaster Medicine, 29, 190-194. doi:10.1017/S1049023X14000284
6. Arnold, P., Paxton, R. A., McNorton, K., Szpunar, S., & Edwin, S. B. (2015). The effect of a hypoglycemia treatment protocol on glycemic variability in critically ill patients. Journal of Intensive Care Medicine, 30(3), 156-60. doi: 10.1177/0885066613511048
7. Adler, P. M. (1986). Serum glucose changes after administration of 50% dextrose solution: Pre- and in-hospital calculations. American Journal of Emergency Medicine, 4(6), 504–506. http://dx.doi.org/10.1016/S0735-6757(86)80004-3