Drop the Beat! – Adenosine in SVT

Drop the Beat! – Adenosine in SVT

Supraventricular tachycardia (SVT) is defined as a dysrhythmia that originates proximal to (or ‘above’) the atrioventricular (AV) node of the heart. It commonly manifests as a regular, narrow complex (QRS interval < 120ms) tachycardia in affected patients. It is most frequently attributable to re-entrant electrical conduction through accessory pathways in the heart, with typical Electrocardiogram (ECG) findings depicting ventricular rates of 150 to 250 beats/min without the preceding P wave usually seen in sinus tachycardias. [1,2]

In the stable adult patient presenting with SVT, where no ‘red flags’ such as shock, altered mental state, ischemic chest pain or hypotension are present, management typically begins with an attempt to convert the rhythm back to its baseline sinus state using vagal manoeuvres.[3] Vagal manoeuvres such as the carotid sinus massage and the Valsalva manoeuvre are effective first-line therapies, terminating approximately 25% of spontaneous SVTs,[4] with the newer, modified Valsalva manoeuvre showing even greater efficacy of 43% conversion.[5] When these fail or are otherwise not feasible to use in patients, management involves the administration of a drug called Adenosine.

The Evolution of Adenosine Use for SVT

In 1927, studies found that the injection of extracts from cardiac tissue into animals appeared to decrease heart rates and that this effect was attributable to an ‘adenine compound’.[6] This compound was later identified as Adenosine, comprised of the purine-based nucleobase Adenine attached to a ribose sugar. Fifty years after its initial discovery, Adenosine began to emerge as a treatment for stabilizing SVTs and has remained a mainstay in its management ever since.[7]

Current guidelines recommend Adenosine for the management of SVT, usually administered through a peripheral intravenous (IV) access initially as a 6 mg bolus. Adenosine has an extremely short half-life (less than 10 seconds) and is therefore rapidly metabolized soon after it enters the body.[8] Therefore, IV dosage is commonly followed by a 20 mL rapid saline flush to facilitate the drug’s transport to cardiac tissue where it can act before being broken down into inactive metabolites. If the 6mg dose does not convert the SVT back to sinus rhythm, subsequent doses are given at 12 mg, also followed by 20-mL saline for rapid infusion.

Pro-Tip: Single syringe technique

Before we dive into the concept of the single syringe method of administering Adenosine, take a look at the segment above. How would you give 6 mg of Adenosine through an IV site, making sure a total of 20 mL saline follows right after, in enough time to make sure you don’t waste that precious 10-second half-life of Adenosine? In many places, one of the two methods are used to make this happen:

  1. Use an IV line to push Adenosine > remove syringe > push 10 mL saline using a pre-filled syringe > remove syringe > push 10mL saline using a second pre-filled syringe.
  2. Fancier places use what’s known as a stopcock, a device usually with 3 ports attached to the IV site. Adenosine syringe is attached to one port and a 10 mL saline flush is attached at a separate port. The process looks something like this: Push adenosine through stopcock port > turn stopcock to open saline port’s access to IV site > push 10 mL saline flush > push an additional 10 mL saline using second syringe or remainder of a 20 mL prefilled syringe.

Now we all know that nurses are indistinguishable from ninjas at times when handling IV medication. However, even the most experienced practitioner is not immune to the occasional stumble when switching between the various syringes and swivels required in the methods above. In fact, a study in 2018 found that, in pediatric patients, adenosine given using the stopcock method delivered suboptimal doses.[9]

In an attempt to improve administration time, a potential work-around was proposed where adenosine could be combined with the flush solution in one 20 mL syringe and pushed altogether.[10] This potentially eliminates any time wasted changing syringes and manipulating stopcocks, but does it still work the same? Fortunately, a few studies have demonstrated the feasibility of the single syringe method, with non-inferior efficacy compared to standard methods of drug administration.[11,12]

Caveats: Coffee Conundrums

Let’s talk a bit about dosage. We mentioned above that guidelines recommend starting at 6 mg and moving to 12 mg for subsequent dosages. These dosages assume uninhibited action of adenosine at its receptors which, unfortunately, may not always be the case in patients. What would inhibit adenosine’s activity, I hear you ask? You’ll want to put down that Caramel Macchiato because the answer (pause for dramatic effect) … is coffee – caffeine to be exact.

Caffeine is known to work by antagonizing adenosine receptors, thereby decreasing adenosine’s biologic effect.[13] A component in many frequently consumed beverages, such as coffee, tea, energy drinks and sodas, and with a half-life of approximately 4-5 hours, caffeine is very likely to be present in the bloodstreams of many Emergency Department patients (and doctors). A 2010 multi-centre study in Australia found that recent ingestion of caffeine less than 4 hours prior to a 6 mg adenosine bolus significantly reduced its effectiveness in treating SVT. [14]

This makes it all the more important to not only include information on any known recent beverage consumption during history taking for patients presenting with SVT, but also to potentially increase dosage for patients with a confirmed or suspected recent ingestion of caffeine. In such cases, it would be reasonable to start at 12 mg adenosine as the first dose, followed by 18 mg subsequent dosages to manage SVT.[15]

A 2010 multi-centre study in Australia found that recent ingestion of caffeine less than 4 hours prior to a 6 mg adenosine bolus significantly reduced its effectiveness in treating SVT.

References and Further Reading

  1. Bibas, L., Levi, M., & Essebag, V. (2016). Diagnosis and management of supraventricular tachycardias. CMAJ : Canadian Medical Association journal = journal de l’Association medicale canadienne, 188(17-18), E466–E473. https://doi.org/10.1503/cmaj.160079
  2. Mahtani, A. U., & Nair, D. G. (2019). Supraventricular Tachycardia. The Medical clinics of North America, 103(5), 863–879. https://doi.org/10.1016/j.mcna.2019.05.007
  3. Advanced Cardiac Life Support Provider Manual, American Heart Association, Mesquite 2016
  4. Lim, S. H., Anantharaman, V., Teo, W. S., Goh, P. P., & Tan, A. (1998). Comparison of Treatment of Supraventricular Tachycardia by Valsalva Maneuver and Carotid Sinus Massage. Annals of emergency medicine, 31(1), 30–35.
  5. Appelboam, A., Reuben, A., Mann, C., Gagg, J., Ewings, P., Barton, A., Lobban, T., Dayer, M., Vickery, J., Benger, J., & REVERT trial collaborators (2015). Postural modification to the standard Valsalva manoeuvre for emergency treatment of supraventricular tachycardias (REVERT): a randomised controlled trial. Lancet (London, England), 386(10005), 1747–1753. https://doi.org/10.1016/S0140-6736(15)61485-4
  6. Drury, A. N., & Szent-Györgyi, A. (1929). The physiological activity of adenine compounds with especial reference to their action upon the mammalian heart. The Journal of physiology, 68(3), 213–237. https://doi.org/10.1113/jphysiol.1929.sp002608
  7. Delacrétaz E. (2006). Clinical practice. Supraventricular tachycardia. The New England journal of medicine, 354(10), 1039–1051. https://doi.org/10.1056/NEJMcp051145
  8. Kazemzadeh-Narbat, M., Annabi, N., Tamayol, A., Oklu, R., Ghanem, A., & Khademhosseini, A. (2015). Adenosine-associated delivery systems. Journal of drug targeting, 23(7-8), 580–596. https://doi.org/10.3109/1061186X.2015.1058803
  9. Weberding, N. T., Saladino, R. A., Minnigh, M. B., Oberly, P. J., Tudorascu, D. L., Poloyac, S. M., & Manole, M. D. (2018). Adenosine Administration With a Stopcock Technique Delivers Lower-Than-Intended Drug Doses. Annals of emergency medicine, 71(2), 220–224. https://doi.org/10.1016/j.annemergmed.2017.09.002
  10. Hayes, B.D. (2019). ‘Trick of the Trade: Combine Adenosine with the Flush’. Academic Life in Emergency Medicine Blog Post https://www.aliem.com/trick-of-trade-combine-adenosine-single-syringe/
  11. Choi, S.C., Yoon, S.K., Kim, G.W., Hur, J.M., Baek, K.W., & Jung, Y.S. (2003). A Convenient Method of Adenosine Administration for Paroxysmal Supraventricular Tachycardia. Journal of the Korean society of emergency medicine, 14, 224-227.
  12. McDowell, M., Mokszycki, R., Greenberg, A., Hormese, M., Lomotan, N., & Lyons, N. (2020). Single-syringe Administration of Diluted Adenosine. Academic emergency medicine : official journal of the Society for Academic Emergency Medicine, 27(1), 61–63. https://doi.org/10.1111/acem.13879
  13. Ribeiro, J. A., & Sebastião, A. M. (2010). Caffeine and adenosine. Journal of Alzheimer’s disease : JAD, 20 Suppl 1, S3–S15. https://doi.org/10.3233/JAD-2010-1379
  14. Cabalag, M. S., Taylor, D. M., Knott, J. C., Buntine, P., Smit, D., & Meyer, A. (2010). Recent caffeine ingestion reduces adenosine efficacy in the treatment of paroxysmal supraventricular tachycardia. Academic emergency medicine : official journal of the Society for Academic Emergency Medicine, 17(1), 44–49. https://doi.org/10.1111/j.1553-2712.2009.00616.x
  15. Hayes, B.D. (2012). ‘Is the 6-12-12 adenosine approach always correct?’ Academic Life in Emergency Medicine Blog Post https://www.aliem.com/is-6-12-12-adenosine-approach-always/
Cite this article as: Mohammad Anzal Rehman, UAE, "Drop the Beat! – Adenosine in SVT," in International Emergency Medicine Education Project, September 14, 2020, https://iem-student.org/2020/09/14/adenosine-in-svt/, date accessed: March 9, 2021

Can I Eat This? – A Helpful Guide To Plant Toxicology – Cardiac Glycosides

CARDIAC GLYCOSIDES

Not only is the identification of toxic plants from their gross appearance a commonly tested topic in Emergency Medicine Board Exams, but it is also a necessary skill for doctors operating in institutions where an established Toxicology division does not exist or where the opinion of a specialist in the field is not immediately available.

This is the second part in a series of blog posts dedicated to providing you with original mnemonics and visual aids that serve to highlight a few classes of common toxic plants prominent for both their inclusion in the academic assessment as well as their prevalence in the community. These memory tools will attempt to highlight key features in the identification of well-known toxic plant species and are designed to aid clinicians from various regions of the globe as well as hone the skills of aspiring toxicologists.

Picture the Scene

A 21-year-old female is brought to your Emergency Department via ambulance due to persistent vomiting, abdominal pain, and some dizziness. She is visibly distressed, clutching her stomach, and reports having vomited at least six times over the past 3 hours. Her brother reports that she had been feeling ill with reported abdominal cramping and diarrhea for the past two days. Earlier that day, she had been given some herbal soup to help with her abdominal cramps by her grandmother, who had prepared it using leaves and flowers from the backyard garden. Soon after drinking the soup, the patient was reported to have multiple episodes of vomiting and began to experience some occasional dizziness, prompting contact of Emergency Medical Services and transfer to the hospital.

Upon initial examination, the patient’s vital signs were significant for a heart rate of 50 beats/minute with a Blood Pressure of 135/76 and spO2 of 95% on room air. No fever, abnormal breathing patterns, or signs of poor perfusion were noted. An Electrocardiogram (ECG) was done and revealed bradycardia, with a first-degree AV block, but no other T wave, QT, ST, or QRS segment abnormalities.

A laboratory workup was initiated, and the patient was given IV Atropine for her bradycardia. A Venous Blood Gas (VBG) was remarkable for hyperkalemia of 6.8 mEq/L with no acid/base disturbance. Therefore, treatment for hyperkalemia was initiated with IV Dextrose and Insulin as per standard management. When bradycardia persisted, a second dose of IV Atropine was given. The patient’s heart rate improved, but the blood pressure was noted to drop down to 95/68. After that, IV fluids were initiated, and the possibility of toxic ingestion explored by asking the patient’s brother for details of the ingredients present in the herbal soup.

The brother contacted the family at home and provided a picture of the plant used, as shown in Figure 1. The in-house Medical Toxicologist was shown the image and confirmed that the patient was suffering from Cardiac Glycoside toxicity secondary to the ingestion of an Oleander plant species.

Figure 1- Photograph of the flower used to make herbal soup. The flower was correctly identified as part of the toxic Oleander species.

Overview of Cardiac Glycoside Toxicity

Cardiac glycosides and related cardenolides represent a group of compounds that exhibit their effects primarily through their action on the Sodium-Potassium (Na+/K+) ATPase pump in cardiac myocytes and other tissues.[1] Inhibition of this pump, as outlined in Figure 2, causes an increase in intracellular Sodium (Na+), with subsequent activation of the Sodium-Calcium (Na+/Ca2+) exchanger, resulting in accumulation of intracellular calcium (Ca2+).

The increased intracellular Ca2+, along with direct stimulation of vagal tone, produces inotropic effects on the heart, increases ventricular ectopy, causes bradycardia, and impaired conduction through the atrioventricular (AV) node. At the same time, the inhibition of the Na+/K+ ATPase pump can lead to hyperkalemia.[2]

Cardiac glycosides are found in a variety of naturally occurring plant and animal species. Acute poisoning often presents with gastrointestinal manifestations (such as nausea, vomiting, abdominal pain or diarrhea), generalized body weakness, and dizziness. However, toxicity can also cause hyperkalemia and cardiotoxicity, represented by bradycardia, heart blocks, and various other dysrhythmias. Death is usually a result of ventricular fibrillation or tachycardia.[3]

Management involves addressing specific symptoms of severe disease. Atropine can be used to increase heart rate and reverse the effects on vagal tone in patients presenting with bradycardia. Reversal of toxicity can be achieved using Anti‐digoxin Fab as with Digoxin overdoses. Hyperkalemia can be managed using a combination of Insulin and dextrose solution to shift potassium back into cells. Activated charcoal may be used for initial decontamination, with Multidose activated charcoal for enhanced elimination.[4]

IV Calcium Chloride or Carbonate use in hyperkalemia was traditionally discouraged in patients suffering from cardiac glycoside poisoning. This was due to concerns that the additional calcium load would result in sustained cardiac contraction, termed as ‘the stone heart.’ However, several studies have since proven that such a phenomenon is unlikely to manifest in patients treated with IV Calcium.[5]

calcium mechanism

Figure 2- Mechanism of action of cardiac glycosides/digitalis drugs

Identifying Plants with Cardiac Glycoside toxicity

The most prominent species of plants known to contain cardiac glycosides include the foxglove plants Digitalis purpurea and Digitalis lanata, Oleander species (e.g., Nerium oleander and Thevetia peruviana), and Lily of the Valley (Convallaria majalis).[6] These plant species are commonly found in numerous tropical and subtropical countries around the world. Unfortunately, toxicity from accidental or intentional ingestion of their toxic leaves, roots, stems, and seeds is not uncommon and has, in several cases, lead to fatal outcomes for patients.[7-11]

cardiac glycosides plant identification

References and Further Reading

  1. Lingrel J. B. (2010). The physiological significance of the cardiotonic steroid/ouabain-binding site of the Na,K-ATPase. Annual review of physiology, 72, 395–412. https://doi.org/10.1146/annurev-physiol-021909-135725
  2. Benowitz, N. (2012). ‘Chapter 61- Digoxin and Other Cardiac Glycosides’ Poisoning & drug overdose. New York, N.Y.: McGraw Hill Medical.
  3. Kanji, S., & MacLean, R. D. (2012). Cardiac glycoside toxicity: more than 200 years and counting. Critical care clinics, 28(4), 527–535. https://doi.org/10.1016/j.ccc.2012.07.005
  4. Roberts, D. M., Gallapatthy, G., Dunuwille, A., & Chan, B. S. (2016). Pharmacological treatment of cardiac glycoside poisoning. British journal of clinical pharmacology, 81(3), 488–495. https://doi.org/10.1111/bcp.12814
  5. Levine, M., Nikkanen, H., & Pallin, D. J. (2011). The effects of intravenous calcium in patients with digoxin toxicity. The Journal of emergency medicine, 40(1), 41–46. https://doi.org/10.1016/j.jemermed.2008.09.027
  6. Hollman A. (1985). Plants and cardiac glycosides. British heart journal, 54(3), 258–261. https://doi.org/10.1136/hrt.54.3.258
  7. Bavunoğlu, I., Balta, M., & Türkmen, Z. (2016). Oleander Poisoning as an Example of Self-Medication Attempt. Balkan medical journal, 33(5), 559–562. https://doi.org/10.5152/balkanmedj.2016.150307
  8. S, Lokesh & Arunkumar.R,. (2013). A clinical study of 30 cases of Acute Yellow Oleander Poisoning. Journal of Current Trends in Clinical Medicine and Laboratory Biochemistry. 1. 29-31.
  9. Haynes, B. E., Bessen, H. A., & Wightman, W. D. (1985). Oleander tea: herbal draught of death. Annals of emergency medicine, 14(4), 350–353. https://doi.org/10.1016/s0196-0644(85)80103-7
  10. Janssen, R. M., Berg, M., & Ovakim, D. H. (2016). Two cases of cardiac glycoside poisoning from accidental foxglove ingestion. CMAJ : Canadian Medical Association journal = journal de l’Association medicale canadienne, 188(10), 747–750. https://doi.org/10.1503/cmaj.150676
  11. McVann, A., Havlik, I., Joubert, P. H., & Monteagudo, F. S. (1992). Cardiac glycoside poisoning involved in deaths from traditional medicines. South African medical journal = Suid-Afrikaanse tydskrif vir geneeskunde, 81(3), 139–141.
Cite this article as: Mohammad Anzal Rehman, UAE, "Can I Eat This? – A Helpful Guide To Plant Toxicology – Cardiac Glycosides," in International Emergency Medicine Education Project, July 17, 2020, https://iem-student.org/2020/07/17/cardiac-glycosides/, date accessed: March 9, 2021

Can I Eat This? – A Helpful Guide To Plant Toxicology – Anticholinergics

A Helpful Guide To Plant Toxicology – Anticholinergics

Introduction

Not only is the identification of toxic plants from their gross appearance a commonly tested topic in Emergency Medicine Board Exams, but it is also a necessary skill for doctors operating in institutions where an established Toxicology division does not exist or where the opinion of a specialist in the field is not immediately available.

Various mnemonics and visual aids serve to highlight a few classes of common toxic plants that are prominent for both their inclusion in the academic assessment as well as their prevalence in the community. This series will sequentially present a series of visual aids and mnemonics that highlight key features in the identification of well-known toxic plant species, designed to aid clinicians from various regions of the globe as well as hone the skills of aspiring toxicologists.

Picture the Scene

A 28-year-old male is brought to your Emergency Department (ED) via ambulance due to a reportedly altered mental status. His wife, who accompanied the paramedics, states that she found him lying unconscious in the grass near a basket he was using to collect berries during an outdoor picnic in the fields. He was arousable at the scene but has had a fluctuating level of consciousness up to arrival to the hospital.

Upon initial examination, the patient is observed to be irritable with irregular, shallow breathing. Vital signs revealed a Blood Pressure of 127/75 mmHg, Heart Rate of 140, Respiratory rate of 24, Temperature of 37.9 C, and spO2 96% on room air. His pupils were found to be equally reactive to light but were significantly dilated, and his mucus membranes were notably dry.

The patient’s wife, believing the cause for her husband’s condition to be ingestion of the berries from the field, approaches you and shows you pictures of the plants she had photographed near where her husband was found. (see below images)

anticholinergic
anticholinergic

Why we care about toxic plant identification

The intoxicated patient, while frequently encountered in the ED, poses a uniquely challenging puzzle for the average ED Physician. Beyond the routine resuscitative and supportive care, the doctor who receives a patient that has consumed an unknown substance is tasked with the burden of deducing what kind of substance was taken and the expected sequelae for the same.

Among the numerous causes of intoxication, ingested plant species are a particularly ambiguous class of toxic substances to identify because the vast majority of intoxicated patients consume them unknowingly with only vague descriptions for what they ate. Often, however, these plants are brought with the patient or are present on their person at the time of arrival.

Whereas a vast majority of cases that present to the Emergency Department may not exhibit similar tell-tale signs and symptoms, the patient in the case described above displayed clinical manifestations typical to an anticholinergic syndrome. Furthermore, the photographs provided by the patient’s wife confirmed the cause of his symptoms as toxic ingestion of berries from the plant species Atropa Belladonna.

Plants with anticholinergic toxicity

The two most important plant species that contribute to this class of toxicity are the Datura stramonium (Jimson weed, angel’s trumpet), and the Atropa Belladonna (Deadly nightshade). The seeds of D. Stramonium and the berry-like fruits and leaves of A. Belladonna contain scopolamine, hyoscyamine and atropine. Ingestion of these parts of the plant results in suppression of Acetylcholine in the body, manifesting as an antimuscarinic syndrome that is characterized by dry skin, altered mental status, flushing, decreased gastrointestinal motility, increased body temperature, tachycardia, pupillary dilation (mydriasis) and urinary retention.

The above constellation of symptoms is usually simplified by using the following phrases:

‘Mad as a Hatter’ – Delirium/Altered Mental Status
‘Hot as a Hare’ – Hyperthermia
‘Red as a Beet’ – Flushing
‘Bloated as a Toad’ – Decreased gut motility/Constipation
‘Blind as a Bat’ – Mydriatic pupils
‘Dry as a Bone’ – Dry skin/decreased sweat production

Management involves benzodiazepines for agitation, adequate hydration, and supportive care. Physostigmine is reserved for cases refractory to Benzodiazepines.

Plant Identification

A useful method of visual identification of the plant species outline above is as follows:

Black in green, Black on green Don’t trust their high, they inhibit Acetylcholine!

jimson weed - Datura Stromonium
Jimson Weed - Datura Stromonium
Atropa Belladonna
Deadly nightshade - Atropa Belladonna
jimson weed - Datura Stromonium
Jimson Weed - Datura Stromonium
Atropa Belladonna
Deadly nightshade - Atropa Belladonna

Mnemonic break-down

  • Black in green

    Black-colored toxic seeds reside within green ‘spiky’ fruit of Datura stramonium (Jimson weed)

  • Black on green

    Black-colored berry-like fruit (often mistaken for common blueberries) nestled on top of greenish petal-like structures and leaves of Atropa Belladonna (Deadly nightshade)

  • Don’t trust their high

    These plant species are commonly ingested for recreational purposes due to reported hallucinogenic properties

  • They inhibit Acetylcholine

    Both cause antimuscarinic syndrome: Dry skin, flushing, decreased GI motility, hallucinations, mydriasis, hyperthermia, tachycardia, urinary retention

Cite this article as: Mohammad Anzal Rehman, UAE, "Can I Eat This? – A Helpful Guide To Plant Toxicology – Anticholinergics," in International Emergency Medicine Education Project, April 6, 2020, https://iem-student.org/2020/04/06/anticholinergics/, date accessed: March 9, 2021

Reference

  • Lim, C.S., Aks, S.E. (2017), ‘Chapter 158 – Plants, Mushrooms and Herbal Medications’, Rosen’s emergency medicine 9th edition, Pg. 1957 – 1973

Salter-Harris Fractures

salter harris

Case Presentation

You are a medical student doing your first clinical shift as part of your Emergency Medicine rotation. A 9-year-old boy is brought in by his father after an injury to his left hand approximately 1 hour back. As explained by the father, the child was playing at home with his elder brother when his left index finger became caught in between a door that had quickly slammed shut. Following the injury, the child was reported to be crying due to severe pain, but had no lacerations or other associated injuries. He was rushed to the hospital and presented in the ED as an anxious, weeping boy who held out his left index finger and pointed to the tip as the region of maximal pain. Mild swelling was noted at the distal interphalangeal joint as well as at the tip of the affected finger. After appropriate analgesia was initiated, the child was sent to the Radiology department for X-ray imaging. The images obtained by the department are shown below in Figures 1.1 and 1.2.

Figure 1.1
Figure 1.1
Figure 1.2
Figure 1.2

Findings

Due to the lack of ideal positioning and suboptimal cooperation from the child and his parent, the radiology technician reports back to you stating that the best images they could obtain were the ones displayed above. Although unclear, you can confidently identify a small break in the bone at the base of the distal phalanx. You mention to the father that you see a fracture on the X-ray and report back to your Attending Physician. 

The Attending Physician decides to take a break from his morning coffee and utters the dreaded question: “What kind of fracture is this?” You try to recall a lecture you had about Salter-Harris fractures but cannot recall the classification of these fractures. As if on cue, the father of the patient finds you shuffling your weight in front of the Attending Physician and asks: “You said he has a fracture, will he have to get surgery for his finger?”

“What kind of fracture is this?”

Salter-Harris Fractures

Salter-Harris Fractures refer to fractures that involve the growth plate (physis). Therefore, these fractures are applicable specifically to the pediatric population, occurring most often during periods of rapid growth (growth spurts) when the growth plate is at its weakest, close to age ranges where children tend to participate in high-risk activities (11-12 in girls and 12-14 in boys) [1].

Originally described in 1963 by Dr Robert Salter and Dr Robert Harris [2], the now infamous Salter-Harris fractures are classified by the region of bone that is affected. Figure 2 displays the gross anatomy of a normal distal phalanx similar to the picture we examined in the X-ray, labelled to reflect the different areas of the bone relative to each other. The types of fractures that can occur are outlined below.

SALTER HARRIS ANATOMY
Figure 2
  • Type I Salter-Harris Fractures (Slipped)

    Type I fractures occur when a longitudinal force is applied across the physis, resulting in a displacement (“slip”) of the epiphysis from the metaphysis. Though relatively infrequent (5%), suspicion of this fracture is raised when the epiphysis is seen to either be displaced to the side of its original position relative to the metaphysis or when the gap between the two segments is widened.

Salter-Harris Type I
Salter-Harris Type I
  • Type II Salter-Harris Fractures (Above)

    Type II fractures are the most common (75%) of the Salter-Harris fractures. As with our patient above, this fracture only involves structures “Above” the epiphysis (Metaphysis + Physis/growth plate) with virtually no fracture or displacement of the epiphysis itself. Fortunately, type I and most type II fractures can be managed conservatively with cast immobilization and splinting.

Salter-Harris Type II
Salter-Harris Type II
  • Type III Salter-Harris Fractures (Lower)

    Type III fractures involve both the physis and the epiphysis. Although relatively uncommon (10%), the involvement of the epiphysis and consequent disruption of the growth plate makes this an intra-articular fracture that usually requires surgical fixation.

Salter-Harris Type III
Salter-Harris Type III
  • Type IV Salter-Harris Fractures (Through)

    Continuing the trend of worse outcomes with higher classification types, Type IV fractures involve all three layers (metaphysis, physis and epiphysis) and thus harbor more adverse outcomes and risks, with management primarily consisting of operative internal fixation. Similar to Type III fractures, this is an intra-articular fracture and also occurs at a similar rate of 10%.

Salter-Harris Type IV
Salter-Harris Type IV
  • Type V Salter-Harris Fractures (Rammed/Crushed)

    The rarest of all the Salter-Harris fractures, type V fractures occur due to high impact compression of the growth plate. Potential disruption of the germinal matrix and compromised vascular supply to the growth plate can lead to growth arrest.

Salter-Harris Type V
Salter-Harris Type V

A convenient method to recall the Salter-Harris classifications is outlined below using the mnemonic “SALTR”

Salter-Harris Classification
Salter-Harris Classification

Case Resolution

You ascertain the patient’s fracture to be a type II Salter-Harris fracture, justifying your answer to the Attending Physician by pointing out that the affected region in the X-ray is limited to the metaphysis and physis with no epiphyseal involvement. Recognizing the potential for parental misconceptions surrounding the diagnosis of fractures in pediatric patients [3], you approach the father and explain that, though there is a fracture present, there is likely no need for any surgical intervention. You advise that the left index finger will be immobilized using a splint and further elaborate on the unlikelihood of this injury to manifest any long-term developmental or growth arrest in the affected region.

References and Further Reading

  1. Levine RH, Foris LA, Nezwek TA, et al. Salter Harris Fractures. [Updated 2019 Aug 13]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2019 Jan
  2. Salter, Robert B.; Harris, W. Robert: Injuries Involving the Epiphyseal Plate, The Journal of Bone and Joint Surgery (JBJS): April 1963 – Volume 45 – Issue 3 – p 587-622
  3. Sofu H, Gursu S, Kockara N, Issin A, Oner A, Camurcu Y. Pediatric fractures through the eyes of parents: an observational study. Medicine (Baltimore). 2015;94(2):e407. doi:10.1097/MD.0000000000000407
Cite this article as: Mohammad Anzal Rehman, UAE, "Salter-Harris Fractures," in International Emergency Medicine Education Project, December 23, 2019, https://iem-student.org/2019/12/23/salter-harris-fractures/, date accessed: March 9, 2021

Learning from The Past

Toxicological Intimations from The Life and Works of Vincent Van Gogh

While his art is now highly renowned and eulogized, Vincent Willem Van Gogh spent his lifetime in considerable obscurity, fraught with numerous unprofitable endeavors, misfortunes and various illnesses leading up to his ultimate suicide at the age of 37. Years of extensive research into the possible ailments that plagued Van Gogh near the end of his life have revealed several factors that could have contributed to both his physical symptoms as well as the art style of his paintings.

van gogh
Vincent Willem Van Gogh - 1853-1890

Seizures

Much of Van Gogh’s neuropsychiatric symptoms, most notably his episodes of seizures, began around the time of his move to the city of Arles in southern France. While the pathology of his seizures has been most famously described by Henri Gastaut (1) as a form of temporal lobe epilepsy, the cause of his disorder remains uncertain. While it is reasonable to point to his poor diet and excessive alcohol consumption as the primary factor for his symptoms, a look into Van Gogh’s substance abuse indicates the possibility of several other causes for his convulsions.

  • Absinthe

    Dr. Hemphill (1961) was the first psychiatrist to link absinthe to Van Gogh’s illness (2). Absinthe is an alcoholic drink that became largely popular around the time of Van Gogh’s move to Paris. Traditionally, it comprises anise, fennel, wormwood and various herbs that undergo distillation. However, it is perhaps most popularly known for its supposed hallucinogenic properties, attributable to the chemical component Thujone. While the oil of wormwood is also known to have some convulsant properties (3), the majority of seizures that occur from consumption of absinthe are likely due to the toxic properties of Thujone. In the year 2000, it was revealed that Thujone possesses the ability to block the γ-aminobutyric acid type A (GABA A) receptor chloride channel (4). GABA works in the human body as a neurotransmitter that inhibits brain cell firing. Binding of GABA to its target receptor causes the influx of Chloride ions into cells, thereby producing inhibitory effects that most commonly cause sedation. Whereas anticonvulsant, sedative and anesthetic medication commonly stimulate the GABA receptor, Thujone antagonizes its effects, resulting in the increased excitation of brain cells that predisposes the body to seizures. Hemphill 1961 noted that, not only was Van Gogh’s consumption of absinthe excessive even by normal standards at the time, he was, in fact, more sensitive to its detrimental effects. To add further insult to injury, the continued use of absinthe during this time caused Van Gogh to develop pica. Pica, usually the consequence of a nutritional disorder, causes individuals to crave the consumption of items that are not considered a source of nutrition (e.g. stones, dirt, hair, paint, etc). The phenomenon usually occurs as a result of need-determined behavior secondary to malnutrition (5). Van Gogh’s pica involved a specific predilection toward consuming ‘turpene’ chemicals such as camphor and turpentine oils.

  • Camphor

    Wilfred Niels Arnold, a biochemist who analyzed the mental health and lifestyle of Vincent Van Gogh (6), connected several of Van Gogh’s odd habits to substance use. While he was hospitalized for having cut off his ear in 1888, the artist suffered from insomnia. In an effort to ameliorate his symptoms, reports suggest that he frequently placed camphor under his pillow to help him fall asleep. In addition to this, as described above, he also routinely ingested the substance as a consequence of his pica disorder. Although originally extracted from the barks of the Cinnamomum camphora tree, camphor is now produced only synthetically from components in turpentine and is found in non-prescription products such as lip balms, skin coolers (Vicks VapoRub) and various creams for muscle aches. During Van Gogh’s time, the substance was likely procured in an oil-based form that he both ingested and used topically. The mechanism of toxicity of camphor is unknown, but it has been associated with depression of the Central Nervous System, producing signs and symptoms such as confusion, hyperreflexia, headache, agitation and seizure. (7)

  • Turpentine

    With his increasing psychosis and advanced disease, Van Gogh’s odd consumption habits eventually extended to turpentine oils in the year 1889. Primarily attributed to his pica, Van Gogh was noted to drink the essence of turpentine as well as chew on his oil colors. Turpentine oils, produced by distilling the resin obtained from trees (mainly pine trees), are comprised of chemicals known as turpenes, most notably pinene. Inhalation of large quantities or ingestion of the compound has been shown to produce convulsions, gastric irritation, dizziness, agitation, cyanosis, coma and even death in patients. (8)

Vision Changes

Speculation exists surrounding the influence of drugs on Van Gogh’s vision. Though most authors now believe this to be a mostly unfounded connection, the predominant use of yellow (Figure 1) coupled with halo-like patterns (Figure 2) observed in some of Van Gogh’s later works have often been attributed to toxicity from digitalis.
Figure 1 – ‘Wheatfield With a Reaper’, 1889 - The abundance of yellow color in paintings such as this one has been said to have been associated with yellow vision seen with Digitalis toxicity
Figure 1 – ‘Wheatfield With a Reaper’, 1889 - The abundance of yellow color in paintings such as this one has been said to have been associated with yellow vision seen with Digitalis toxicity
Figure 2 – ‘The Starry Night’, 1889  - Turbulent flows and spirals used to represent stars have been linked to  ‘visual halos’ infamous in Digitalis toxicity
Figure 2 – ‘The Starry Night’, 1889  - Turbulent flows and spirals used to represent stars have been linked to  ‘visual halos’ infamous in Digitalis toxicity

While researchers believe there to be very little evidence of digitalis use in Van Gogh’s life, the association, at the very least, provides a useful mnemonic for medical students to familiarize themselves with the vision changes related to digitalis toxicity.

  • Digitalis

    Digitalis is a cardiac glycoside that primarily acts on the cardiac myocyte by inhibiting the Na+/K+ ATPase pump (outlined in Figure 3). Under normal conditions, this pump acts to exchange intracellular Na+ for K+. Therefore, blocking its activity results in an accumulation of intracellular Na+, which then allows the adjacent Na+/Ca2+ exchange channel to use the excess intracellular Na+ to bring in more Ca2+, resulting in a net increase in intracellular Ca2+ which acts as an inotrope for the cardiac cells.

Figure 3 – Mechanism of action of Digoxin/Digitalis on cardiac myocytes
Figure 3 – Mechanism of action of Digoxin/Digitalis on cardiac myocytes

Digitalis is said to purport its effects on vision through a similar mechanism. In this case, acting on Na+/K+ ATPase channels in the retina results in changes to the arrangement of rods and cones, thereby propagating the symptoms of ‘Xanthopsia’- a term used to describe a distortion in color perception with a tendency toward visualizing colored halos.

The presumption that Van Gogh was exposed to digitalis arose from the fact that, during those times, digitalis (extracted from the plant species, known commonly as the foxglove) may have been used to treat epilepsy. In fact, a plant resembling the foxglove was noted in Van Gogh’s portrait of his psychiatrist (Figure 4).

Figure 4 – Portrait of Dr. Gachet - Dr. Gachet, the psychiatrist, supposedly charged with the treatment of Van Gogh’s Epilepsy is seen painted here with a flower that intriguingly resembles the foxglove plant (from which Digitalis is derived)
Figure 4 – Portrait of Dr. Gachet - Dr. Gachet, the psychiatrist, supposedly charged with the treatment of Van Gogh’s Epilepsy is seen painted here with a flower that intriguingly resembles the foxglove plant (from which Digitalis is derived)

Worsening Mental State

Finally, great debate exists surrounding the cause for Van Gogh’s worsening mental state during the last years of his life. While everything from malnutrition to Acute Intermittent Porphyria has been implicated in the development of his cognitive decline, an interesting toxicological cause that may have been, at least in part, a culprit for his condition is lead poisoning.

  • Lead Poisoning

    The prevalence of lead-based paints in those times, coupled with Van Gogh’s peculiar consumption of oils and paint (pica), suggests both inhalation and ingestion as possible routes of lead exposure for Van Gogh. While exposure does not necessarily confirm poisoning in this case, some of Van Gogh’s evident neuropsychiatric decline does match the psychotic features associated with lead poisoning (also referred to as ‘Saturnism’). An outline of common manifestations of lead poisoning is mapped below (Figure 5)

Figure 5 - Features of lead poisoning
Figure 5 - Features of lead poisoning

Conclusion

Since most of the information obtained on Van Gogh’s illness is extracted from unreliable accounts and excerpts of letters he wrote toward the end of his life, any causal association, toxicological or otherwise, would ultimately be pure conjecture. At the very least, however, the relations outlined above provide an educational insight into the possibilities and mechanisms by which the substances prevalent in Van Gogh’s lifestyle could, in part, be contributory to his tendencies and even his psychiatric disease.

References and Further Reading

  1. Gastaut H: La maladie de Vincent van Gogh envisagée a la lumière des conceptions nouvelles sur l épilepsie psychomotrice. Ann Méd Psychol (Paris) 1956; 114:196–238
  2. Hemphill RE (1961): The illness of Vincent van Gogh. Proc Roy Soc Med 54: 1083–1088
  3. Simonetti G. Simon & Schuster’s Guide to Herbs and Spices. New York: Simon & Schuster; 1990. pp. 261–262
  4. Hold K M, Sirisoma S I, Ikeda T, Narahashi T, Casida J E. Proc Natl Acad Sci USA. Alpha-thujone (the active component of absinthe): gamma-aminobutyric acid type A receptor modulation and metabolic detoxification. 2000;97:3826–3831
  5. Richter CP. Self-selection of diets. Essays in Biology. Berkeley, CA: University of California Press; 1943
  6. Vincent van Gogh: chemicals, crises, and creativity, Author: Wilfred Niels Arnold, Published by Birkhäuser, 1992
  7. Phelan WJ, 3rd. Camphor poisoning: over-the-counter dangers. Pediatrics 1976; 57:428–431, Klingensmith WR. Poisoning by camphor. J Am Med Assoc 1934; 102:2182–2183
  8. Pande TK, Pani S, Hiran S, Rao VVB, Shah H, Vishwanathan KA (1994) Turpentine poisoning: a case report. Forensic Sci Int 65: 47–49
Cite this article as: Mohammad Anzal Rehman, UAE, "Learning from The Past," in International Emergency Medicine Education Project, August 7, 2019, https://iem-student.org/2019/08/07/learning-from-the-past/, date accessed: March 9, 2021

A Case Of Cyanide Poisoning From Vitamin B17

Since their advent in the 1930s, ‘vitamin pills’ have shown a steady rise in both variety and consumption patterns in patients. Guided by the promise of a healthier lifestyle and overall wellness, the use of vitamin supplements has become increasingly commonplace and you would be hard-pressed to find a patient who isn’t on some form of regular vitamin. Most of these nutritional adjuncts are either indicated for chronic conditions or, at the very least, harmless additions to daily regimens and do not usually warrant a second thought when described during patient encounters in the ED. However, not all supplements are as benign as they might seem. The following case report details the events that unfolded when a 45-year-old male patient accidentally ingested more tablets than were indicated for a vitamin he had purchased online.

Case Presentation

A 45-year-old male presented to the Emergency Department with complaints of fatigue, shortness of breath and anxiety following a possible over-ingestion of vitamin supplement tablets. As per the patient, he ordered a bottle of vitamin supplements online and admitted to misreading the instructions on the label. Instead of the recommended one tablet per day dose, he reported taking eight tablets for the first time earlier that morning. The tablets were bought without the need for prescription and, according to the patient’s research, were meant to be “good for promoting long life and preventing cancer.” Upon arrival to the ED, the patient was visibly anxious and mildly diaphoretic, stating that “I know I took too many tablets. Am I going to be okay?”

Physical Exam

Examination revealed a tired-looking patient with vital signs significant only for mild tachycardia of 105 and spO2 95% on room air. Otherwise, physical exam was normal. 

ABG

The initial ABG and preliminary lab tests revealed no significant findings, mildly elevated lactate of 1.8, for which the patient was placed on fluids with observation.

Being a particularly busy shift at the Emergency Department, the patient’s presentation coupled with his history of seemingly harmless vitamin ingestion, did not produce an immediate cause for concern. Nevertheless, he was monitored frequently until his investigations returned, during which time he remained clinically stable and without any subjective complaint besides a persistent feeling of fatigue.

A second ABG was performed and, despite the fluids, demonstrated a rise in his lactate levels to 2.6. By this time, the patient’s companion had made their way to the hospital, carrying with them the bottle of pills he reported he took prior to the onset of his symptoms. The bottle of supplements was filled to about ¾ of its capacity, with the label indicating that each capsule contained 250mg of Vitamin B17.

Given the persistence of fatigue and rising lactate, the physician decided to perform an internet search on whether any adverse effects were linked to the over-ingestion of vitamin B17. While most sources claimed the supplement was relatively safe, with many ayurvedic webpages praising the vitamin’s numerous benefits, it was soon found that the vitamin had been shown in studies to be associated with the development of cyanide toxicity when taken in large amounts.

However, this toxicity apparently only seldom manifested in individuals who only consumed vitamin B17. Instead, the cases of cyanide toxicities observed occurred more frequently in groups of patients who had concomitant consumption of Vitamin C.

Returning back to the patient, further history taking revealed that the patient had, in fact, consumed vitamin C for the past one month after he had about flu and had failed to mention it earlier as it had ‘slipped his mind at the time.’ Considering the risks evident in the patient’s ingestion history and his worsening fatigue (at 30 minutes after the ED arrival, the patient had now become increasingly somnolent with profuse diaphoresis, maintaining O2 saturation at 94-96% on room air), the decision was made to manage the patient as a case of cyanide toxicity and hydroxycobalamin was administered.

What is Vitamin B17?

Vitamin B17, also known as Amygdalin, is a naturally occurring chemical compound that is found most famously in the seeds of fruits such as apricots, bitter almonds, apples, peaches and plum (1). At the molecular level, amygdalin is formed as a chemical combination of Glucose, Benzaldehyde and Cyanide. The cyanide component in amygdalin can be released by the action of Beta-Glucosidase and Emulsin- both of which are not present in human tissues. However, microorganisms present in human intestinal linings have been found to possess similar enzymes that effectively promote cyanide release from the Amygdalin compound. The resulting cyanide toxicity is therefore almost 40 times more toxic by the oral route when compared with IV injection of the compound (2).

A modified form of amygdalin has been available under the brand name ‘Laetrile’ since the early 1950s as an alternative treatment to fight cancer, though most studies have failed to show any such benefit in humans (3). While the US FDA continues to insist on the drug’s obvious cyanogenic effects, there exist numerous advocates promoting the potential benefits of taking Amygdalin. Despite years of regulation on the original Laetrile supplement, unregulated forms of Amygdalin (or Vitamin B17 as it is often called) continue to circulate the market and are available in most outlets without the need for a prescription.

Since the toxicity of amygdalin depends on intestinal conversion, peak levels of cyanide are usually reached at around 2 hours post-ingestion. A curious phenomenon was evidenced in studies which found that the conversion of amygdalin to cyanide in vitro was further accelerated when amygdalin was ingested with foods containing beta-glucuronidase (such as bean sprouts, peaches, celery, and carrots) or with a concurrent intake of high doses of vitamin C (4,5).

Cyanide Toxicity - Principles & Management

Oral intake of 500 mg of amygdalin may contain up to 30 mg of cyanide (6). A minimum lethal dose of cyanide is approximately 50 mg or 0.5 mg/kg body weight (7). Our patient had ingested eight 250mg tablets, totaling 2000mg of amygdalin, thereby exposing him to a dose of cyanide well above the lethal dose.

Cyanide has a famously dangerous mechanism of toxicity. It binds to the ferric ion on cytochrome oxidase in mitochondria and blocks the electron transport chain, thus halting oxidative metabolism and leading to cell death by interfering with mitochondrial oxygen utilization leading to cell death, hypoxia and lactic acidosis (8). Mild to moderate cases of cyanide toxicity manifest as tachycardia, headache, confusion, nausea, and weakness. Severe cases may present with cyanosis, coma, convulsions, cardiac arrhythmias, cardiac arrest, and death.

Treatment involves addressing the patient’s vitals, oxygen saturation and acidosis as well as administering the appropriate antidote as detailed in the Table below. A sequence of these medications can be incorporated or hydroxycobalamin can be administered alone, as was done in the case above.

Cyanide Toxicity Medication

Medication

Dosage

Mechanism of Action

Notes

Amyl Nitrite pearls
0.3mL (1 amp) inhaled prior to establishing IV
Induces methemoglobinemia (binds cyanide)
First component of cyanide kit Discontinue once IV started
Sodium Nitrite
300mg (10 mg/kg) IV over 3-5 minutes
Induces methemoglobinemia (binds cyanide)
Second component of cyanide kit Do NOT use if suspected concurrent Carbon Monoxide poisoning
Sodium Thiosulfate
12.5 g IV over 10-20 minutes
Binds cyanide to form thiocyanate (less toxic) which is excreted in urine
Third component of cyanide kit
Hydroxycobalamin
5 g IV over 15 minutes
Binds cyanide to form cyanocobalamin (Vitamin B12) which is excreted in urine
Can be used as a single agent May cause transient hypertension

Conclusion

As with most cases of toxic ingestion, the key to effective management is appropriate stabilization followed by rapid identification of the potential toxicity through focused history taking and physical examination of the patient. In cases such as the one outlined above, where the ingested agent is unfamiliar but poses a potential threat, efforts should be made to probe deeper into the potential side effects, interactions and toxicities of such drugs and the Poison Control Center contacted immediately when and where available to expedite successful treatment of affected patients.

For our patient, the decision to administer hydroxycobalamin was followed by admission to the ICU with serial investigations done to monitor for any metabolic derangements. The patient showed remarkable improvement in his symptoms over the course of 24 hours and was eventually discharged in a stable condition.

References and Further Reading

  1. National Center for Biotechnology Information. PubChem Compound Database; CID=656516,
  2. https://pubchem.ncbi.nlm.nih.gov/compound/656516
    http://toxnet.nlm.nih.gov/cgi-bin/sis/search2/r?dbs+hsdb:@term+@DOCNO+3559
  3. Laetrile (Vitamin B17 or Amygdalin): Benefits, Myths and Food Sources, https://www.healthline.com/nutrition/laetrile-vitamin-b17
  4. Bromley J., Hughes B. G. M., Leong D. C. S., Buckley N. A. Life-threatening interaction between complementary medicines: Cyanide toxicity following ingestion of amygdalin and vitamin C. Annals of Pharmacotherapy. 2005;39(9):1566–1569. doi: 10.1345/aph.1E634
  5. Conjoint use of laetrile and megadoses of ascorbic acid in cancer treatment: possible side effects, 1979 Sep;5(9):995-7, PMID: 522711
  6. Newton G. W., Schmidt E. S., Lewis J. P., Conn E., Lawrence R. Amygdalin toxicity studies in rats predict chronic cyanide poisoning in humans. Western Journal of Medicine. 1981;134(2):97–103.
  7. Shragg T. A., Albertson T. E., Fisher C. J., Jr. Cyanide poisoning after bitter almond ingestion. Western Journal of Medicine. 1982;136(1):65–69
  8. Physician Beware: Severe Cyanide Toxicity from Amygdalin Tablets Ingestion- 2017; 2017: 4289527, DOI: 10.1155/2017/4289527
Cite this article as: Mohammad Anzal Rehman, UAE, "A Case Of Cyanide Poisoning From Vitamin B17," in International Emergency Medicine Education Project, July 15, 2019, https://iem-student.org/2019/07/15/a-case-of-cyanide-poisoning-from-vitamin-b17/, date accessed: March 9, 2021

Lover’s Fracture

A 35-year-old construction worker was brought in by the ambulance to the Emergency Department. He was reported to have fallen from scaffolding at the height of approximately 4 meters and landed onto the concrete floor below feet first. He was found conscious by paramedics but in obvious pain, holding his right leg. Upon initial examination in the ED, the patient remains vitally stable but complains of severe, persistent pain in his right ankle and heel. After adequate analgesia, an X-ray of the right ankle and foot revealed signs of a calcaneal "Lover’s" fracture (Figure 1).

Figure 1
Figure 1: Image courtesy of Annelies van der Plas, and J.L. Bloem - http://www.startradiology.com/internships/general-surgery/ankle/x-ankle/

Calcaneal Fractures

Before we begin our discussion on calcaneal fractures, it is important to highlight the major anatomical structures visible on a standard X-ray of the ankle and foot.

Figure 2
calcaneus and foot anatomy

Figure 2 shows a lateral x-ray of the right ankle, demonstrating the calcaneus as the bone – commonly referred to as the heel – that makes up the majority of the hindfoot.

As would be expected, the size and position of the calcaneus predispose the bone to various forms of injury. A calcaneal fracture is most often sustained after a road traffic accident or a fall from significant height onto the feet as was the case with our patient. Due to the mechanism of injury, it is often colloquially dubbed as “Lover’s fracture” or the “Don Juan fracture”(1).

Epidemiology

Among fractures of the hindfoot, calcaneal fractures comprise 50-60% of all tarsal bone fractures (2). These fractures are usually intra-articular (3) and occur more commonly in young men aged between 20 and 40 years. Diseases which decrease bone density, such as osteoporosis, invariably increase the risk for development of the fracture when injury occurs.

Patient evaluation

Patients with calcaneal fractures will often present in severe pain, though they may not always be able to localize the exact source for their pain. Swelling at the ankle or heel along with bruising (ecchymosis) can also be expected. Due to the mechanism of fall, injury usually occurs bilaterally. Most patients are unable to bear any weight onto the affected limb.

The lower extremity or extremities in question should undergo a thorough neurovascular exam, as diminished pulses distal to the injury (dorsalis pedis) could indicate arterial compromise and mandate aggressive investigation with angiography or Doppler scanning. Though the gold standard for diagnosing calcaneal fractures remains a CT scan, a plain film X-ray is usually obtained first which should include an Antero-Posterior (AP), a lateral, and an oblique view.

Bohler’s Angle and Critical Angle of Gissane

Historically, physicians would measure Bohler’s angle and the critical angle of Gissane in cases where a calcaneal fracture was not clearly evident on a plain X-ray. Outlined in Figure 3, a calcaneal fracture would be suspected if Bohler’s angle was below 20 degrees or the critical angle of Gissane was noted to be more than 140 degrees. Bohler’s angle was found to be a lot more diagnostically reliable when compared to the critical angle of Gissane (4). However, both these methods of diagnosis are now considered obsolete and the same research that studied that utility of the angles found that Emergency Physicians were able to accurately identify calcaneal fractures approximately 98% of the time without the measurement of either angle.

Figure 3
853 - bohler angle - calcaneus
854 - Gissane angle- calcaneus

Figure 3- Bohler’s Angle and Critical angle of Gissane

Management

The goal of initial management in the Emergency Department is centered on adequate pain relief, immobilization and wound care (including antibiotics when there are signs of a contaminated wound). [See the link for open fractures and antibiotic choices.]

An important point to note is that the mechanism of injury in calcaneal fractures (namely fall from height) is a form of axial loading. The energy from landing on the ground will often be transmitted up through the body, usually to the spine causing compression fractures of the vertebrae. The patient, however, may not complain about pain in other areas due to the overwhelming and distracting pain in the calcaneus. Therefore, all calcaneal fractures should be managed with a high index of suspicion for associated injuries.

Other potential complications include compartment syndrome, wound infection, malunion and osteomyelitis. All patients diagnosed to have calcaneal fractures should be managed by a multidisciplinary team that includes an Orthopedic Surgeon to ensure definitive management and repair of the fracture.

Take Home Points

  • High energy impact with axial loading, usually from a road traffic accident or a fall from height should raise suspicion of a calcaneal fracture.

  • Perform a thorough evaluation of the site of injury and suspect associated injuries (check the spine and remember to check the other foot for concomitant injury).

  • Maintain adequate analgesia (these fractures hurt!) and involve the Orthopedic Surgeon as soon as the diagnosis is made.

References and Further Reading

  1. Lee P, Hunter TB, Taljanovic M. Musculoskeletal colloquialisms: how did we come up with these names? Radiographics. 2004;24 (4): 1009-27. doi:10.1148/rg.244045015
  2. Davis D, Newton EJ. Calcaneus Fractures. [Updated 2019 Mar 13]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2019 Jan
  3. Jiménez-Almonte JH, King JD, Luo TD, Aneja A, Moghadamian E. Classifications in Brief: Sanders Classification of Intraarticular Fractures of the Calcaneus. Clin. Orthop. Relat. Res. 2019 Feb;477(2):467-471
  4. Jason R. K., Eric A. G., Gail H. B., Curt B. H. & Frank L. Boehler’s angle and the critical angle of gissane are of limited use in diagnosing calcaneus fractures in the ED. American Journal of Emergency Medicine. 24, 423–427 (2006)
Cite this article as: Mohammad Anzal Rehman, UAE, "Lover’s Fracture," in International Emergency Medicine Education Project, June 28, 2019, https://iem-student.org/2019/06/28/lovers-fracture/, date accessed: March 9, 2021