Author Archives: Janeske Vonkeman

An EM Approach to Syncope in Adults

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Medical Student Pearl

Samarth Fageria

Med 3

Memorial University of Newfoundland Class of 2024

Reviewed by Dr. J Gross

Copy Edited by Dr. J Vonkeman

Pdf Download: EMSJ An EM Approach to Syncope by SFargeria

 

Case

A 60-year-old male presented to the ED after experiencing recurrent episodes of syncope. The first episode occurred at a convenience store in an upright position. He denied prodrome and exertional activity at the time of syncope. After a transient loss of consciousness, he woke up confused with urinary incontinence. He felt nauseous and had emesis in the ambulance on the way to ED. He had two more episodes of syncope over the span of two hours. On assessment in the ED, he endorsed a past history of light-headedness preceded by laughing and holding his breath. He denied dyspnea and chest pain. He had no significant past medical history. There was no family history of cardiovascular disease and syncope, and social history was unremarkable.

 

On examination, he was alert and oriented. He had a minor laceration on his forehead from the fall. His respiratory and cardiovascular exams were unremarkable, neurological exam was normal. In the ED, his blood work was unremarkable. He was placed on telemetry when he had two more episodes of syncope. The monitor showed 20-second-long sinus pauses corresponding with the syncopal episodes. Cardiology was consulted and he was temporarily placed on intermittent transcutaneous pacing.

 

 

Differential Diagnosis of Syncope2

True Syncope

1. Reflex (autonomic hypersensitivity)

  • Vasovagal, carotid sinus hypersensitivity, situational

2. Orthostatic hypotension

  • Volume depletion, autonomic failure

3. Cardiac

  • Valvular (aortic stenosis, mitral stenosis), dysrhythmias (bradyarrhythmia, ventricular tachyarrhythmia, supraventricular tachyarrhythmia), mechanical (pacemaker dysfunction), cardiomyopathy, infiltrative (eg. hemochromatosis, sarcoidosis, amyloidosis), acute MI, ARVC, cardiac tamponade, acute aortic dissection

Other Causes

1. Medication/ Drug-induced

  • Anti-hypertensives, QT prolonging meds, insulin, alcohol, anti-depressants, anti-glycemic agents, diuretics, anti-anginal agents, etc

2. Transient Loss of Consciousness (TLOC)

    • Traumatic brain injury, seizure disorders, intoxications, hindbrain TIA, conversion disorders and metabolic abnormalities

 

Background

Syncope is defined as a brief, sudden, transient loss of consciousness due to cerebral hypoperfusion1. The three broad categories of syncope are reflex, orthostatic and cardiac syncope. The most common cause of cardiac syncope includes dysrhythmias1. A good past medical history of cardiovascular disease is important as it is 85-94% sensitive and 64-83% specific in predicting a cardiac etiology of syncope1.

Diagnostic Workup

Diagnostic workup for syncope requires a thorough history, physical exam, and a 12-lead ECG. Cardiac monitoring is necessary in patients that present to ER with an acute presentation of syncope, and a strong suspicion for cardiac etiology2. History should consist of identifying high-risk features that warrant a prompt cardiology consult2. A detailed HPI should consist of asking about an absence of a prodrome, exertional or supine syncope, concomitant trauma, past medical history of cardiovascular disease and family history of sudden cardiac death (<50 years)2. Low-risk features include presence of a prodrome, specific triggers (eg. dehydration, stress, laughter), syncope while upright and the absence of cardiovascular disease2. Vital signs and a cardiac exam should be completed2. If cardiac causes of syncope cannot be ruled out on first assessment, a 12-lead ECG should be placed to assess for dysrhythmias or conduction disease, and serial troponin values should be collected2.

 

Though there are multiple clinical decision rules for syncope, the following have been externally validated: Evaluation of Guidelines in Syncope Study (EGSYS), San Francisco Syncope Rule and Osservatorio Epidemiologico sulla Sincope nel Lazio (OESIL)1. Patients that are stratified as high risk require admission for further evaluation. EGSYS predicts the probability of cardiac syncope at two years based on abnormal ECG findings (eg. BBB, sinus bradycardia), heart disease (eg. ischemic, structural), palpitations before syncope, as well exertional and positional syncope, symptoms of prodrome (nausea/vomiting) and predisposing/precipitating factors1. An admission is warranted if the patient scores a three or higher as there is a 21% mortality risk at two years1. The OESIL risk score estimates a 1-year all-cause mortality in patients presenting with syncope1. The factors include age (>65), history of cardiovascular disease, lack of prodrome and abnormal ECG characteristics (eg. BBB, AV conduction disorders and hypertrophy)1. Admission is warranted for one or more variables1. The Canadian Syncope Risk Score can be used in patients presenting to ER with syncope to predict a 30-day serious adverse events2.  It consists of factors such as abnormal QRS axis, corrected QT interval >480 ms, elevated troponin (>99th percentile of normal population) and ED diagnosis based on evaluation to stratify patients into risk categories: very low (-3 to -2), low (-1 to 0), medium (1 to 3), high (4 to 5) and very high (6 to 11)2.

The Canadian Journal of Cardiology recommends a disposition algorithm for patients presenting to ER with syncope that is based on history of a serious medical condition and high-risk features3. Figure 1 illustrates an approach to disposition from the ER. Patients that have an unclear etiology and intermediate risk should be considered for an urgent cardiology assessment.

 

Figure 1: A disposition plan for patients presenting to the ER with syncope (Canadian Cardiovascular Society 2020).

Best Practice for Treatment

Given the benign course, treatment for vasovagal syncope is based on lifestyle modification, education and reassurance2. Lifestyle modification consists of educating patients on identifying and managing prodromes early and managing triggers (eg. dehydration, defecation, micturition, laughing, coughing and crowded environments)2.

Treatment for orthostatic syncope also relies on lifestyle modification, education and reassurance2. Lifestyle modification consists of re-adjusting diuretics, ACE-inhibitors, angiotensin receptor blockers, calcium channel and beta blockers to ensure optimal blood pressure and hydration control2.

Managing cardiac syncope requires addressing the underlying etiology through antiarrhythmic medications (eg. tachyarrhythmias), cardiac pacing (eg. bradyarrhythmias), catheter-directed ablation and ICD insertion1. Cardiac pacemaker therapy is indicated for patients that have intermittent sinus node disease if correlation is identified between sinus pauses on ECG and syncope3. Selected patients that are diagnosed with the bradycardia-tachycardia form of sick sinus syndrome, can benefit from a percutaneous cardiac ablative technique3.  Dual-chamber pacing is recommended for patients with sinus node dysfunction provided there is an increased risk of AV block4.

Case continued

The patient was admitted and had no further asystole after receiving atropine and intermittent transcutaneous pacing. He was accepted for a dual-chamber pacemaker insertion and was discharged with the diagnosis of syncope with sinus arrest and vagal overtones.

Take Home Points

  1. Patients presenting to the ER with new-onset syncope require a thorough history and physical exam to rule out cardiogenic causes.
  2. Validated clinical decision-making tools can be helpful to supplement clinical judgement for assessing the risk of a future cardiac event, identifying the need for a cardiology consult and creating a disposition plan.

References

  1. Runser LA, Gauer RL, Houser A. Syncope: Evaluation and Differential Diagnosis. Am Fam Physician. 2017;95(5):303-312. https://www.aafp.org/pubs/afp/issues/2017/0301/p303.html#:~:text=A%20standardized%20approach%20to%20syncope,%2C%20physical%20examination%2C%20and%20electrocardiography
  2. UpToDate. www.uptodate.com. https://www.uptodate.com/contents/syncope-in-adults-clinical-manifestations-and-initial-diagnostic-evaluation
  3. Sandhu RK, Raj SR, et al. Canadian Cardiovascular Society Clinical Practice Update on the Assessment and Management of Syncope. Can J Cardiol. 2020;36(8):1167-1177. doi:10.1016/j.cjca.2019.12.023 https://www.onlinecjc.ca/article/S0828-282X(19)31549-1/fulltext
  4. Brignole M, Moya A, de Lange FJ, et al. 2018 ESC Guidelines for the diagnosis and management of syncope. Eur Heart J. 2018;39(21):1883-1948. doi:10.1093/eurheartj/ehy037https://academic.oup.com/eurheartj/article/39/21/1883/4939241?login=false
  5. Dakkak W, Doukky R. Sick Sinus Syndrome. In: StatPearls. Treasure Island (FL): StatPearls Publishing; July 18, 2022. https://www.ncbi.nlm.nih.gov/books/NBK470599/

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Under pressure: Anorectal abscesses… to drain or not to drain?

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Resident Clinical Pearl

Victoria Landry

iFMEM R3

Reviewed by Dr. J Mekwan

Copy Edited by Dr. J Vonkeman

PDF Download: EMSJ Anorectal Abscess by VLandry

Case

A 57yo male presents to the emergency department with complaints of a lump near his rectum and pain with sitting which developed over the past week. He is afebrile with normal vital signs. He tells you that about 6 months ago this same thing occurred and drainage was attempted in the ED but was unsuccessful. A colorectal surgeon subsequently drained it successfully under local anesthetic in clinic later the same day. He has had no recurrence of symptoms until the past week. He smokes and has hypertension controlled with medication but is otherwise healthy.

He denies pain with defecation and has not had any rectal bleeding nor changes in bowel habits. He feels otherwise well and denies fevers or chills.

On exam you find a tender firm mass in the subcutaneous tissue lateral to his rectum on the left side. There is minimal overlying erythema and no fluctuance.

Key Point #1: Always do a Digital Rectal Exam

  • Palpate in all directions to localize area of tenderness1
  • Should be unremarkable after you get past the anal verge2 – if tenderness, mass, induration past anal verge, do a CT scan to assess for deeper abscess

You think back to your perirectal anatomy and recall the spaces where abscesses can develop.

Figure 1: Transverse anorectal anatomy3

Figure 2: Longitudinal anorectal anatomy3

 

  Perianal Ischiorectal Intersphincteric Supralevator Postanal
Incidence 40-45% 20-25% 20-25% <5% 5-10%
Location Outside anal verge, red, swollen, fluctuant, easily palpable at anal verge Between rectum and ischial tuberosity, outside sphincters, palpable through rectal wall or lateral to anal verge on buttocks Lower rectum, between sphincters, inferior to levator ani (tender indurated mass in rectum) Above levator ani (tender indurated mass in rectum) Posterior to rectum, Deep to external sphincter, inferior to levator ani
Symptoms Painful perianal mass Buttock pain Rectal fullness, throbbing, worse with defecation Perianal and buttock pain Rectal fullness and pain near coccyx
Fever, ↑WBC No Possibly Possibly Yes Yes
Fistula formation ++ + +++ +++ –
ED I&D Yes Possibly: I&D/needle aspiration only if abscess is superficial and fluctuant No No:

Consult surgery for urgent drainage

 No

Table 1: Types of abscesses3

** caution as mass may be bigger/deeper than anticipated – prudent to defer to surgery for their expertise

Figure 3: Anorectal abscess locations4

Key Point #2: Get a CT scan to define the abscess for any of the following2

  • Unable to see the abscess superficially
  • Patient is unable to tolerate the DRE due to significant pain
  • Induration, bogginess or tenderness in the supralevator space (above the sphincter muscle)
  • If the extent of the abscess is uncertain4

Note: can use POCUS to evaluate location of abscess, but caution against false reassurance as to extent/depth, and safer to rely on palpable fluctuant mass to determine if I&D is safe

 

Figure 4: Perianal abscess on CT1

Management5

  • Simple, isolated, fluctuant perianal abscess4
    • Bedside I&D
    • Goal is to relieve the pus under pressure2
  • Ischiorectal abscess2
    • Can consider I&D only if superficial, but prudent to get a CT first
    • Consult surgery for their expertise
  • Intersphincteric, Supralevator, Postanal
    • CT to define the abscess
    • Consult surgery

Key Point #3: Err on the side of caution

Only do I&D in the ED if the following criteria are met3 [3]

  • Perianal abscess (+/- ischiorectal) is small and superficial
  • Patient
    • Is Well-appearing
    • Is Cooperative
    • Has no complicating factors (DM, immune compromise etc.)

Incision and Drainage of simple perianal abscess2

  • Local anesthetic – lidocaine with epinephrine
    • Infiltrate superficial skin where you will poke with needle
    • occasionally procedural sedation is needed3
  • Needle poke +/- aspiration (18guage) or pinpoint incision over painful region to localize purulent pocket4
  • Inject more local anesthetic2
  • Enlarge the incision
    • Make incision as close to anal verge as possible to minimize the length of any potential fistula2,5,6
    • Cruciate (with trimming of the flaps) or elliptical incision over fluctuant part of abscess is preferred over a linear incision to keep incision open and draining without painful packing2
    • If linear only, will need packing to prevent premature closure
    • Note: loop drainage technique not recommended for I&D in the ED7
  • Break up loculations with finger (increased tactile feedback and better control) or hemostat +/- irrigation with saline7
  • Cover with bulky dressing4
  • Ideally, close follow up until complete healing (up to 8wks) to monitor for recurrence and for fistula formation5
  • Uncomplicated perianal abscesses do not require antibiotics after successful drainage2.

Figure 5: Cruciate incision4

Instruct the patient to WASH8

  • W – warm water sitz baths 5-10min BID-QID PRN, with Epsom salts (start the day after I&D)
    • Water >40°C helps decrease anal canal pressure
  • A – analgesics (NSAIDs, topical 1-2% lidocaine gel)
  • S – stool softeners (PEG, senna)
  • H – high fiber diet +/- fiber supplement
  • Uncomplicated perianal abscesses do not require antibiotics after successful drainage2.

Indications for antibiotics (+/- tetanus +/- admission to hospital with surgical consult)4

  • Surrounding cellulitis
  • Immune compromise
  • Valvular heart disease
  • Diabetes
  • Systemic symptoms (Fever, ill appearing, leukocytosis)
  • Elderly

Note: Send off a wound culture before giving antibiotics

Antibiotic choice5:

  • Systemic: piperacillin-tazobactam
  • Oral: Amoxicillin-clavulanate or Metronidazole + ciprofloxacin

A word on fistulas

  • Fistulas are a connection between two epithelium-lined surfaces, characterized by persistent or recurrent anal drainage. They are seen in Crohn’s, TB, cancer, FB reactions, and as a complication of anorectal abscesses. Treatment is surgical3
  • ~50% of anorectal abscesses form a fistula overtime2
  • Suggest surgical consultation after drainage of perianal abscess as fistula formation is common4
  • Fistulas may be missed on CT scan; MRI is more sensitive for diagnosis2     

Take home points: 

  1. Always do a rectal exam as part of the initial evaluation
  2. Have a low threshold to get a CT scan to define the abscess
  3. Reserve I&D in the ED for perianal abscesses that are visible, superficial and fluctuant

References

  1. Farah, Jennifer, Mason, Jessica, and Werner, Jessie, “Perirectal Abscess & Pilonidal Cyst.” [Online]. Available: https://www.emrap.org/episode/gastro/perirectal
  2. Jhun, Paul and Cologne, Kyle, “Anorectal Infections,” HIPPO EMRAP, vol. 15, no. 9, pp. 17–18, Sep. 2015.
  3. Parrillo, “Anorectal Emergencies,” presented at the EMRAP, Temple University Hospital EM Residency, Feb. 2004. [Online]. Available: https://www.emrap.org/episode/september2004/anorectal
  4. Berberian J.G., & Burgess B.E. Tintinalli J.E., & Ma O, & Yealy D.M., & Meckler G.D., & Stapczynski J, & Cline D.M., & Thomas S.H.(Eds.), “Anorectal disorders,” in Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e, McGraw Hill, 2020. [Online]. Available: https://accessmedicine-mhmedical-com.ezproxy.library.dal.ca/content.aspx?bookid=2353&sectionid=219642697
  5. Streitz Matthew, Long Brit, “Anorectal Disease,” in CorePendium, Burbank, CA: CorePendium, LLC, 2022. [Online]. Available: https://www.emrap.org/corependium/chapter/reclLjrt5HvPGSIDv/Anorectal-Disease#h.d78nqbylr3x
  6. Bleday, Ronald, Perianal and perirectal abscess. uptodate.com, 2022. [Online]. Available: https://www.uptodate.com/contents/perianal-and-perirectal-abscess
  7. Cavanaugh, Megan and Ormon, Rob, “Anorectal Disorders.” [Online]. Available: https://www.emrap.org/episode/april2011/anorectal
  8. Lipp, Chris, “Anorectal Disorders.” [Online]. Available: https://canadiem.org/crackcast-e096-anorectal-disorders/

 

 

 

 

 

 

 

 

 

 

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EM Grand Rounds: Practical Points in Aboriginal Health

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Dr. Tiffany O’Donnell (MD, CCFP, C. ISAM)

Andrea Paul-McCoy (Dalhousie NP Student, RN BN)

 

Resources:

Commonly Used Indigenous Terms & Phrases You May Not Be Familiar With

The Indian Act: A Summary

Indigenous Services Canada (ISC)

Non-insured health benefits for First Nations and Inuit

Jordan’s Principle

Truth and Reconciliation Commission of Canada: Calls to Action

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Approach to Inguinal and Femoral Hernias in the Emergency Department

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Medical Student Pearl

Julia Short

Med 2

DMNB Class of 2025

Reviewed by Dr D Lewis

Copy Edited by Dr. J Vonkeman

PDF Download: EMSJ Approach to Inguinal and Femoral Hernias in the ED by JShort

Case

A 52-year-old male patient presents in the ER with a lump in their right groin. The lump protrudes when they cough and when laying on their left side, although it re-enters the abdomen on its own. You wonder if it could be a femoral or an inguinal hernia, and how to go about differentiating between the two.

Introduction

A hernia is defined as an organ, or part of an organ, that protrudes through the body wall in which it is normally contained. The etiology of a hernia can be due to congenital anatomical malformations or from acquired weakening of the body wall tissues. There are various subtypes of abdominal hernias, while groin hernias consist of inguinal and femoral hernias. Throughout their lifetime, males have a 27 to 43% chance of developing a groin hernia, while females have a 3 to 6% lifetime prevalence1. Although it is much more likely that a groin hernia is inguinal in nature (they account for 96% of groin hernias), it is clinically useful to identify and distinguish between the types of groin hernias. Additionally, there are important clinical features that must not be overlooked when characterizing a groin hernia.

Distinguishing inguinal from femoral hernias

An important landmark in determining the hernia origin is the inguinal ligament. Inguinal hernias protrude superior to the inguinal ligament, while femoral hernias present inferior to the inguinal ligament (Figure 1). This is because femoral hernias protrude from the femoral ring, located medial to the femoral vein. As a result, in males, femoral hernias will never course into the scrotum. Femoral hernias also present more lateral than inguinal hernias and may be difficult to differentiate from lymph nodes. Although they account for only 3% of all groin hernias, 40% of femoral hernias present as urgent due to bowel strangulation or incarceration1. Females are more likely to develop femoral hernias, while males are more likely to develop inguinal hernias.

Figure 1. Groin anatomy © 2023 UpToDate7

Distinguishing between direct and indirect inguinal hernias

Direct inguinal hernias originate medially, near the pubic tubercle and external inguinal ring. They protrude through Hesselbach’s triangle as a result of weakness in the floor of the inguinal canal. On exam, a bulge near the external (superficial) inguinal ring is suggestive of a direct inguinal hernia. In contrast, indirect inguinal hernias protrude near the midpoint of the inguinal ligament, at the internal (deep) inguinal ring (Figure 2). In males and females respectively, the internal inguinal ring is where the spermatic cord and round ligament exit the abdomen. A bulge in this area therefore suggests an indirect inguinal hernia. This type of hernia is the most common in all ages and sexes, accounting for approximately two thirds of all inguinal hernias2. In males, the indirect hernia often courses into the scrotum, which can be palpated if the patient strains or coughs. In contrast, it is rare for a direct hernia to course into the scrotum.

Figure 2. Anatomical comparison of direct and indirect inguinal hernias © 2020 Dr. Vaibhav Kapoor8

Clinical Approach

General considerations for investigating groin hernias include assessing the symptoms at presentation as well as any “red flag” physical findings. Patients commonly complain of dull or heavy types of discomfort when straining, which resolves when straining stops. Most groin hernias occur on the right side. Common physical findings include a bulge in the groin, which can indicate the type of hernia based on location relative to the inguinal ligament (Figure 3). However, in female or obese patients, the layers of abdominal wall may make the hernia more difficult to locate. In these cases, ultrasound or other imaging is needed to detect hernias. Clinicians should also determine if the hernia is reducible, or if the herniated bowel can be returned to the abdominal cavity when moderate pressure is applied externally.

Figure 3. Locations of femoral and inguinal hernias on examination © 2023 UpToDate7

 

Physical examination has a 76 to 92% sensitivity and 96% specificity for diagnosing groin hernias, although imaging may also be required1,2. Nausea, vomiting, fever, moderate-to-severe abdominal pain, localized tenderness, or bloating may indicate more sinister pathology such as bowel incarceration (when the hernia contents cannot return to the abdominal cavity), strangulation (when the blood supply to the involved bowel section is compromised) or necrosis.

Figure 5. CT images of A) femoral hernia (courtesy of Chris O’Donnell9 and B) inguinal hernia (courtesy of Erik Ranschaert10)

Management

Uncomplicated or asymptomatic hernias in males can be monitored through watchful waiting. Surgical repair is a definitive treatment for inguinal hernias and should be considered for symptomatic or complex hernias. If repair is needed for an uncomplicated inguinal hernia, a laparoscopic repair is recommended. Watchful waiting is not recommended for femoral hernias – these patients should have a laparoscopic repair (when anatomically feasible).

Manual reduction of the hernia can be performed by following the GPS Taxis technique. Taxis is a non-invasive technique for manual reduction of incarcerated tissues in a hernia to the original compartment5. “GPS” is an acronym to remind clinicians to be gentle, be prepared, and be safe when performing taxis5. Conscious sedation with intravenous diazepam and morphine is recommended for the procedure. Consider having an anesthetist present for the procedure if the patient is frail. Provide appropriate early resuscitation by monitoring vital signs, administering oxygen therapy and establishing IV access. Place the patient in Trendelenburg position. Begin the GPS Taxis technique by palpating the fascial defect around the base of the hernia and gently manipulating hernia contents back into the abdominal cavity. Use gentle manipulation pressure over 5-10 minutes until a gurgling sound is heard (indicating successful reduction of bowel).

 

Taxis guided by ultrasound may increase success rates for reduction.

https://sjrhem.ca/taxis-reduction-of-inguinal-hernia/

Figure 4. Colourized clip demonstrating PoCUS assisted Taxis reduction of an inguinal hernia11

 

It should be noted that the major contraindication to performing GPS Taxis is bowel strangulation within the hernia. A rare but serious complication of manual reduction is reduction en masse, when a loop of bowel remains incarcerated at the neck of the hernia after manual reduction6. This can lead to early strangulation, intestinal necrosis, sepsis, organ failure and death. Femoral hernias and indirect inguinal hernias are at higher risk of reduction en masse from manual reduction attempts.

References:

  1. UpToDate – Classification, clinical features, and diagnosis of inguinal and femoral hernias in adults
  2. Hammoud M, Gerken J. Inguinal hernia. StatPearls. 2022 Aug 15.
  3. UpToDate – Overview of treatment for inguinal and femoral hernia in adults
  4. Bates’ Guide to Physical Examination and History Taking, 12th ed. (pdf). Chapter 13: Male Genitalia and Hernias
  5. Pawlak M, East B, de Beaux AC. Algorithm for management of an incarcerated inguinal hernia in the emergency settings with manual reduction. Taxis, the technique and its safety. Hernia, 25, 1253-1258. 2021 May 25.
  6. Yatawatta A. Reduction en masse of inguinal hernia: a review of a rare and potentially fatal complication following reduction of inguinal hernia. BMJ Case Rep. 2017 Aug 7.
  7. UpToDate – Classification, clinical features, and diagnosis of inguinal and femoral hernias in adults
  8. Kapoor, V. Difference between and inguinal and umbilical hernia. 2020. Retrieved from: https://www.drvaibhavkapoor.com/difference-between-inguinal-and-umbilical-hernia.html
  9. Patel, MS. Femoral hernia. Radiopaedia. 2022 Dec 28. Retrieved from: https://radiopaedia.org/articles/femoral-hernia
  10. Fahrenhorst-Jones, T. Inguinal hernia. Radiopaedia. 2022 Apr 12. Retrieved from: https://radiopaedia.org/articles/inguinal-hernia
  11. PoCUS assisted Taxis reduction of an inguinal hernia. Video obtained courtesy of Dr. David Lewis.

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EM Grand Rounds: 2SLGBTQIA+ Health in the ED

Posted on by

Dr. J Vonkeman

 

Resources:

 

Gender Inclusive Language Resources

General language

Language for clinical settings

 

Education for Health Care Providers

Rainbow Health Ontario

TransCare BC

Gender Diversity Education

 

Guidelines:

TransCare BC Primary Care Tool Kit

Sherbourne Health Trans Health Care

UCSF Transgender Care

 

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Headaches and Herpes Zoster

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Headache and Herpes Zoster

Medical Student Pearl

 

James Tang

Dalhousie University Class of 2023

Reviewed by: Dr. Erin Slaunwhite

Copyedited by: Dr. Janeske Vonkeman

Case

Mr. H is a 57 yo gentleman who presents to the ED complaining of a 3-day history of headache. He describes a progressive worsening of a constant dull ache unilaterally above his left eye. It’s currently a 4-5/10 in severity and does not radiate. He has not had any nausea or vomiting, and no phonophobia but asks you to dim the lights in the room if that’s possible. He has no previous history of the same. He has not noticed any shooting pains associated with eating or drinking cold foods/liquids. He denies any associated autonomic symptoms on that side. Mr. H tells you he’s tried Tylenol and Advil at home and although it seemed to help a bit initially, the pain has continued to worsen over the last couple of days. He hasn’t noted any changes in the severity of his headache with physical activity.

Mr. H has no relevant past medical history and does not take any regular medications. He enjoys drinking 1-2 beers on the weekends, does not use cannabis, and has never used any other recreational drugs.

On physical exam, Mr. H appears his stated age and appears quite tanned from his job in construction. His vital signs are within normal limits. On close inspection, you make note of an area of erythematous macules and papules forming on his left forehead and extending 1-2 cm above and below his scalp line. The area is mildly tender to touch. His cranial nerve exam was otherwise normal. His remaining neuro exam, as well as head and neck, cardiac, respiratory, and abdominal exams were all normal.

A general approach to primary headache – Tension TIC TAC TOE

The International Headache Society (IHS) outlines specific diagnostic criteria for headache disorders within their International Classification of Headache Disorders (ICHD 3rd edition).1 Below is an abbreviated summary of the select common diagnoses that the ICHD discusses in much greater detail2-5:

Danger signs – features suggestive of secondary headache (e.g. space-occupying lesion, sub-arachnoid hemorrhage, cervical artery dissection, giant cell arteritis, infection, trauma, etc)2,4,5:

  • Systemic symptoms including fever, weight loss, progressive N/V
  • Neoplasm history
  • Neurologic deficit (including confusion, weakness, vision loss, numbness, impaired alertness, side locked headache)
  • Onset is sudden or abrupt (thunderclap)
  • Older age (> 50 yo)
  • Pattern change from previous headaches
  • Positional headache
  • Precipitated by Valsalva or exertion
  • Papilledema
  • Progressive headache and atypical presentations
  • Pregnancy or puerperium
  • Post-traumatic onset of headache
  • Pathology of the immune system such as HIV

Patients with danger signs suggestive of secondary headache should be considered for imaging. If a primary headache is suspected but imaging is performed for no other reason than reassurance, it can be detrimental to the patient if the results return incidental findings (e.g. vascular lesion) likely unrelated to the headache.

But our patient’s presentation doesn’t really seem to fit into any of these categories…

Herpes Zoster

In immunocompetent individuals, the diagnosis of herpes zoster is based solely on the clinical presentation: unilateral, usually painful vesicular eruption with a well-defined dermatomal distribution (see Figure 1). Prodromal symptoms include malaise, headache, photophobia, abnormal skin sensations, and occasionally fever. These symptoms may occur one to five days before the appearance of the rash. Age is the most important risk factor for the development of herpes zoster. A dramatic increase in the age-specific incidence of herpes zoster begins at approximately 50 years of age with 40% occur in people at least 60 years of age.6 It is estimated that approximately 50% of persons who live to 85 years of age will have had an episode of herpes zoster.6

Figure 1. Vesicular eruption in keeping with herpes zoster ophthalmicus with a crusted skin rash following the V1 dermatomal distribution and does not cross midline.7

Antiviral therapy is the first-line treatment and should be initiated within 72 hours of rash onset to increase the rate of healing, decrease the duration of acute herpes zoster, and decrease severity and pain. Ideally, initiation of antiviral therapy should be started during the pre-eruptive phase of herpes zoster, but often the diagnosis can only be confidently made once the distinctive rash presents.

See Table below for antiviral doses9:

Pain management

For acute herpes zoster, mild to moderate pain may be controlled with acetaminophen and/or nonsteroidal anti-inflammatory drugs. For those with moderate pain not responding to acetaminophen and nonsteroidal anti-inflammatory drugs, a short course of a short acting opioid such as hydromorphone or morphine could be considered or a course of corticosteroids. If the pain does not rapidly respond to opioid analgesics or if opioids are not tolerated, the addition of an adjunctive therapy should be considered including nortriptyline, gabapentin, or pregabalin. Despite these adjunctive therapies not having been extensively studied in patients with acute herpes zoster pain, they have evidence for other forms of nerve-type pain.8 The addition of corticosteroids to acyclovir decreases the pain of acute herpes zoster and speeds lesion healing and return to daily activities. Combination therapy with corticosteroids and antivirals should be considered in older patients with no contraindications.8

Theoretical models suggest that reducing pain during the acute phase of herpes zoster may stop the initiation of the mechanisms that cause chronic pain, thus reducing the risk of postherpetic neuralgia.8

 

Postherpetic neuralgia

Postherpetic neuralgia is the most common complication of herpes zoster.9 It occurs in ~30% of patients older than 80 years and ~20% of patients 60 to 65 years; it is rare in patients younger than 50 years.6 Postherpetic neuralgia may persist from 30 days to more than 6 months after the lesions have healed, and most cases resolve spontaneously.9 Although antiviral medications slow the production of the virus and decrease the viral load in the dorsal root ganglia, evidence showing that these medications alter the incidence and course of postherpetic neuralgia is inconsistent.8 The major risk factors for postherpetic neuralgia are older age, greater acute pain, and greater rash severity.8

Case conclusion

Mr. H’s headache did not fit into any specific category of headache as is often the case. Although he did meet the criteria for certain danger signs (e.g. age >50), imaging was forgone due to the finding of an erythematous maculopapular rash over his forehead. Mr. H’s rash followed the dermatomal distribution of the ophthalmic branch of the trigeminal nerve and was highly suspicious of an early herpes zoster outbreak.

The patient was given a prescription for valacyclovir to take for 7 days with instructions to seek care if lesions break out close to his eye or his pain becomes unmanageable with over-the-counter analgesia. Herpes zoster opthalmicus can be a sight-threatening condition that requires close ophthalmology follow up if there is any concern of lesions near or in the eye or the patient has clinical signs or symptoms. Mr H inquired about getting the shingles vaccine and was advised to follow up with his family doctor to arrange this following resolution of his rash.

Key Takeaways

  • Have a structured approach to understanding the different classes of primary headaches
  • Know the danger signs that could be suggestive of a secondary headache
  • Clinical judgement should be prioritized in determining who to image
  • Herpes zoster is a clinical diagnosis in immunocompetent individuals
  • Appropriate pain management of acute herpes zoster and vaccination can help prevent chronic pain syndromes

 

References

  1. The International Classification of Headache Disorders – ICHD-3. Accessed June 24, 2022. https://ichd-3.org/
  2. Evaluation of Acute Headaches in Adults. Accessed June 24, 2022. https://www.aafp.org/pubs/afp/issues/2001/0215/p685.html
  3. Primary care management of headache in adults Clinical Practice Guideline | September 2016 2 nd Edition. Published online 2016.
  4. Ponka D, Kirlew M. Top 10 differential diagnoses in family medicine: Headache. Can Fam Physician. 2007;53(10):1733. Accessed June 24, 2022. /pmc/articles/PMC2231438/
  5. Do TP, Remmers A, Schytz HW, et al. Red and orange flags for secondary headaches in clinical practice: SNNOOP10 list. Neurology. 2019;92(3):134-144. doi:10.1212/WNL.0000000000006697
  6. Epidemiology, clinical manifestations, and diagnosis of herpes zoster – UpToDate. Accessed June 24, 2022. https://www.uptodate.com/contents/epidemiology-clinical-manifestations-and-diagnosis-of-herpes-zoster
  7. Darren Shu JT, Ghosh N, Ghosh S. Herpes zoster ophthalmicus. BMJ : British Medical Journal (Online). 2019;364. doi: https://doi.org/10.1136/bmj.k5234.
  8. Herpes Zoster and Postherpetic Neuralgia: Prevention and Management. Accessed June 24, 2022. https://www.aafp.org/pubs/afp/issues/2011/0615/p1432.html
  9. Clinical Overview of Herpes Zoster (Shingles) | CDC. Accessed June 24, 2022. https://www.cdc.gov/shingles/hcp/clinical-overview.html
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Journal Club – Diagnostic Accuracy of ECG for Acute Coronary Occlusion resulting in MI

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Presenter: Dr. Nick Byers (iFMEM R2)

Host: Dr. Colin Rouse

Article:

Research question/PICOD

  • Question:
    • Does shifting from a STEMI/NSTEMI paradigm to a new approach (ACO-MI/ non-ACO-MI) result in better identification of the patients who need acute reperfusion therapy?
  • Population:
    • Adult ED patients with ACS Symptoms
  • Intervention/Comparison:
    • STEMI/NSTEMI vs ACOMI/NACOMI
  • Outcome:
    • Composite ACO defined as one of:
      • A) Total occlusion or presence of culprit lesion on angiography with a peak troponin I level equal to or greater than 1.0 ng/mL plus an at least 20% rise within 24 h
      • B) A highly elevated peak troponin (greater than 5.0 ng/mL), which was shown to be correlated with ACO
      • C) Cardiac arrest before any troponin rise has been documented with supporting clinical evidence of possible ACO
    • All cause in hospital mortality
    • All cause long term mortality
  • Secondary Outcomes: 
    • Time from ECG to coronary angioplasty or CABG
    • The sensitivity and specificity of current criteria in diagnosing ACO
    • The sensitivity and specificity of ECG without ST-segment elevation to diagnose ACO (accuracy of ECG interpretation of acute coronary occlusion without STEMI criteria)
    • The specificity of ECG with STEMI criteria (correct ECG interpretation of false positive STEMI criteria)
    • The sensitivity of ECG with STEMI criteria (correct ECG interpretation of false negative STEMI criteria)
    • The outcome according to ECG subclassifications (outcomes of the patients who are labeled as STEMI and the patients who are labeled as having NSTEMI but have acute coronary occlusion)
  • Design:
    • Single center, retrospective case-control study in Turkey

Results

Authors conclusions

“We believe that it is time for a new paradigm shift from the STEMI/non-STEMI to the ACOMI/non-ACOMI in the acute management of MI”

 

Discussion at Journal Club

Strengths

  • 3000 patients included, 1000 per arm
  • Reviewers were blinded, disagreements were resolved by a 3rd independent reviewer
  • EKGs were reviewed again 3 months later to decrease inter-observer variability
  • Consecutive patients with an initial diagnosis of MI (i.e. not a convenience sample)
  • All patients received guideline-recommended medical treatment
  • There were documented criteria of ECG findings to classify the ECGs

Weakness

  • This was a retrospective study and at a single centre.
  • When troponins were taken was not controlled for/accounted for in any way
  • Control group age, medical comorbidities, and cardiac risk factors were much less
  • Their results suggest 17% of patients in N-ACOMI (N-STEMI Subgroup B) with angiographic ACO were missed (slide 16 results)
  • Study wasn’t powered enough to indicate modest benefit of early intervention over late
  • Extrapolating results to the real world may be difficult because ecg interpretation

 

Bottom line/suggested change to practice/actions

  • This single center retrospective chart review suggests that considering coronary occlusion vs. just ST elevation on ekg decreases long-term mortality, and has a better sensitivity, specificity, PPV, and NPV.
  • This could be a great way of getting patients better access to PCI for occlusive lesions, though inter-operator variability and time constraints are likely to be difficult to implement

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