Peritonsillar Abscess Considerations and Treatment

Flimsy on Quinsy: Considerations and procedures to help diagnose and treat peritonsillar abscess  

Author: Iain McPhee- PGY1

Case study:

A 30 y.o. female presented to the emergency department with a 2-3 day history of sore throat, a unilateral, right sided oral pain that was worsening, and mild right ear ache. Although she was able to swallow food and liquid with discomfort, she reported an increased pooling of saliva in her mouth. She became more concerned when she noticed voice changes and decided to come to the hospital. 

On exam, she looked well and her vitals were within normal limits. On examination of the oral cavity there was a noted mild deviation of the uvula to the left. There was clearly demarcated erythema of both the hard palate and soft palate on the right side. Her right tonsil was only mildly enlarged and the presence of tonsillar stones were appreciated bilaterally. There was very mild fluctuance when palpating the junction between the hard and soft palate. There was an obvious dysphonia (Hot potato voice).

Background:

Peritonsillar abscess (PTA) (Quinsy) and peritonsillar cellulitis (PTC) are often indistinguishable, sharing similar clinical signs and symptoms (1). As management differs depending on the condition, several aspects warrant consideration in the differentiating process

Considerations

  1. Assess for severe upper airway obstruction
    • Look for signs of trismus, suprasternal retractions and anxious appearance. If present consider airway management.
  2. Computed tomography of the neck
    • Consider if you suspect signs of deep neck infection like a retro or parapharyngeal abscess. The CT scan should be obtained with contrast to help identify an abscess (4)
  3. Ultrasound guided exam 
    • Intraoral ultrasound has been shown to be a superior method to both diagnose and assist in the execution peritonsillar abscess drainage when compared to classic landmark-based needle aspiration (2,3). 
  4. Time
    • In the absence of a significant/apparent fluctuating mass in the mouth, consideration of the amount of time the symptoms have been present can help distinguish between the two conditions. Peritonsillar cellulitis is considered a transition phase of peritonsillar inflammatory process which leads to abscess formation (1). Look for 1-2 day history of symptoms as peritonsillar cellulitis, Abscesses are more likely to form between 2-8 days.

Algorithm: Approach to diagnosis and treatment of peritonsillar abscess in the emergency department

https://www.uptodate.com/contents/image?csi=59e98f58-4a45-4ff2-b021-31528346c088&source=contentShare&imageKey=EM%2F112062

Intraoral Ultrasound approach to drainage (as described on emdocs)

http://www.emdocs.net/unlocking-common-ed-procedures-peritonsillar-abscess-drainage/

  1. Use intracavitary probe with cover (Fig 1).
    • Examine affected area and locate abscess 
    • Also locate depth of carotid artery and any potential vascular anatomy anomalies (Fig 2).

      Figure 1: Intracavitary Probe with cover

      Figure 2: Anechoic abscess and carotid artery highlighted in red

       

  2. Analgesia/anesthesia
    • Consider IV analgesia, anxiolytics
    • Anesthetize oral cavity using topical spray like cetacaine or nebulized lidocaine
    • Inject lidocaine with epinephrine into the area of abscess with 18g needle with cut sheath (Fig 3).

      Figure 3 : Scalpel with taped guard and

  3. Optimize Abscess visualization 
    • Insert laryngoscope blade to a depth that is comfortable for the patient. Ask patient to hold laryngoscope (Fig 4)

      Figure 4: Laryngoscope blade optimizing view

  4. Drainage
    • Once adequate visualization is achieved, approach superior pole of abscess with sheathed spinal needle and continuously aspirate when advancing until pus is reached (Fig 5).
    • Consider incision with scalpel with protective guard and used 
    • Insert curved hemostat into abscess space to break up remaining loculations

      Figure 5: Anatomical picture showing superior pole

 

References

  1. Mohamad I, Yaroko A. Peritonsillar swelling is not always quinsy. Malays Fam Physician. 2013 Aug 31;8(2):53-5. PMID: 25606284; PMCID: PMC4170468.
  2. Costantino TG, Satz WA, Dehnkamp W, Goett H. Randomized trial comparing intraoral ultrasound to landmark-based needle aspiration in patients with suspected peritonsillar abscess. Acad Emerg Med. 2012 Jun;19(6):626-31. doi: 10.1111/j.1553-2712.2012.01380.x. PMID: 22687177.
  3. Froehlich MH, Huang Z, Reilly BK. Utilization of ultrasound for diagnostic evaluation and management of peritonsillar abscesses. Curr Opin Otolaryngol Head Neck Surg. 2017 Apr;25(2):163-168. doi: 10.1097/MOO.0000000000000338. PMID: 28169864.
  4. Galioto NJ. Peritonsillar abscess. Am Fam Physician. 2008 Jan 15;77(2):199-202. PMID: 18246890.

Procedures and Algorithms

  1. http://www.emdocs.net/unlocking-common-ed-procedures-peritonsillar-abscess-drainage/
  2. https://www.uptodate.com/contents/image?imageKey=EM%2F112062&topicKey=EM%2F6079&search=peritonsillar%20cellulitis&rank=1~19&source=see_link

 

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A Summary of Bronchiolitis

A Summary of Bronchiolitis: A review of bronchiolitis, evidence behind various treatment regimens, and suggested admission criteria – A Resident Clinical Pearl

 Melanie Johnston, R3

Integrated FMEM, Dalhousie

Reviewed by Dr. Patricia Dutton

Copyedited by Dr. Mandy Peach

Respiratory illnesses are the second most common ED presentation for paediatric patients, particularly during the winter months, in Canada. 1,2 These paediatric patients with respiratory pathologies are at risk of rapid clinical deterioration; a thorough history and exam with careful attention to respiratory evaluation is critical. Three of the most common paediatric respiratory complaints presenting to the ED include croup, asthma, and bronchiolitis. This pearl will focus on a review of bronchiolitis, its presentation, evaluation, and the evidence behind various treatments.

What is bronchiolitis:

Bronchiolitis is a viral lower respiratory tract infection. It is characterized by obstruction of small airways cause by acute inflammation, swelling/edema, and necrosis of the cells lining the small airways.2 Airways are further narrowed by increased mucous production. The most common causes are respiratory syncytial virus (RSV), influenza, rhinovirus, adenovirus, and parainfluenza.2 These viruses are transmitted by secretions from the nose/mouth and via respiratory droplets in the air. Co-infection with multiple viruses occurs in 10-30% of hospitalized children.2

Figure 1: Pathophysiology of Bronchiolitis.3

 

Epidemiology:
RSV season generally begins in November and persists until April. Bronchiolitis generally presents with a first episode of wheezing before the age of 24 months during the winter months.2 It is the most common reason for admission to hospital in the first year of life in Canada, and more than one-third of children will be affected by bronchiolitis in their first two years of life.2

Presentation:

Bronchiolitis may present with a wide range of symptoms from mild upper respiratory tract infection symptoms (cough, rhinorrhea, fever) to respiratory distress (tachypnea, wheeze, grunting, indrawing, abdominal breathing, and retractions).4 The peak severity of illness usually occurs on day 2-3 of the illness with resolution over 7-10 days.2,6 Cough can persist in infants for up to three weeks after onset.

Pediatric populations at risk for more serious illness include:
– Age <3 months
– Infants born prematurely (<35 weeks gestation)
– Chronic lung disease
– Congenital heart disease
– Chronic neurological conditions
– Immunodeficiency
– Trisomy 21

Patients with the above risk factors are at risk of rapid clinical deterioration even if presenting early in illness with mild symptoms.2,5

Diagnosis:


The diagnosis of bronchiolitis is considered to be clinical based on history and physical exam. The illness generally begins with a 2-3 day prodrome of mild URTI symptoms including cough, fever, rhinorrhea. This may progress to tachypnea, wheeze, and signs of respiratory distress.2 If respiratory distress is interfering with feeding, there may be signs of dehydration (delayed cap refill, dry mucous membranes, no tears produced with crying). Initial assessment should focus on overall appearance, breathing, and circulation. A tool to assist in establishing a general first impression of the paediatric patients stability is the paediatric assessment triangle. Abnormalities in any domain of the triangle (appearance, work of breathing, circulation) should be noted and factored into initial workup with potential to decompensate, with abnormalities in two domains indicative of potentially serious illness.

Figure 3: Pediatric Assessment Triangle.1

Signs of respiratory distress to note on exam include:

– Tachypnea
– Intercostal/subcostal retractions
– Accessory muscle use
– Nasal flaring
– Grunting
– Colour change or apnea
– Wheezing
– Low O2 saturation (<90%)

In stratifying the severity of illness in bronchiolitis, the Royal Children’s Hospital of Melbourne has proposed the following chart to assist with assessment:

Figure 4: Stratifying severity of illness in bronchiolitis, adapted from RCHM.5

Investigations

Bronchiolitis is considered to be a clinical diagnosis. As such, the majority of patients won’t require any additional investigations. If there is diagnostic uncertainty, then the following investigations may be considered:

Management:

Bronchiolitis is a self-limiting disease with peak severity generally at day 3-4 of illness.2,5,6 Most children have mild disease and can be managed with supportive care at home. For those ultimately admitted, focus in hospital is on supportive care with assisted feeding, nasal suctioning, and oxygen therapy as needed.

Disposition:

Most children do well and the symptoms will peak by day 3-5 of illness.

Criteria for safe discharge home include:
– O2 > 90-92%
– Adequate oral hydration
– Mild respiratory symptoms
– Access to reliable follow-up care if needed.2

Criteria for hospital admission include:

– Persistent oxygen saturation <92% and requiring supplemental oxygen AND/OR
– Unable to maintain oral hydration (fluid intake 50% of normal), requiring IV or NG fluids AND/OR
– Persistent moderate-severe respiratory distress
– Apnea (observed or reported)
– Children with risk factors for severe disease (see above).2

Admission or a period of observation in the ED can be used to document feeds and monitor vital signs/oxygen status. Other considerations for admission to hospital include social circumstances, comfort of caretaker in managing child at home, distance to healthcare facility in case of deterioration, and the phase of illness.

Resources:

1. Pediatric Respiratory Illnesses, Dr Allan Shefrin. Jan 30, 2020. Accessed at https://criticallevels.ca/2020/01/30/episode-3-paediatric-respiratory-illnesses-dr-allan-shefrin/

  1. Bronchiolitis: Recommendations for diagnosis, monitoring and management of children one to 24 months of age. Canadian Pediatric Society. Friendman, J., Rieder, M., Walton, J. et al. Nov 3, 2014. Accessed at https://emergencymedicinecases.com/wp-content/uploads/filebase/pdf/CPS-guidelines-bronchiolitis.pdf.

    3. Bronchiolitis. Cleveland Clinic. Accessed online at: https://my.clevelandclinic.org/health/diseases/8272-bronchiolitis

  2. Bronchiolitis, Bottom Line Recommendations. Trekk: Translating Emergency Knowledge for Kids. October 2020. Accessed online at: https://trekk.ca/system/assets/assets/attachments/502/original/2021-01-08-Bronchiolitis_v_3.0.pdf?1610662513

    5. Bronchiolitis, Clinical Practice Guidelines. The Royal Children’s Hospital Melbourne. Accessed online at: https://www.rch.org.au/clinicalguide/guideline_index/Bronchiolitis/

    6. Bronchiolitis, Episode 59. Emergency Medicine Cases. Accessed online at https://emergencymedicinecases.com/episode-59-bronchiolitis/

    7. Bronchiolitis in children: diagnosis and management. NICE guideline. June 1, 2015. Accessed online at: https://www.nice.org.uk/guidance/ng9/resources/bronchiolitis-in-children-diagnosis-and-management-pdf-51048523717

    8. https://www.connectedcare.sickkids.ca/quick-hits/2019/8/29/volume6-efnk4-nyn48-max8h-rczlx (Pediatric assessment triangle)

    9. Bronchioitis, accessed online at: https://en.wikipedia.org/wiki/Bronchiolitis.

 

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A case of Herpetiform Keratitis- Clinical evaluation and important considerations.

A case of Herpetiform Keratitis- Clinical evaluation and important considerations: A Resident Clinical Pearl

Bonnie He, PGY1

Ophthalmology, Dalhousie University

Reviewed by: Dr. Cherie Adams

Copyedited by: Dr. Mandy Peach

Case

A 68-year-old female presented to SJRH Emergency Department with a three-day history of atraumatic worsening of right eye pain, photophobia, and decreased vision. She denied any experience of flashing lights or “curtain falling”. She reported a long-standing history of glaucoma for which she was previously prescribed brimonidine (alpha-agonist) ophthalmic drops and was prescribed travoprost (prostaglandin) ophthalmic drops approximately one week prior to presentation. Additional ophthalmologic history revealed used of glasses, but not contact lenses, and bilateral cataract surgery two years previously. Of particular note, she recounted an episode of “sores from her upper lip along the side of her nose to right lower eyelid” in the past for which she was treated with oral valacyclovir. Further history positive for hypertension, for which she is prescribed ramipril, and type 2 diabetes mellitus, for which is is prescribed metformin. She is a retired schoolteacher, non-smoker, social drinker and denies any recreational drug use.
Visual acuity from 20 feet with spectacle correction revealed was 20/100 on the right (OD) and 20/30+1 on the left (OS). Her intraocular pressures were OD 17 and OS 19. Examination revealed mild upper and lower eyelid edema and moderate conjunctival injection. Fluorescein staining of the right cornea revealed four small dendritic epithelial defects (Figure 1) at about the 6 o’clock position. External and slit lamp examination of the left eye was normal. Fundoscopic examination to check the optic disc, macula, retinal vessels, and periphery were deferred.

Figure 1A: 4 small dendritic epithelial lesions can be seen at the 6’oclock position.

 

Figure 1B: Classic dendritic corneal epithelial lesions 17.

OPHTHALMOLGIC ASSSESSMENT:

Ocular complaints are common in emergency care settings. Yet, the quantity and quality of ophthalmology education varies significantly across Canada, with both medical students and residents report receiving insufficient ophthalmic medical education from medical education curricula.1-3
Proper history and physical examination taking skills are crucial to the appropriate management of patients with a red eye. The American Academy of Ophthalmology recommends the 8-point physical exam as a systematic approach to any eye problems:

  1. Visual acuity
    • Position the patient 20ft or 6m away from the Snellen chart to test for distance vision
    • Document whether it is their best corrected visual acuity, (ie. did they have their glasses or contact lens on at the time of the exam)
  2. Pupils
    • In dim room light, check for:
      1. Direct response by looking for pupil constriction in the eye being shined
      2. Consensual response by looking for pupil constriction in the other eye (eye that is not being shined)
  • Rapid Afferent Pupillary Defect (RAPD) with the swinging light test by shining light back and front between eyes
  1. Extraocular motility and alignment
    • Conduct a “H test” to test for the 9 cardinal positions of gaze by tracing out the letter “H” in the air while monitor their eyes for 3 S’s: speed, smoothness, and symmetry
    • Ask patient to follow your finger with their eyes while keeping their head still in the center and note for any double vision at certain gazes
  2. Intraocular pressure
    • The Icare tonometer requires no local anesthetic
    • Insert probe into tonometer and anchor the tonometer to the seated patient’s eyebrow.
    • Slowly bring tonometer probe towards patient light until the light turns green – now you’re ready to press the button that will automatically measure the patient’s intraocular pressure
  3. Confrontation visual fields
    • At about 1 arm’s-length away, test each eye individually by holding up 1 or 2 fingers and ask patient how many fingers they see
    • Ask patient to close their OS and fixate on your nose. Close your OS to assess with your open OD.
    • To check OS, ask the patient to close their OD and fixate on your nose. Close your OD to assess with your open OS.
  4. External examination
    • Assess for any obvious globe rupture, ecchymoses, deformities or lesions around the eye
    • Check to see if there’s any ptosis (lid drooping)
  5. Slit lamp examination (watch this video to learn how to perform a slit lamp exam: https://www.youtube.com/watch?v=gHW5OYj1Gf8
    • Assess for the following structures
    • Lids/lashes/lacrimal system: edema, erythema, lesions
    • Conjunctiva/sclera: injection, subconjunctival hemorrhage
    • Cornea: foreign body, fluorescein stain + cobalt blue light to assess corneal integrity (ie. corneal abrasions, herpetic dendrites), Seidel test (leakage of aqueous humour)
    • Iris: round (normal) vs. peaked (abnormal)
    • Anterior chamber: any hyphema, hypopyon, cells, flare
    • Lens: opacity
  6. Fundoscopic examination
    • In the emergency department, fundoscopy is typically undertaken in the undilated eye.
    • May consider dilating the eye with tropicamide (dilating drop) to visualize the back of the eye with the slit lamp or direct ophthalmoscope
    • Assess for the following structures:
      1. Optic nerve: cup-to-disc ratio, pallor, symmetry between eyes
      2. Macula: foveal light reflex
  • Vessels: Arteriovenous (AV) nicking, silver or copper wiring,
  1. Periphery: bleeding

DISCUSSION:

Given the patient’s endorsed history suggestive of ipsilateral V2 herpes zoster and classic dendritic corneal lesions, the leading differential diagnosis for her acute on chronic ocular pain in this case would be zoster keratitis, though herpes keratitis should also be considered, particularly in patients with identified history and recent episode of orolabial cutaneous HSV. Interestingly, she was started on travoprost for her glaucoma a week prior to her presentation. Topical ocular hypotensive agents, including travoprost, are known to have a myriad local and systemic side effects including: superficial punctate keratitis, corneal erosion, bradycardia, hypotension, and bronchoconstriction, are common.4,5 However, of particular interest in this case,  multiple clinical and animal studies have reported that topical prostaglandins for ocular hypertension are culprits  associated with herpes simplex virus (HSV) keratitis or varicella-zoster virus (VZV) keratitis.6-13 It is thought that prostaglandin analogues such as travaprost may induce the reactivation of HSV keratitis by releasing endogenous prostaglandins in the iris and ciliary muscles.9,14-16 Therefore it could also be very well possible that she may have developed HSV keratitis.

 

Irrespective of which differential was truly causing this patient’s symptoms the antiviral treatment for zoster ophthalmicus and HSV keratitis are the same: valocylcovir 1g TID PO x 7 days (or acyclovir 800mg po five times daily if cost of valcyclovir is prohibitive) and arrangements were made for next-day ophthalmologist consultation.

 

BOTTOM LINE:

Always take a thorough ophthalmologic history for patients with ocular complaints, including complete medication history.

Always ask about contact lens use in a history in any patient with a painful red eye.

Always conduct a complete physical exam for patients with ophthalmologic complaints using the AAO 8-point framework described above.


REFERENCES

  1. Sim D, Hussain A, Tebbal A, Daly S, Pringle E, Ionides A. National survey of the management of eye emergencies in the accident and emergency departments by senior house officers: 10 years on—has anything changed? Emerg Med J. 2008;25(2):76-77. http://emj.bmj.com/content/25/2/76.abstract. doi:10.1136/emj.2007.049999.
  2. Noble J, Somal K, Gill HS, Lam W. An analysis of undergraduate ophthalmology training in Canada. Canadian Journal of Ophthalmology. 2009;44(5):513-518. http://www.sciencedirect.com/science/article/pii/S0008418209801130. doi:https://doi.org/10.3129/i09-127.
  3. Gostimir M, Sharma RA, Bhatti A. Status of Canadian undergraduate medical education in ophthalmology. Canadian Journal of Ophthalmology. 2018;53(5):474-479. http://www.sciencedirect.com.ezproxy.library.ubc.ca/science/article/pii/S0008418216309553. doi:https://doi-org.ezproxy.library.ubc.ca/10.1016/j.jcjo.2017.11.015.
  4. Inoue K. Managing adverse effects of glaucoma medications. Clinical ophthalmology (Auckland, N.Z.). 2014;8:903-913. https://pubmed.ncbi.nlm.nih.gov/24872675 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4025938/. doi:10.2147/OPTH.S44708.
  5. Anwar Z, Wellik SR, Galor A. Glaucoma therapy and ocular surface disease: current literature and recommendations. Curr Opin Ophthalmol. 2013;24(2):136-143. doi:10.1097/ICU.0b013e32835c8aba [doi].
  6. Kroll DM, Schuman JS. Reactivation of herpes simplex virus keratitis after initiating bimatoprost treatment for glaucoma. Am J Ophthalmol. 2002;133(3):401-403. doi:S0002939401013605 [pii].
  7. Wand M, Gilbert CM, Liesegang TJ. Latanoprost and herpes simplex keratitis. Am J Ophthalmol. 1999;127(5):602-604. doi:S0002939499000501 [pii].
  8. Alm A, Grierson I, Shields MB. Side effects associated with prostaglandin analog therapy. Surv Ophthalmol. 2008;53 Suppl1:93. doi:10.1016/j.survophthal.2008.08.004 [doi].
  9. Soomro MZ, Moin M, Attaulla I. Latanoprost and Herpetic Keratitis. Pakistan Journal of Ophthalmology. 2011;27(4).
  10. Kothari MT, Mehta BK, Asher NS, Kothari KJ. Recurrence of bilateral herpes simplex virus keratitis following bimatoprost use. Indian J Ophthalmol. 2006;54(1):47-48. doi:10.4103/0301-4738.21617 [doi].
  11. Ekatomatis P. Herpes simplex dendritic keratitis after treatment with latanoprost for primary open angle glaucoma. Br J Ophthalmol. 2001;85(8):1008-1009. doi:10.1136/bjo.85.8.1007a [doi].
  12. Morales J, Shihab ZM, Brown SM, Hodges MR. Herpes simplex virus dermatitis in patients using latanoprost. Am J Ophthalmol. 2001;132(1):114-116. doi:S0002939401010121 [pii].
  13. Villegas VM, Diaz L, Izquierdo NJ. Herpetic keratitis in a patient who used two different prostaglandin analogue ophthalmic solutions: a case report. P R Health Sci J. 2008;27:348+. https://link.gale.com/apps/doc/A189052227/HRCA?u=anon~6a050068&sid=googleScholar&xid=2c140d29.
  14. Dios Castro E, Maquet Dusart JA. Latanoprost-associated recurrent herpes simplex keratitis. Arch Soc Esp Oftalmol. 2000;75(11):775-778.
  15. Gordon YJ, Yates KA, Mah FS, Romanowski EG. The effects of Xalatan on the recovery of ocular herpes simplex virus type 1 (HSV-1) in the induced reactivation and spontaneous shedding rabbit models. J Ocul Pharmacol Ther. 2003;19(3):233-245. doi:10.1089/108076803321908356 [doi].
  16. Kaufman HE, Varnell ED, Toshida H, Kanai A, Thompson HW, Bazan NG. Effects of topical unoprostone and latanoprost on acute and recurrent herpetic keratitis in the rabbit. Am J Ophthalmol. 2001;131(5):643-646. doi:S0002939400009107 [pii].
  17. Yu, Hubert (2019) Canadiem Medical Concepts: Approach to Corneal Disorders in the ED

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Cunningham Technique for dislocated shoulder reduction

Cunningham Technique for dislocated shoulder reduction: A Resident Clinical Pearl

Rebecca Fournier, PGY1 

Family Medicine, Dalhousie University

Reviewed by Dr. Chris Doiron

Copyedited by Dr. Mandy Peach

Case

38yo woman presenting with right shoulder pain after falling on ice. Unable to adduct right arm across body. Pain is minimal when resting quietly. Xray confirms anterior dislocation. You recently read about a sedation sparing technique to reduce her shoulder and decide to attempt it.

The Cunningham technique has been shown to be an effective and simple method to reduce a dislocated shoulder. The technique is based on the theory that the humeral head remains outside the glenoid fossa due to tension in the muscles surrounding the shoulder, primarily the biceps. Without the use of sedation or analgesia, the Cunningham technique relaxes the muscles to encourage self reduction. When used as the first technique of choice, Puha et al (2016) found a success rate of 76.9 compared to more traditional methods at 87%+. However, attempting Cunningham technique first allowed avoidance of sedation and was not found to increase pain or duration of hospital stay.

Cunningham Technique

A. Patient Selection and Preparation

1. Ideal patient is calm, in minimal pain, able to take direction, understands and willing to participate in procedure.
2. May consider Ativan 0.5 to 1 mg prior to procedure with goal for calm, thoughtful patient able to participate in the reduction. In most cases, Ativan is not required for a successful reduction

B. Patient position

1. Performed with awake, seated patient. Encourage good posture to maximize success
2. Patient and examiner sit opposite one another eye to eye
3. Patients arm position

a. Held adducted at side: critical to success, may be limiting if patient uncomfortable in this position or body habitus restricts adduction at the side.
b. Elbow flexed to 90 degrees

4. Examiner position
a. Examiner rests one hand firmly on top of the patient’s dorsal forearm, applying downward pressure
b. Opposite hand will perform massage aspect of technique

C. Technique
1. Examiner applies gentle, steady pressure downward on dorsal forearm
2. With free hand, examiner massages upper extremity proximal muscles

a. Start at deltoid and trapezius
b. Move distally to biceps and triceps

3. As the patient’s musculature begins to relax, some may experience apprehension.

a. Patient positioning: an awake, seated patient. Encourage good posture with shoulders up and back + chest pushed forward to maximize success.

b. Gently reassure patient that this sensation indicates progress and continued relaxation is key to success
c. Premedication with Ativan prior to procedure may additionally facilitate this transition

4. Anticipate Shoulder to spontaneously relocate

a. May take as long as 15 minutes to relocate
b. Often times an audible “clunk” is not heard, check often to verify if reduction has been successful

5. Confirm reduction with post procedure xray

Take away points:

– Requires no sedation (requires awake patient!) or analgesia
– Pick the right patient! Must be calm, able to take direction, willing to participate, and trust provider
– Attempting Cunningham procedure first avoids risks of sedation and analgesia without increasing length of stay
– Cunningham method is all about positioning and relaxation; let the humeral head find its way back to the glenoid. Check out the videos for a step by step by visual.
– Confirm reduction with post procedure xray

 

References

Gudmundsson TH, Bjornsson HM. [Reduction of shoulder dislocation with the Cunningham method]. Laeknabladid. 2017 Sep;103(9):373-376. Icelandic. doi: 10.17992/lbl.2017.09.150. PMID: 29044033.

Puha B, Gheorghevici TS, Veliceasa B, Popescu D, Alexa O. CLASIC VERSUS NOVEL IN REDUCTION OF ACUTE ANTERIOR DISLOCATION OF THE SHOULDER: A COMPARISON OF FOUR REDUCTION TECHNIQUES. Rev Med Chir Soc Med Nat Iasi. 2016 Apr-Jun;120(2):311-5. PMID: 27483710

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A Peanut Problem or Pimple Popper Predicament

 A Peanut Problem or Pimple Popper Predicament – A Resident Clinical Pearl

Grace Dao PGY1

Family Medicine, Dalhousie University

Saint John, NB

Reviewed by: Dr. Chris Vaillancourt

Copyedited by: Dr. Mandy Peach

 

Case Presentation

A 30-year-old otherwise healthy female presented to the ED with concerns about an “allergic reaction” to peanut butter. She reported that she woke 30 minutes prior to her presentation in the ED with a severely swollen red and disfigured lip. Her face had looked normal upon going to bed the evening prior. Her last meal was a peanut butter sandwich, which she eats frequently without difficulty. She described having some “wheezes” and “chest tightness” to the triage RN. When seen by writer, she denied any trouble breathing. She denied any issues the night prior before going to bed. She denied any GI upset, such as cramping, nausea, vomiting or diarrhea. Besides the swollen lip, she denied noticing any other skin changes; she denied any itchy sensation. Past medical history was unremarkable; she had no history of prior allergic reaction and no known allergies. She took no medications. Review of systems was negative, besides she noted that there was pimple at the base of her nose that she had “popped” yesterday.

On exam, all vitals were within normal limits besides a HR of 110. Respiratory exam revealed no obvious stridor or increased work of breathing; there was no swelling of the tongue or uvula on inspection of the mouth, clear air entry and exit were appreciated bilaterally. A faint wheeze was appreciated bilaterally. Cardiovascular and abdominal examinations were within normal limits. A skin exam revealed a diffusely red and swollen upper lip, with skin the above the vermillion border also showing swelling and redness. Increased erythema/pus at the R nostril sill was appreciated in the area of the previously popped pimple. The lip was tender and very warm to the touch.

With 2 system involvement (lip swelling and wheezes on respiratory exam); she was treated as anaphylaxis initially and given 0.5 mg Epinephrine IM, which did not lead to any change in her symptoms. However, it would be quite unusual for an IgE mediated reaction to present this late after ingestion. A peanut allergy especially, as most of these present before age 3.

Initial bloodwork showed a normal CBC, Cr and electrolytes. CRP was elevated at 67.1. Due to no change in symptoms with anaphylaxis treatment and concerns re an infectious etiology a CT facial bones was ordered after discussion with the radiologist on call. CT report showed a broad zone of cellulitis with an evolving central abscess. ENT was consulted who reported that incision and drainage was required, and that the infection likely came from the popped pimple. They performed an incision and drainage of the abscess in the ED, took wound cultures and started empiric antibiotics, and arranged for outpatient follow-up. In discussion with the ENT, it was noted that this presentation is typical of CA-MRSA cellulitis, and, thus, antibiotics to cover MSRA were required.

Anaphylaxis

While not the outcome in this case, it is important to be familiar with the various constellation of symptoms/signs that make anaphylaxis a likely and the initial management of this “can’t miss” diagnosis, which are outlined in the included figures1,2.

Lip Cellulitis and Abscess

Interestingly, after this case, a case study of a similar presentation was found in the literature where a MRSA lip infection was initially misdiagnosed as angioedema/anaphylaxis3. The diagnosis was discovered later, after the patient was unresponsive to anaphylaxis treatment and a history of a popping a pimple on their chin the day prior was elicited. Because Methicillin-resistant Staphylococcus aureus (MRSA) soft tissue infection also has a characteristic presentation of erythema, edema, and often, areas of fluctuance it can have a similar appearance to the typical angioedema that can be found in anaphylaxis.

See Reference 3. This CT was performed after incision and drainage; thus, no abscess is appreciated

While it is important to be vigilant towards the presentation of anaphylaxis, cellulitis is another diagnosis that it important not to miss4. Like other infections, complications of cellulitis include bacteremia, endocarditis, septic arthritis, osteomyelitis, metastatic infection, sepsis and toxic shock syndrome.  In patients with suspected erysipelas or cellulitis it is important to consider the possibility of an abscess, which requires incision and drainage. Findings in keeping with a skin abscess would be a painful, erythematous, fluctuant nodule.

The central face is not the most common area to develop cellulitis; however, it is an important area to recognize cellulitis. Untreated cellulitis in this area, can lead to septic cavernous thrombosis because the veins in this region are valveless.

Other diagnoses to consider for angioedema without history consistent with IgE mediated reaction or infection:

  1. Hereditary or acquired angioedema
  2. Mast cell disorder
  3. Idiopathic angioedema

 

Bottom Line: Always consider anaphylaxis in someone with apparent lip angioedema. However, it is also important to keep infection on the differential for a swollen lip, particularly if symptoms are not responding to therapy. Asking about prior injuries/skin lesions in the previous days can help clarify likelihood of infection. Also, as a personal takeaway, I should probably stop popping pimples.

References:

  1. Sampson, H. A. , Munoz-Furlong A., Campbell, R.L., et al. (2016). Second symposium on the definition and management of anaphylaxis: Summary report: Second National Institute of Allergy and Infectious Disease/Food Allergy and Anaphylaxis Network Symposium. J Allergy Clin Immunol 2006; 117:391. https://doi.org/10.1016/j.jaci.2005.12.1303
  2. Campbell, R.L. & Kelso, J.M. (2021). Anaphylaxis: Acute diagnosis. UpToDate. Retrieved December 30th, 2021 from : https://www.uptodate.com/contents/anaphylaxis-acute-diagnosis?search=anaphylaxis&topicRef=392&source=see_link#H1929228973
  3. Lucerna, A. R., Espinosa, J., & Darlington, A.M. (2015). Methicillin-resistant Staphylococcus Aureus Lip Infection Mimicking Angioedema. The Journal of Emergency Medicine 49 (1), 8-11 https://doi.org/10.1016/j.jemermed.2014.12.022.
  4. Spelman, D. & Baddour, L.M. (2021). Cellulitis and skin abscess: Epidemiology, microbiology, clinical manifestations, and diagnosis. UpToDate. Retrieved January 2nd, 2022 from: https://www.uptodate.com/contents/cellulitis-and-skin-abscess-epidemiology-microbiology-clinical-manifestations-and-diagnosis?search=cellulitis%20&source=search_result&selectedTitle=3~150&usage_type=default&display_rank=2#H1368100182

Cover image from: https://www.uptodate.com/contents/an-overview-of-angioedema-clinical-features-diagnosis-and-management?search=angioedema&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1

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Frailty: A Slow Burning…Emergency?

Frailty: A Slow Burning…Emergency? A Resident review on Advanced Care Planning in the ED

 

Robert Hanlon PGY1

Dalhousie Family Medicine

Saint John NB

Reviewed by Dr. Fraser MacKay

Copyedited by Dr. Mandy Peach

Chart: 95 year old male arrived by ambulance for generalized weakness…

PMHx: Mild Dementia, left hip arthroplasty 5 years ago from a fall at home (which also broke his left wrist), hypertension, atrial fibrillation, GERD, hearing loss, and anxiety/depression.

Social Hx: Lives with his daughter. Has a son. No admissions in the past 2.5 years.

Patient is lying supine on the stretcher and appears disheveled and  in emotional distress. He looks pale and emaciated with sunken facial features. He is staring at the ceiling and is slightly startled when you speak.

The patient is alert and oriented only to person. He answers questions with short sentences. His voice is shaky and anxious. He does not understand why he is in hospital or how he got here. He says he lives with his daughter. It seems he was living independently with some assistance, but recently requires more help. He claims he doesn’t walk much and really cannot bath, dress, or feed himself without his daughter. He, however, feels that he is still managing at home. He is afraid to be admitted to hospital.

 

Physical exam reveals pupils 3mm, equal and reactive to light. No RAPD, CN 2-12 are intact. Muscle bulk is reduced, but tone is normal.  Strength is 4/5 for both upper and lower limbs. There is normal ROM of his neck and limbs. Lungs have decreased air entry bilaterally but are clear. Cardiac exam reveals normal S1 and S2 with a systolic ejection murmur over the aortic valve area. Abdomen is soft, nondistended and non-tender. No pressure sores are noted at the coccyx or heels.

 

You call the daughter for some collateral. She says she is too distressed and not able to talk at this time. You call the son, and he identifies himself as the POA and his sister as the SDM. He lives in another city. He informs you that his father’s health has steadily declined since his fall 5 years ago. They have known about the dementia diagnosis for 8 years now and that his father first showed symptoms of declining memory after their mother died 9 years ago. Up until 5 years ago he had been living on his own with some assistance from family. After the fall, his family decided to have him come live with them. He says his sister has been taking care of their father, but that in the past 2 years the demands are out-weighing her abilities. He confirms that the patient is not able to complete their ADLs without assistance and that IADLs are impossible for his father. He had previously been using a walker to ambulate, but now he is unable to walk more than 2-3 steps. Despite this struggle, both the daughter and father do not want anyone in the house to help.

 

You ask when was the last time he saw his family physician – it was about 2.5 years ago right before the pandemic hit. He has had no in-person visits since, only phone calls for prescription refills. Although living with his daughter, he retains his family physician from his previous home when he lived independently. It has become increasingly difficult to get the patient to appointments of any kind.

 

You inquire about a code status: The son states that the discussion about SDM and POA had just occurred last week. The patient has been talking with both the daughter and son and often says that he is ‘ready to die and just wants this over with’. Together the son and daughter feel that a DNR order was appropriate, but the patient has not been asked outright what his wishes are.

This scenario is a common occurrence in Emergency Department’s across Canada and North America.

However, reading the scenario there is a sense that it is not a sudden acute emergency, but rather a slow burning issue that has reached a breaking point. You may ask yourself: why is this patient presenting to the Emergency Department? Is it appropriate? And, what does this type of presentation tell us about our care system and the experiences of frail patients?

 

There are many potential factors that have led to this patient’s current presentation. The main health issue being he is a 95 year old frail elderly male presenting with failure to thrive due to worsening dementia and physical decline.

However, I would like to focus on two specific areas of geriatric care. Advanced Care Planning and Local Resources for Caregivers

Advanced Care Planning

Looking at the scenario, there were multiple opportunities for this family, along with their health care providers, to discuss advanced care planning. This is in no way intended to place blame on any individual, group, or provider; yet, because there was a lack of communication/planning, the patient and their caregiver suffered a preventable crisis. Discussing advanced care plans is awkward; it can be unpleasant to discuss one’s end-of-life course or to cause family members distress. Nevertheless, the end-of-life experience is inevitable and the evidence shows that planning can help improve satisfaction with care and allow families to cope with loss (1,2). It is well established that being a care-giver for a complex-elderly patient is both mentally and physically demanding (3). Knowing this as care-providers, it is prudent to encourage elderly patients and their families to seek advanced planning early in a disease course or, better yet, before an illness. This way the individual is able to begin to reflect on their values and what they would like to prioritize in terms of their health and end-of-life experience. As well, starting early allows the conversation to be on-going over many years, which helps all those involved commit to the plan (1,2). Family physicians are best suited to encourage these early conversations.

But what can be done in the emergency department?

 

The reason this patient has presented to the emergency department is that his level of need surpassed his caregiver’s abilities; today just happened to be the day the caregiver could not function anymore in their role. Because of the poor access to primary care and little follow-up, this family had little choice but to choose the hospital as their point of entry.

 

The number of people over the age of 65 visiting emergency departments has been steadily increasing for decades, and older adults typically require more tests, stay longer, and are more frequently admitted to the hospitals (4,5,6). They are at greater risk of revisits, hospitalization, functional decline, and death after an emergency department visit (4). In elderly patients, an emergency visit is often a sign for declining health, which should prompt opportunities to change the clinical course of older patients.

 

Predicting the course or progression of disease in elderly patients is challenging. However, close monitoring of a patients’ experiences are likely to help clarify disease severity and drive better care. This provides Emergency Physicians with an opportunity to screen for frequent visitors and assess the level of frailty in patients. Frailty is a condition that occurs from multisystem decline and it compromises a person’s ability to recover from stressors (7).

 

The gold standard for assessing frailty is the comprehensive geriatric assessment (7). However, this is typically done through a geriatric service or as an in-patient assessment. There are streamlined tools that look to stratify risks for elderly patients visiting the emergency department. The Identification of Seniors at Risk (ISAR) and the Silver Code (SC) tools have been found to be useful in stratifying risk in both acute and long-term hospitalization, revisits, and death (8).

As score increases as does the risk of return visits, hospital admission and death.

 

One systematic review, suggested that the ISAR alone was not suitable for identifying seniors at risk (9). There are also the Clinical Frailty Scale (CFS), which was found to be strong at predicting in-patient death and admission to geriatrics (10,11). As well as the Study of Osteoporotic Fracture frailty index (SOF), which was strong at predicting functional decline (11).

Whatever tool that is used, it is important to remember it is a tool; used only to guide and inform care, but it is also important to consider the physical exam and clinical gestalt in assessing frailty.

 

If emergency physicians are able to help risk stratify frail patients, then the conversation at the end of a visit is an opportunity to shape expectations and suggest options for the prevention or early recognition of decline, and to encourage them to follow-up with their primary care physician (if they have one). This information can be used to help facilitate/motivate patients and their families to discuss and plan the future of their care.

 

Local Resources in NB

As providers at any entry point to the healthcare system, both primary care and emergency physicians ought to be familiar with local resources that can help patients in the community. The Government of New Brunswick has created an excellent guide for caregivers of older adults.

https://www2.gnb.ca/content/dam/gnb/Departments/sd-ds/pdf/Seniors/CaregiversGuide.pdf

 

As well there is a program called Social Supports NB, which can either be accessed via website or by telephone at 211.  https://socialsupportsnb.ca/en/

 

There is also the NB Home Support Association http://nbhsa.ca/english/about-us

 

 

References:

 

  1. Lum HD, Sudore RL, Bekelman DB. Advance care planning in the elderly. Med Clin North Am. 2015 Mar;99(2):391-403. doi: 10.1016/j.mcna.2014.11.010. Epub 2014 Dec 23. PMID: 25700590.
  2. Detering K M, Hancock A D, Reade M C, Silvester W. The impact of advance care planning on end of life care in elderly patients: randomised controlled trial BMJ 2010; 340 :c1345 doi:10.1136/bmj.c1345
  3. Hawken T, Turner-Cobb J, Barnett J. Coping and adjustment in caregivers: A systematic review. Health Psychol Open. 2018;5(2):2055102918810659. Published 2018 Nov 9. doi:10.1177/2055102918810659
  4. Frumkin K. Toppling Oranges: Death, Disability, Decline, and Readmission of Community-Dwelling Elderly Patients After an Emergency Department Visit. J Emerg Med. 2020 Feb;58(2):339-345. doi: 10.1016/j.jemermed.2019.12.014. Epub 2020 Jan 28. PMID: 32005609.
  5. Latham LP, Ackroyd-Stolarz S. Emergency department utilization by older adults: a descriptive study. Can Geriatr J. 2014 Dec 2;17(4):118-25. doi: 10.5770/cgj.17.108. PMID: 25452824; PMCID: PMC4244125.
  6. Shenvi CL, Platts-Mills TF. Managing the Elderly Emergency Department Patient. Ann Emerg Med. 2019 Mar;73(3):302-307. doi: 10.1016/j.annemergmed.2018.08.426. Epub 2018 Oct 2. PMID: 30287120.
  7. Theou O, Searle SD. Using frailty tools as prognostic markers in patients who are acutely ill. CMAJ. 2018 Feb 20;190(7):E182-E183. doi: 10.1503/cmaj.170902. PMID: 29565017; PMCID: PMC5828888.
  8. Di Bari M, Salvi F, Roberts AT, Balzi D, Lorenzetti B, Morichi V, Rossi L, Lattanzio F, Marchionni N. Prognostic stratification of elderly patients in the emergency department: a comparison between the “Identification of Seniors at Risk” and the “Silver Code”. J Gerontol A Biol Sci Med Sci. 2012
  9. Yao JL, Fang J, Lou QQ, Anderson RM. A systematic review of the identification of seniors at risk (ISAR) tool for the prediction of adverse outcome in elderly patients seen in the emergency department. Int J Clin Exp Med. 2015;8(4):4778-4786. Published 2015 Apr 15.
  10. Wallis SJ, Wall J, Biram RW, Romero-Ortuno R. Association of the clinical frailty scale with hospital outcomes. QJM. 2015 Dec;108(12):943-9. doi: 10.1093/qjmed/hcv066. Epub 2015 Mar 15. PMID: 25778109.
  11. Jørgensen R, Brabrand M. Screening of the frail patient in the emergency department: A systematic review. Eur J Intern Med. 2017 Nov;45:71-73. doi: 10.1016/j.ejim.2017.09.036. Epub 2017 Oct 3. PMID: 28986161.

 

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Quadriceps Tendon Rupture

Quadriceps Tendon Rupture – A Resident Clinical Pearl

Ida Szarics, PGY2

Dalhousie University

Reviewed by Dr. Paul Keyes

Copyedited by Dr. Mandy Peach

A 52 year old male presents to the ED with a right knee injury. He slipped while running, landing awkwardly on his right knee, with his foot caught behind him. He felt a “pop” and immediately had severe sharp right knee pain. He was unable to weight bear and states that his knee was swollen immediately afterwards. He denies any other injuries. He is otherwise healthy and is on no medications.

On exam, his vitals are within normal limits. There is obvious swelling of the right knee and has a palpable defect 2 cm above the patella which is extremely tender to palpation. He is unable to perform a straight leg raise. The remainder of the knee exam is non-contributory and he is neurovascularly intact.

He is clinically diagnosed with a quadriceps tendon rupture.

Above: Patients with complete quadriceps tendon ruptures will often present with a palpable defect within 2 cm above the patella. Image from: https://coreem.net/core/quadriceps-tendon-rupture/

 

Quadriceps tendon rupture: Mechanism

Quadriceps are the knee extensors, therefore rupture is most likely when the knee is flexed with simultaneous quadriceps contraction.1

-Age <40: Less common. Often occurs in athletes, particularly those who do not stretch activity, as a result of jumping and landing with the knee flexed. Patellar tendon rupture is more common in this age group

-Age >40: More common. Weaker tendons rupture more easily, so a fall onto a knee, or trying to prevent a fall onto the knees is typical.

 

Risk factors,2, 3

-Age (more common in patients >40 years of age)

-Male gender

-Type 2 Diabetes

-Renal disease

-Medications associated with tendon rupture (fluoroquinolones)

 

ABOVE: Anatomy of the muscles of the anterior thigh. Quadriceps tendon ruptures typically happen at the tendon’s insertion at the patella. Source: https://www.physio-pedia.com/Quadriceps_Tendon_Tear

 

Diagnosis

-Typically a clinical diagnosis, and is one of the “cannot miss diagnosis” in acute knee injuries.

-There is often a palpable defect ~2 cm above the patella where the tendon has been torn.

-Patients with a complete tear will be unable to perform a straight leg raise.

-Patients with a partial tear are unable to extend their knee against resistance – the ability to forcibly extend the knee against resistance is a critical part of the knee exam.

Investigations

XRays:

-May show a patella that is below expected anatomic position (patella baja). Of note, patella alta (or high-riding patella) can be a sign of patellar tendon rupture.

Ultrasound

-Can be a useful modality if diagnosis is uncertain. Often primary investigation available in the ED to supplement clinical exam findings.

MRI

-Best diagnostic modality, but cannot be obtained in the ED – this is typically a modality ordered by surgeons for surgical planning

ABOVE: Normal Knee XRay (left) and low-riding patella (right). The Insall Salvatti Index is the ratio of the patellar tendon length (red line) to the patellar length (yellow line). Normal is 0.8-1.2. Source: https://radiopaedia.org/articles/insall-salvati-ratio

 

Management

-Early surgical repair is important to maximize recovery, especially in complete tears. The distal tendon is avascular, so it will not heal well non-operatively.1

-Non-operative treatment (RICE, splinting, non-weightbearing) may be an option in partial tears or in patients with poor baseline mobility.

-Either way, orthopedic surgery should be consulted within a timely matter, usually within a week, to guide management. As time goes on difficulty of repair increases, as does probability of failed repair.  The ED physician should provide adequate analgesia as needed, immobilize the knee, and advise non-weightbearing while the patient is in the ED.

Back to our patient

Orthopedic surgery is contacted, and a plan is made to see the patient in clinic the following day to plan surgical repair. The patient’s knee is immobilized in extension, and an outpatient MRI is ordered. The patient undergoes surgical repair later that week.

References:

1Sharareh, Ben. (2021). Quadriceps Tendon Rupture. Orthobullets. https://www.orthobullets.com/knee-and-sports/3023/quadriceps-tendon-rupture

2 Von Fange, T.J., (last updated, 2021). Quadriceps Tendon and Muscle Injuries. UpToDate.

3 Nori, S., (2018) Quadriceps tendon rupture. J Family Med Prim Care. 7(1): 257–260.

 

 

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PoCUS in Early Pregnancy – a review

PoCUS in Early Pregnancy – a Resident Clinical Pearl (RCP)

Dr. Victoria Landry, R3

Integrated Family Medicine Emergency Medicine Program

Saint John, NB

Edited by Dr. Rawan AlRashed, PoCUS fellow

Copyedited by Dr. Mandy Peach

PoCUS use by the emergency physician for the diagnosis of uncomplicated intrauterine pregnancy have been proven to be affective in expiditing patient management and decreasing the length of stay in the emergency department. In a metanlaysis done by Stein et.al. emergency physiscain performed PoCUS was found to be 99.3% sensitive in ruling out ectopic pregnancy by detecting an Intauterine pregnancy (IUP). In this review, ultrasound findings in the first trimester will be highlighted.

Indication: Confirmed or suspected pregnancy with abdominal pain, vaginal bleeding, syncope, or hypotension(2)

Technique

Start with trans-abdominal ultrasound (TAUS) (1,2)

  • Use abdominal probe (deep penetration, wide field view; use “obstetrics” or “gynecology” preset)
  • Acoustic window is a full bladder (anechoic structure in the near field). Uterus is a homogenous structure beneath bladder
  • Place abdominal probe midline longitudinally/sagitally immediately superior to symphysis pubis with probe marker toward patient’s head. Adjust depth so uterus is in middle of screen. Sweep left and right till uterus disappears in each view.
  • Rotate probe 90° into transverse plane with marker toward patient’s right side. Sweep up and down till uterus disappears in each view.
  • To improve image: Turn the gain down, sweep slowly

Then Consider the use of transvaginal ultrasound (TVUS) if available, and qualified to use  (1)

  • Requires empty bladder, Patient in lithotomy position.
  • Ultrasound gel on probe, latex condom over top (ensure no air bubbles), then sterile lubricant
  • Reference mark toward ceiling (in sagittal orientation), insert 4-5cm into vagina, sweep left and right
  • Turn probe 90° C to be in coronal plane and marker to the right of the patient – sweep anterior and posterior

General principles (1)

  • follow the endometrial stripe (echogenic line within uterus) along its entire course (left to right in longitudinal view, cervix to fundus in transverse view), looking for evidence of a pregnancy
  • You are trying to rule in an intrauterine pregnancy (IUP) (as opposed to rule out an ectopic) – assume all pregnancies are ectopic until proven otherwise(2)

 

Figure 1 – Longitudinal/sagittal view (TAUS): (1)

Figure 2 – Transverse view (TAUS): (1)

Discrimination zone (βHCG levels below which you cannot see an IUP)(2, 3)

  • TVUS – βHCG 1500-2000 mlU/ml
  • TAUS – βHCG 5000-6000 mlU/ml
  • If No definite IUP (NDIUP) above these levels, strongly consider ectopic!

Findings:

Inutrauterine pregnancy

  • The “double ring sign is the earliest sign of a definitive IUP. Diagnosing an intrauterine pregnancy (IUP) requires visualization of all 3 structures inside the uterus. (1,2)
  • Decidual reaction – hyperechoic (white) line in uterus (2) represents endometrium thickening – begins around day 14 post-fertilization (1)
  • Gestational sac – anechoic (black) round area within decidual reaction, contains amniotic fluid, seen at 4-5wks (TVUS), 6wks (TAUS) (2)
  • Yolk sac +/- fetal pole within the gestational sac(2)
    • Yolk sac: circular echogenic layer, looks like a cheerio, visible when gestational sac is 10mm by TVUS (~5-6wks GA), 20mm by TAUS (~6-7wks GA) (1)
    • Fetal pole: echogenic structure; develops around the same time as yolk sac but visualized on US ~1wk later(1)

Figure 3 – Double ring sign(1)

Figure 4 – Double ring sign(4)

Figure 5 – Fetal pole(1)

Measurements

Mean sac diameter

  • Obtain sagittal view of gestational sac, measure height and length of sac using mean sac diameter calculation package, rotate probe 90º to obtain transverse view of gestational sac, measure width of sac
  • MSD (mm) + 30 = Gestational age (days)

 

Crown-rump length (CRL) = Top of skull to base of pelvis(1)

  • >5mm without visible fetal heart = unlikely to proceed to viability
  • CRL (mm) + 42 = gestational age (days)
  • The most accurate method of dating the pregnancy(3)

 

Fetal cardiac activity = proof of live IUP(1)

  • detectable ~6wks on TVUS (fetal pole is >5mm), 7-8wks on TAUS (fetal pole is >10mm) (1)
  • Normal IUP with fetal cardiac activity is reassuring!
    • absence of cardiac activity will likely result in miscarriage, presence of cardiac activity reduces risk of miscarriage (HR >100 consistent with good fetal outcome)
  • Technique(3)
    • Locate fetal pole, optimize depth, turn on M-mode (never doppler as it subjects fetus to high US energy and may be harmful)(1,2), place caliper over beating heart, measure and calculate heart rate
    • Note: must be within gestational sac, well away from uterine wall (don’t confuse with highly vascular decidual reaction)(1)
    • Normal FHR Ranges
      • 6-7wks: 100-120bpm
      • 8wks: 145-170bpm
      • 9+wks: 120-160bpm

 

Other findings and descriptions

No definitive intrauterine pregnancy (NDIUP) (2)

  • if any single criteria of IUP is missing

DDx for NDIUP(2):

  • Early normal pregnancy (βHCG below discrimination zone)
  • Threatened/spontaneous abortion
  • Anembryonic pregnancy (blighted ovum)
  • Molar pregnancy
  • Ectopic pregnancy

Threatened abortion: abnormal bleeding during pregnancy; normal IUP on US(3)

Inevitable abortion: vaginal bleeding with open os; normal IUP or product of conception (POC) near cervix on US(3)

Incomplete abortion: open os with retained POC; US shows anything from debris to embryo; abnormal uterine contents confirms dx(1)

Complete abortion: empty uterus + positive βHCG +/- closed os; same findings as for ectopic therefore requires formal US + serial βHCG(1)

Ectopic pregnancy (3)

  • NDIUP (no definitive intrauterine pregnancy) above βHCG in discriminatory zone
  • Scan adnexa for signs of ectopic
    • Tubal ring sign (thick hyperechoic ring around a tubal mass)
    • Ring of fire sign (also seen in corpus luteum cysts; high velocity flow seen on color doppler around the
    • gestational sac + fetal pole with cardiac activity outside the uterus is diagnostic of an ectopic
  • assess pouch of douglas for free fluid
  • suspicious for ectopic: ectopic mass, fluid in cul de sac, absent IUP, abnormal βHCG pattern (normally rises at least 50% in 48hr period)

Corpus luteal cyst(2,3)

  • develops due to growth, instead of normal regression, of corpus luteum
  • appears very similar to ectopic, but will move with the ovary in response to transducer manipulation instead of independent, tubal ring is thinner and less echogenic, cystic fluid is more clear and anechoic (rather than “clumpy” with echoes)
  • ovarian cyst characteristics: outside the uterus, circular, well circumscribed, do not taper to solid organs

Blighted ovum (anembryonic pregnancy)(1,2)

  • abnormally large gestational sac with no embryonic contents
    • gestational sac >20mm without yolk sac visible à suspect blighted ovum
    • >25mm without yolk sac visible à blighted ovum virtually certain (Eliminates diagnosis of ectopic)
  • Positive βHCG (higher than expected for GA)
  • Confirm with formal US

Molar pregnancy (1,3)

  • Tumor due to uncontrolled proliferation of trophoblasts (cells that surround blastocyst and later become the placenta)
  • Complete mole: no fetal/embryonic tissue; abnormally elevated βHCG >100,000 mIU/ml
  • Partial mole: may contain (abnormal) fetal structures
  • Presentation: hyperemesis, larger uterus than expected, vaginal bleeding, anemia, signs of hyperthyroidism, pregnancy-induced hypertension
  • US: appears as a “snowstorm” or “cluster of grapes” in uterus – fairly homogenous mass full of small, fluid-filled (black) holes; no detectable fetal cardiac activity
  • Needs gyne referral for surgical evacuation(2)

Pitfalls

  • Pseudogestational sac (1, 3)
    • contains no yolk sac, usually more irregularly shaped or pointy-edged than a true gestational sac, border is not as echogenic, and fluid may contain some echoes
    • Intrauterine fluid collections occur in 9-20% of ectopic pregnancies
    • Unless all 3 criteria met for double ring sign, pt requires formal US
  • Extrauterine pregnancy(1)
    • Recognize uterine tissue and always confirm bladder-uterus juxtaposition(2)
  • Interstitial and cornual ectopic pregnancies(1)
    • Rare but dangerous – tend to rupture later therefore produce more rapid hemorrhage than other ectopics
    • Myometrium around interstitial and cornual pregnancies is thin and uneven(2)
    • Measure the “myometrial mantle” (the thinnest part of myometrium around the gestational sac) – should be >5-7mm thick (thinner is concerning for cornual or interstitial ectopic pregnancy) (2)
  • Multiple pregnancies(2)
    • In multiple gestation, each fetus needs to meet the criteria for IUP
    • Heterotopic pregnancies = combined IUP and ectopic pregnancy
      • Risk is 1:30,000 in general population
      • Risk increases to 1:100 with fertility treatment (e.g. IVF)

Figure 7 – Extrauterine pregnancy(1)

Figure 8 – Normal myometrial mantle(1)

Figure 9 – Cornual ectopic pregnancy(1)

Key points(1)

  • False positive IUP can have devastating consequences
  • Any positive βHCG + no definitive IUP = presumed ectopic
    • Pt stable + no free fluid à formal US + quantitative βHCG
      • If no ectopic mass, repeat formal US and βHCG in 48hrs with consideration of patient risk of ectopic pregnancy
      • Follow up with OB to be arranged
    • Always consider other diffrerntail diagnosis for patient presentation before discharging them home.

Figure 10 – Clinical application(2)

 

References:

  1. Socransky, S., &amp; Wiss, R. (2016). Obstetrical EDE. In Essentials of point-of-care ultrasound: The EDE book (pp. 61-90). The EDE 2 Course.
  2. Long, N. (2020, March 02). VanPOCUS: 1st Trimester Obstetrics • LITFL • Ultrasound Library. Retrieved October 15, 2020, from https://litfl.com/vanpocus-1st-trimester-obstetrics/
  3. Dinh, V. (n.d.). Obstetric/OB Ultrasound Made Easy: Step-By-Step Guide. Retrieved October 15, 2020, from https://www.pocus101.com/obstetric-ob-ultrasound-made-easy-step-by-step-guide/
  4. Flores, B., Smith, T., & Joseph, J. (n.d.). OB/Gyn. Retrieved October 15, 2020, from https://www.thepocusatlas.com/obgyn-1

 

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Just the Facts: Sympathectomy for Frostbite

Just the Facts: Sympathectomy for Frostbite – A Resident Clinical Pearl

Robert J. Dunfield

PGY-3 – Integrated Family Medicine/Emergency Medicine Program

Reviewed by: Dr. Devon Webster

Copyedited by: Dr. Mandy Peach

Case:

You’re working in a rural emergency department when a 76 year old man is brought in by ambulance after being found laying in a snowbank on the side of the road, next to his parked car. The temperature outside is -20°C and it’s snowing quite heavily. As far as you can gather, the man has a history of cognitive impairment and lives alone.

You perform an appropriate initial resuscitative workup. His core temperature is warmed to 36.5°C and he is stabilized, but complains of ongoing left hand pain. You note that the man’s left hand has the following features: it is cold, throbbing, his phalanges are covered in blisters, surrounded by edema. You suspect frostbite.

Figure 1: Frostbite. [Peer-Reviewed, Web Publication] Herndon, A. Amick, A. (2021, Mar 15). Health Risks Imposed by the Beach. [NUEM Blog. Expert Commentary by Lank, P]. Retrieved from http://www.nuemblog.com/blog/health-risks-imposed-by-the-beach.

  1. What features on clinical examination distinguish first, second, third, and fourth degree frostbite? [1, 2]

In the emergency department setting, distinguishing between degrees of frostbite is not accurate and not clinically useful. Similar to burns, it is more useful in the acute setting to classify frostbite as superficial or deep to help determine prognosis. Tissue involvement can change through rewarming and progress with time. All frostbite injuries are treated with a similar approach, no matter the degree of involvement.

Classically, however, frostbite injuries have been categorized as first, second, third, or fourth degree. The following table outlines the characteristics for each of these classifications.

Clinical features indicating favourable prognosis:
* Intact sensation to pinprick
* normal skin color
* large blisters with clear fluid

Clinical features indicating poor prognosis:
* Non-blanching cyanosis
* Dark fluid-filled blisters
* Hard, non-deforming skin.

2. What treatment options are available for rewarming a peripheral frostbite injury? [1, 3, 4, 5, 6]

The treatment for frostbite requires a careful approach that starts immediately during the pre-hospital stage. These patients should:

1) be removed from the cold environment,
2) have any cold and wet clothing removed,
3) begin rewarming of affected area in circulating warm water bath (37 to 39*C)

*Avoid rewarming with dry heat, vigorous rubbing, or fire.

Once these patients have arrived to your emergency department, initial resuscitation of the whole patient should be the primary focus of treatment. Follow your ABC’s and ensure their core temperature is stabilized prior to focusing on the frostbitten limb.

 

In terms of rewarming, the traditional approach has implicated the following interventions:

1) Analgesia: thawing can be extremely painful. Administer anti-inflammatories and/or short acting opioids as needed.

2) Warm and wet immersion: immerse the frostbitten limb in circulating water/saline warmed to 37 to 39°C.

3) Fluid resuscitation: as needed, particularly if there is concern for cold diuresis in the setting of hypothermia.

4) Movement: encourage gentle movement of the affected limb as tolerated, but ensure no rubbing/friction is applied to the frostbitten area.

5) Topical aloe vera q6h: this treatment has shown to be effective in fighting the arachidonic acid cascade that promotes inflammation and prostaglandin formation, thereby reducing tissue damage in frostbite. Can be considered when available.

6) Tetanus toxoid

7) Careful wound care: this is an important aspect of ongoing management. Prior approaches to frostbite discuss the possibility of debridement of blisters and soft tissue, but this does not need to occur in the acute setting. Incision and drainage of white, cloudy blisters remains controversial.

8) Affected limb elevation

 

3. What management options exist for post-rewarming pulse deficits in frostbite? [1, 5, 6, 7]

If a hand continues to demonstrate ongoing evidence of ischemia or rewarming therapy fails to achieve reperfusion, the following management strategies are suggested:

1) If not already done, emergently consult local frostbite management expertise, such as plastic or vascular surgery.

2) Consider vascular imaging of the affected area.

3) Intravenous or intraarterial thrombolytic (Tpa 0.15 mg/kg bolus then 0.15 mg/kg over 6 hours). After Tpa is administered, start IV unfractionated heparin (2 mg/kg/min) for 24 to 72 hours. This reduces the risk of digital amputation.

4) Iloprost* IV (where available) 2 mg/kg/min, 6 hours per day for 5 days.
*Iloprost is not currently available commercially in Canada, but many Canadian physicians working in northern regions of the country are currently advocating for its increased availability. Iloprost is an arterial vasodilator, often used in pulmonary arterial hypertension.

 

4. What role does local anaesthetic play in rewarming a frostbitten hand? [8, 9]

Studies have assessed the role of regional anesthesia to create a chemical sympathectomy for patients with frostbite. Hand surgeries performed under local anaesthetic have shown to reduce sympathetic innervation of the hand, resulting in hyperemia (increased blood flow) while simultaneously providing pain control. Hyperemia is likely a result of the sympathetic blockade that results in increased blood flow and vasodilatation peripherally. This peripheral nerve block focuses on the ulnar and median nerves.

One study looked at 39 patients undergoing carpal tunnel release. It showed that a volar nerve block resulted in 74% of patients having a temperature increase of >1°C in their distal fingers following distal forearm anaesthetic block.

Concerns about finger vasoconstriction as a result of epinephrine use in anaesthetic injected at the wrist, theoretically worsening ischemia and necrosis risk in the fingers, are currently unfounded. Local anaesthetic without epinephrine comparatively will have a shorter duration of hyperemia and analgesia.

In general, there is limited research available around the use of local anaesthetic in frostbite.
No clear guidelines outlining indications and contraindications to local anaesthetic sympathectomy in the treatment of frostbite presently exist. Currently, its use as an adjunct to other routine management of acute frostbite is recommended.

5. How is a local anaesthetic sympathectomy performed in the hand? [8]

1) Materials needed:

-Aseptic cleaning wipe/solution
-10 mL syringe
-1% lidocaine with epinephrine
-18G needle (to draw up local anaesthetic)
-27G needle (to inject local anaesthetic)
-Sterile marking pen

2) Identify your landmarks: injection of the local anaesthetic should be performed between the palmaris longus and flexor carpi ulnaris tendons, just proximal to the wrist crease. Mark the area.

3) Clean the area with an antiseptic solution.

4) Inject 10 mL of 1% lidocaine to the area landmarked, subfascially. There is no need to fan the needle during this injection.

5) Continue to monitor the temperature of the involved fingers. It is possible the area near the wrist infiltrated by the local anaesthetic will blanche, but the hand and fingers distal to this area should become warmer and hyperemic.

 

  1. How long do the effects of local anaesthetic sympathectomy last? [8]

It is estimated that hyperemia will last for approximately 2 hours. Numbness may last up to 6 hours.

https://handsurgery.org/multimedia/files/preCourse/Frostbite%20treatment%20with%20blocks.pdf

 

SUMMARY AND KEY POINTS:

-Classifying frostbite in an acute setting is notoriously unreliable due to the ability of the insult to progress over time. Your approach to frostbitten patients should be consistent despite their initial tissue involvement.

-Initial management of the frostbite patient should focus on resuscitation and core rewarming.

-Removing the patient’s exposure to hypothermia and cause of frostbite, pain control, warm and wet rewarming, tetanus vaccination, topical aloe vera, wound care, considering thrombolysis, and consulting experts in frostbite management are core tenants of frostbite care.

-Consider local anaesthetic sympathectomy using distal volar wrist nerve block as an adjunctive therapy in patients with hand frostbite.

-Iloprost is currently unavailable commercially in Canada but advocacy is ongoing to increase its availability for treatment of frostbite, especially in northern areas of the country.

 

REFERENCES:

 

  1. Tintinalli, J.E., Ma, O.J., Yealy, D.M., Meckler, G. D., Stapczynski, J.S., Cline, D., Thomas, D.M. (2016). Tintinalli’s emergency medicine: A comprehensive study guide(Ninth edition.). New York: McGraw-Hill Education. Chapter 208: Cold Injuries.
  2. Comp, L. Brrr! ED Presentation, Evaluation, and Management of Cold Related Injuries. net: Practice Updates. 2018; Last updated: May 21, 2018. Accessed: June 01, 2021. Available from: http://www.emdocs.net/brrr-ed-presentation-evaluation-and-management-of-cold-related-injuries/
  3. Thomas, A. CRACKCast E139 – Frostbite. org. 2017; Last updated: December 28, 2017. Accessed: June 01, 2021. Available from: https://canadiem.org/crackcast-e139-frostbite/
  4. Handford, C., Buxton, P., Russell, K., Imray, C. E., McIntosh, S. E., Freer, L., Cochran, A., & Imray, C. H. 2014. Frostbite: a practical approach to hospital management. Extreme physiology & medicine3, 7. https://doi.org/10.1186/2046-7648-3-7
  5. Basit, H., Wallen, T.J., Dudley, C. 2021. Frostbite. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from: https://www.ncbi.nih.gov/books/NBK536914/
  6. Poole, A., and Gauthier, J. 2016. Treatment of severe frostbite with iloprost in northern Canada. CMAJ, 188 (17-18): 1255-1258. https://doi.org/10.1503/cmaj.151252
  7. Yun, T. 2021. ‘It’s a promising result’: Made-in-Yukon treatment reducing amputations in most severe frostbite cases. CTV News: Health News. Last updated: March 3, 2021. Accessed: June 01, 2021. Available from: https://www.ctvnews.ca/health/it-s-a-promising-result-made-in-yukon-treatment-reducing-amputations-in-most-severe-frostbite-cases-1.5331820
  8. Chandran GJ, Chung B, Lalonde J, Lalonde DH. The hyperthermic effect of a distal volar forearm nerve block: a possible treatment of acute digital frostbite injuries? Plast Reconstr Surg. 2010 Sep;126(3):946-950. doi: 10.1097/PRS.0b013e3181e60400.
  9. Rakower SR, Shahgoli S, Wong SL. Doppler ultrasound and digital plethysmography to determine the need for sympathetic blockade after frostbite. J Trauma. 1978 Oct;18(10):713-8. doi: 10.1097/00005373-197810000-00006.
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A bad trip… to the ICU – A case presentation and general overview of poisonous mushroom ingestion

A bad trip… to the ICU – A Resident Clinical Pearl  on poisonous mushroom ingestion

Scott Fenwick 

PGY-1 Family Medicine, Dalhousie University

Reviewed by: Liam Walsh, Clinical Pharmacist

Copyedited by: Dr. Mandy Peach

Case Presentation:

A 43yo otherwise healthy female presents to the ED with 30 hours of intractable nausea, vomiting, diarrhea, and diffuse crampy abdominal pain. 12 hours prior to the onset of these symptoms, she had foraged six wild mushrooms, fried them with butter, and ate them with her dinner. She had used a wild mushroom reference guide and thought these “pristine white” mushrooms would be a safe steak topping.

In the ED, she was alert and oriented with a GCS of 15 and no apparent encephalopathy. Her vitals were BP 109/68, P 93, T 37, RR 16, O2 97% RA. She was retching and vomiting clear emesis, which settled some with ondansetron 8mg IV. Clinically, she looked dehydrated but otherwise not toxic. Her abdomen was soft and diffusely tender. Cardiorespiratory exams were unremarkable. There were no skin findings.

A 1L bolus of normal saline was administered. Serum laboratory studies, drawn approximately 42 hours post-ingestion returned as follows:

Urinalysis showed trace blood, ketones and protein. ECG showed normal sinus rhythm.

The marked elevation in liver enzymes and abnormal coagulation studies were concerning for hepatocellular injury and fulminant hepatic failure. The local Internal Medicine consultant was contacted, and the patient was transferred to the ICU at the nearest liver transplant center.

In consultation with pharmacy and poison control, it was determined that the most likely offending mushroom was Amanita virosa, more commonly know as a Destroying Angel.

The patient was started on NAC, activated charcoal, penicillin G, cimetidine, vitamin C, and IV silibinin (milk thistle). Consideration was given to percutaneous cholecystostomy, as the toxin can accumulate in the gallbladder, but this was not anatomically feasible at the time.
Laboratory studies peaked at 72 hours post-ingestion as follows

Vitamin K was given to lower the INR. Creatinine continued to climb and was 835 prior to initiation of hemodialysis. Liver studies slowly trended downward with ALT 9774, AST 4586, and INR 1.7 at 96-hours post-ingestion. Ultimately, liver function values returned to normal and enzymes levels continued to trend downward—making liver transplant not necessary.

Overview of Toxic Mushroom Ingestion:

Epidemiology:

According to the 2019 Annual Report of the American Association of Poison Control Centers’ National Poison Data System, more than half of toxic mushroom ingestions occur in children under the age of 6. Serious toxicity and mortality, however, is more common in foraging adults, as they are more likely to consume larger quantities of a misidentified mushroom. Data for Atlantic Canada was difficult to obtain, but the Ontario Poison Centre received 72 calls related to mushroom exposures in September 2020, generally the peak month for exposures.

Poisoning Syndromes:

Only 20% of the time is the offending mushroom correctly identified, so we often rely on the clinical presentation to identify the likely species and relevant treatment. UpToDate lists 12 different mushroom toxins and 14 unique corresponding syndromes:

  • Acute gastroenteritis (<6hrs) without liver failure
  • Delayed gastroenteritis (6-12hrs) and delayed liver failure
  • Acute gastroenteritis and delayed renal failure
  • Hallucinogenic
  • CNS depression and excitation
  • Disulfiram-like reaction
  • Cholinergic excess
  • Delayed renal failure
  • Delayed rhabdomyolysis
  • Erythromelalgia
  • Delayed encephalopathy
  • Immune-mediate hemolytic anemia
  • Shiitake dermatitis
  • Allergic bronchioalveolitis

The syndrome from this case, bolded above, is delayed liver toxicity and delayed gastroenteritis.

This syndrome follows 3 phases:

  • Phase I: Dysentery – nausea, vomiting, diarrhea (6-24hrs post-ingestion)
  • Phase II: Apparent recovery (24-36hrs post-ingestion)
  • Phase III: Fulminant hepatic and multisystem organ failure (48-96hrs post-ingestion)

Poisonous Mushrooms in New Brunswick:

The New Brunswick Museum has compiled a catalog of the mushroom species discovered in the province. One of the deadliest mushrooms in the province is the Destroying Angel. This nickname refers to a group of mushroom species under the genus Amanita. Amanita virosa is commonly found in New Brunswick and Nova Scotia. They are pristine white and often located in wooded areas or next to trees/shrubs in suburban areas. They are most prevalent in the summer and fall.

In their button stage, Destroying Angels can be confused with white mushrooms that you might buy at the grocery store. Destroying Angels produce an amatoxin—a selective inhibitor of RNA polymerase II, leading to an interruption in protein synthesis and cell death. Amatoxins are especially toxic to the GI tract, liver and kidneys.

Notably, in the NB Museum catalog, there are no reports of Amanita phalloides, aka the Death Cap, in New Brunswick. In Canada, they are more commonly found in British Columbia.

EM Approach:

History:

  1. What did they look like? Ask for photos from the patient’s phone or samples if they have them. Identification assays are available but not always useful in the acute setting.
  2. Were the mushrooms collected in a field or along/underneath trees? Many toxic mushrooms are in wooded areas.
  3. How many types of mushrooms were ingested?
  4. How long after ingestion did symptoms develop? Less than 6hrs is associated with lower risk of—but does not exclude—potentially lethal ingestion.
  5. How much was eaten? Were there multiple times of ingestion?
  6. Did others eat the mushrooms? If so, do they have similar symptoms?

Physical Exam:

  • Assess hydration status
  • Assess for encephalopathy or other signs of fulminant hepatic failure

Laboratory studies:

Treatment:

  • Ondansetron for N/V, do not use anti-diarrheal agents
  • IVF for dehydration and electrolyte abnormalities
  • If a serious ingestion cannot be excluded, patients should be admitted for 24-48hrs for observation and serial bloodwork

Evidence-based recommendations for suspected amatoxin poisoning:
o Multiple dose activated charcoal: 0.5g/kg (max 50g) q4h for 4 days post-ingestion.

o Silibinin: loading dose of 5 mg/kg IV, followed by a continuous infusion at a dose of 20 mg/kg/day for 6 days or until clinical recovery.

If IV silibinin is not available, oral milk thistle capsules (Silymarin) are an effective alternative. The initial dose is 50-100mg/kg q8h, and titrated up to 200mg/kg q8h as tolerated, with a maximum single dose of 2-3g. IV Silibinin is available only through Health Canada’s Special Access Program. Pharmacy should be contacted early to assist with this process if it’s being considered.

o Penicillin G: 300,000 to 1,000,000 units/kg/day given as a continuous IV infusion. A small amount of research shows no benefit to adding this if IV silibinin is available. If penicillin allergy, consider ceftazidime 4.5 g every 2 hours.

o NAC protocol: initial loading dose of 150 mg/kg (max 10g), next a 4-hour infusion at 12.5 mg/kg/hr, then a 16-hour infusion at 6.25 mg/kg/hr. The 16-hour dose may be repeated if significant hepatic dysfunction persists.

o Cimetidine: 300 mg IV every 8 hours until clinical improvement (evidence in animal studies only)

o Vitamin C: 3 g IV daily until clinical improvement (evidence in animal studies only)

o Dextrose for hypoglycemia

o Lactulose for hyperammonemia

o Vitamin K +/- FFP for coagulopathy

o Dialysis for AKI

o Early consultation with liver transplant center

  • Treatments for other mushroom poisoning syndromes can be found in this chart

Bottom Line:

Ask if the patient has photos of the mushrooms on their phone, or if they can describe their appearance. Call local poison control with this information.

Obtain a clear history to determine the interval between time of ingestion and time of symptom onset. Acute gastroenteritis onset (<6hrs from ingestion) is associated with favourable outcomes, and delayed gastroenteritis (usually 6-12hrs from ingestion) is more likely to have liver and/or renal failure.

Liver studies may be normal until 24-36 hours and generally peak at 72-96 hours post-ingestion.

Early treatment and consultation/transfer to a liver transplant center is imperative.

 

References:

Cover photo: https://www.deviantart.com/dreadillustrations/art/Poison-Mushrooms-774297817

Gummin, D. D., Mowry, J. B., Beuhler, M. C., Spyker, D. A., Brooks, D. E., Dibert, K. W., Rivers, L. J., Pham, N., & Ryan, M. L. (2020). 2019 Annual Report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 37th Annual Report. Clinical toxicology (Philadelphia, Pa.)58(12), 1360–1541. https://doi.org/10.1080/15563650.2020.1834219

Nelson, L. S., Howland, M. A., Lewin, N. A., Smith, S. W., Goldfrank, L. R., Hoffman, R. S., & Flomenbaum, N. E. (2019). Goldfrank’s toxicologic emergencies (11th ed.). Mc Graw Hill Education.

Shannon, M. (2007). Haddad and Winchester’s clinical management of poisoning and drug overdose (4th ed.). Saunders.

NB Museum Mushroom Checklist: http://website.nbm-mnb.ca/mycologywebpages/Checklists/NBMushrooms/NBMushroomChecklist.html

Tavassoli, M., Afshari, A., Arsene, A. L., Mégarbane, B., Dumanov, J., Bastos Paoliello, M. M., Tsatsakis, A., Carvalho, F., Hashemzaei, M., Karimi, G., & Rezaee, R. (2019). Toxicological profile of Amanita virosa – A narrative review. Toxicology Reports, 6, 143–150. https://doi.org/10.1016/J.TOXREP.2019.01.002

Amanita virosa photo: https://www.tehrantimes.com/news/423947/Mushroom-poisoning-kills-18-in-Iran

White mushroom photo: https://www.stockfood.com/images/00395464-Several-button-mushrooms

Amanita phalloides photo: http://www.bccdc.ca/about/news-stories/stories/2020/death-cap-mushrooms-make-fall-appearance-in-urban-areas

 

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When you catch more than fish – Fish Hook Removal

When you catch more than fish – a Resident Clinical Pearl on Fish Hook Removal

Melanie Johnston

PGY2, FMEM Program, Dalhousie University

Reviewed & Copyedited by Dr. Mandy Peach

Introduction

Fishing is a common recreational activity in the Maritime provinces and fishhook injuries are common presentations among both recreational and commercial fishers, particularly during the warm weather months. Individuals may try to remove the fishhook themselves prior to presenting to the emergency department. While some may be successful, many will require evaluation and management in the emergency department for removal.

The majority of fishhook injuries are penetrating soft tissue injuries involving the hands, feet, or head, but can involve any body part.1 Most injuries involve superficial structures because of the forces applied to the fishing line that drive the barb parallel to the skin and keep it from penetrating deeper structures. There are four commonly used techniques to remove fishhooks, and the choice of technique will depend on the body part affected, depth of penetration, and the type of fishhook.2

Initial Evaluation

To determine the most appropriate technique for removal:

  • Determine what type of fishhook was being used (shape, size, # of hooks, location and # of barbs)
  • Perform a thorough neurovascular exam both proximal and distal to wound
  • Assess penetration depth; if difficult to assess, radiographs should be utilized for further evaluation (rule out bone and joint involvement)
  • Determine if tetanus immunization status is up to date

Figure 1: Types of fishhooks (A) Simple single barbed fishhook, (B) Multiple- barbed fishhook, (C)Treble fishhook.1

Complicated Fishhook Injuries

While the majority of fishhook cases are uncomplicated, those that require specialist referral and follow-up include:
– fishhook injuries involving the eyeball or orbit
– fishhook injuries with joint/tendon involvement
– fishhook injuries involving vital structures (carotid, radial artery, testicle, urethra)

In these cases, specialist consultations are warranted prior to fishhook extraction.1-3

Figure 2: Fishhook injury involving eye.5

Preparation for Fishhook Removal

Wound preparation: remove any additional materials attached to the fishhook (fishing line, lures, weights) using scissors/wire cutters. Surrounding skin should then be cleansed (betadine, chlorhexidine, saline irrigation).1

Pain control: Local or regional anesthesia is sufficient for most cooperative patients. If the hook is embedded in fingers or toes consider a digital block. Young children may warrant procedural sedation if uncooperative.

Tetanus prophylaxis: Status should be verified and prophylaxis given when indicated.

Four Primary Techniques for Fishhook Removal

The four primary techniques described for the removal of fishhooks are:

  • retrograde
  • string-yank
  • needle cover
  • advance and cut.1-3

The retrograde and string-yank methods generally result in the least amount of tissue trauma.

The needle cover and advance and cut techniques are generally reserved for more difficult fishhook removals.

It may take multiple techniques and attempts before a fishhook can be successfully removed. The physician should take care not to be struck by the hook on removal and eye protection should be worn.

 

Figure 3: Fishhook structure.6

 

Retrograde “Back Out” technique:

Lowest success rate. Works well for barbless/superficial embedded hooks.1

Figure 4: Retrograde technique.1

  • Apply downward pressure to the shank of the hook (helps to rotate the gook and disengage the barb)
  • Back the hook out of the skin along the path of entry
  • If any resistance/catching of the barb is experienced, should stop and consider other removal techniques

 

String-Yank Technique:

Modification of the retrograde technique. Considered to be least traumatic as it creates no new wounds.1 Generally works best on small-medium sized hooks. Cannot be performed on parts of the body that are not fixed (eg. earlobe).

Figure 5: String-Yank Technique

  • Wrap a 3-0 silk culture around the midpoint of the bend in the fishhook with the free ends of the string held tightly (can achieve a better grip wrapping the free ends around a tongue depressor or around the providers fingers)
  • Stabilize the involved skin area against a flat surface as the shank is depressed parallel against the underlying skin
  • Apply a firm quick pull parallel to the shank while continuing to exert pressure on the fishhook
  • Examine hook to ensure that the barb is intact and has been removed

Failure of this technique is most often due to non-forceful pull.

 

Needle Cover Technique:

Works well for removal of large hooks with single barbs that are superficially embedded and can be easily covered by a needle.3

Figure 6: Needle Cover Technique

  • Advance an 18 gauge (or larger) needle along the entrance wound of the fishhook
  • Direction of insertion of needle should be parallel to the shank, with the bevel pointing towards the inside of the curve of the fishhook (allows the needle to engage the barb)
  • Advance the fishhook to disengage the barb, then pull and twist so that the point of the hook enters the lumen of the needle
  • Back the fishhook out of the path of entry, moving the needle along with the fishhook

 

Advance and Cut Technique:

Almost always successful, irregardless of fishhook size. Disadvantage of this technique is additional trauma to surrounding tissue. This technique is most effective when the point of the fishhook is located near the surface of the skin.3

Figure 7: Advance and Cut technique

  • Using a needle driver (or pliers), advance the fishhook, including the entire barb, through the skin
  • Cut the advanced portion (including barb) free with pliers or other cutting tool
  • Remove the remaining portion of the fishhook back out of the original entrance wound (should be no resistance)

 

Post Fishhook Removal Wound Care
– Explore wound for possible foreign bodies (bait)
– Generally wound is left open to heal by secondary intention
– Rinse wound with normal saline irrigation post fishhook removal
– Consider application of antibiotic ointment and simple dressing
– Majority of individuals with superficial wounds do not require prophylactic antibiotics; consider in those who are immunosuppressed or who have poor wound healing (diabetics, peripheral vascular disease).

  • The most common pathogens involved in fishhook wound infections are Staph aureus, and Strep pyogenes originating from the patients’ skin flora. As such oral antibiotic coverage could include five days of: Keflex, Penicillin, Amoxicillin, Clindamycin, Septra.
    – Antibiotics for any deep wound involving tendons, cartilage, or bone
    – Discuss monitoring for signs/symptoms of infection and return for reassessment if any complications
    – Patients who receive antibiotics should be scheduled follow up evaluation in 2-3 days to assess for signs of infection

 

Bottom Line: Fishhook injuries are common emergency department presentations among both recreational and commercial fisherman. The majority of these injuries are superficial, soft tissue injuries that can be managed with one of the four techniques described above.

The initial evaluation of these patients should include a thorough neurovascular exam and assessment to determine any features that would deem the injury complicated (joint/bone involvement, orbit/eyeball involvement, vascular injury) requiring specialist consultation or further investigations (Xray).

The choice of technique utilized will vary depending on type of fishhook, location of injury, depth, and practitioner comfort. Some injuries may require multiple attempts and techniques before the hook will be successfully removed.

Post fishhook removal, the wound should be thoroughly irrigated and left to heal by secondary intention. The majority can be managed with antibiotic creams and at-home monitoring for signs of infection, but those at risk of poor wound healing can be considered for prophylactic antibiotics.

 

References:
1. Gammons, M.; Jackson, E. Fishhook Removal. Am Fam Physician. 2001 Jun 1;63(11):2231-2237. Retrieved from https://www.aafp.org/afp/2001/0601/p2231.html.

  1. Bothner, J. Fishhook removal techniques. Updated Mar 01, 2020. Retrieved from: https://www.uptodate.com/contents/fish-hook-removal-techniques?search=fishhook%20removal%20&source=search_result&selectedTitle=10~150&usage_type=default&display_rank=10#H13

  2. Riveros, T., Kim, J., Dyer, S. Trick of the Trade: Fishhook Removal Techniques. 2018, Jan 8. Retrieved from: https://www.aliem.com/trick-fishhook-removal-techniques.

  3. Cover photo: https://www.outdoorlife.com/photos/gallery/fishing/2012/04/survival-skills-how-remove-fish-hook-and-treat-injury/

  4. Inchinogolo, F. Fish-hook injuries: a risk for fisherman. Head & Face Medicine
    Volume 6, Article number: 28 (2010)

  5. Fish hook structure, retrieved from: https://en.wikipedia.org/wiki/Fish_hook
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A life threatening case of Hiccups

A life threatening case of Hiccups – A Resident Clinical Pearl

Mark McGraw, PGY3 FMEM program,  Dalhousie University Saint John

Reviewed by Dr. Luke Taylor

Copyedited by Dr. Mandy Peach

Introduction:

Its mid morning on an acute shift in the emergency department and you hear a familiar but somewhat out of place sound coming from around the corner. You look up to see the triage nurse walking in a middle-aged male patient who is hiccuping constantly. The patient looks unwell and is pale, but he is able to walk into the department without assistance. The triage nurse asks the charge doc where she should place the patient. He has had intractable hiccups for over a week and has been unable to sleep or eat anything. His chief complaint is hiccups and weakness. She notes he also has a small infected cyst on his back that is being treated with Keflex from one of the local surgeons and had a subjective fever at home. Vitals on triage were normal but she was concerned because he just didn’t look right. You suggest he take a trauma bed and state you’ll see him now based on his appearance and wonder to yourself how often a trauma bed is taken up with someone who has a chief complaint of hiccups….

A little background:

Hiccups are a bit of a physiologic anomaly and appear to have no protective effect or evolutionary purpose. Hiccups can be found early in life and are can be found as early as the second trimester of pregnancy. The incidence of hiccups in the general pediatric and adult population is unknown but its fair to say the majority of people have experienced them at some point in their lives. To most, hiccups are nothing more than a brief annoyance or embarrassing distraction but in some cases they can herald sinister pathologies.

Hiccups result from inappropriate closure of the glottis through a reflex arc that consists of the phrenic nerve, vagus nerve, and thoracic sympathetic chain. During inspiration our glottis remains patent allowing unimpeded airflow into the lungs. The hiccup reflex triggers glottis closure, typically triggered during the swallowing to prevent aspiration, about 30 milliseconds after the onset of inspiration resulting in a rush of air against a closed glottis.

The majority of problematic hiccup cases arise from stimulation, inflammation, or injury to nerves of the afferent reflex arc. Two of the most common causes of benign hiccups are gastric distension from eating a large amount of food or consuming carbonated beverages and relaxation of the glottis due to alcohol ingestion.

The differential for hiccups is broad. UpToDate lists over 50 items on its differential for persistent/intractable hiccups grouped as CNS disorders, vagus/phrenic irritation, GI disorders, thoracic disorders, CV disorders, toxic/metabolic causes, postoperative, drug induced, and psychogenic.

Hiccups under 48 hours

In patients with hiccups lasting less than 48 hours and without red flag symptoms or other warning signs it is reasonable to try physical maneuvers to stop hiccups. The goal of all these maneuvers is stimulation/irritation of the afferent reflex arc.

• Breath holding or Valsalva maneuvers (increasing hypercapnia),
• Sipping or gargling cold water (nasopharynx irritation)
• Swallowing a spoonful of dry sugar (nasopharynx irritation),
• Pulling a patient’s knees to his/her chest and having them lean forward (decrease diaphragmatic pressure)

Hiccups over 48 hours

There is little quality evidence on the treatment of hiccups. In general, if an etiology is suggested from the history and physical target treatment, i.e. using a PPI in patients with underlying GERD, should be considered.

A 2015 systematic review suggested the use of baclofen and gabapentin as first line agents in treating hiccups with metoclopramide and chlorpromazine used as second line agents. A follow up systematic review in 2017 published in the journal of emergency medicine found that only baclofen and metoclopramide had randomized control trials supporting their efficacy. Baclofen was found to be particularly effective for treatment of intractable hiccups associated with stroke.

Treatment options:

• Baclofen 5 to 10 mg PO TID,
• Gabapentin 100 to 400mg PO TID,
• Metoclopramide 10mg PO TID or QID,
• Chlorpromazine 25mg PO TID,

A recent case report published in the American Journal of Emergency Medicine (Kocak et al., 2020) demonstrated almost immediate termination of hiccups in a patient following a subdermal injection of lidocaine and thiocolchicoside into the sternocleidomastoid muscle and epigastric region.

 

 

Back to our case

Our patient settles into a bed in the trauma bay and his repeat vitals show a declining blood pressure and increasing heart rate. His only complaint at this time continues to be his persistent hiccups. Cardiac, respiratory, abdominal and CNS exams are unremarkable. When you assess the “small lump” on his back you find an area of erythema extending from the superior tip of his scapula to his L1/L2 region inferiorly with a large softball size nodule around the lateral border of his scapula. You initiate empiric therapy with pip/tazo and clindamycin and call for an urgent CT scan and surgical consult.

While prepping for the scan the patient asks about treatment for his hiccups. You decide to try metoclopramide 10mg IV, which does nothing to alleviate his hiccups. His CT scan confirms a massive abscess extending from his deltoid muscle to his obliques with infiltration into the muscle and fascia. He is taken to the OR by a team of 3 surgeons for emergent debridement of his necrotizing fasciitis. After a brief stay in the ICU he is transferred to the surgical floor where you find out his hiccups have resolved.

Summary
The next time you are working in the emergency department and a patient presents with hiccups here are a few helpful points to remember:

• Patients with hiccups lasting less than 48 hours in the absence of red flag / systemic symptoms typically do not require medical workup or treatment.
– Physical maneuvers to terminate hiccups may provide relief for patients in the ED.
• Patients with persistent hiccups over 48 hours warrant a full physical exam and laboratory studies tailored to the patient’s history as hiccups may be the initial manifestation of an underlying neoplasm, infection, or metabolic disorder.
• If no underlying etiology is found there is reasonable evidence to support empiric treatment with metoclopramide 10mg PO TID or baclofen 5 to 10mg PO TID.
• In patients with persistent hiccups secondary to another disease process empiric treatment may be a useful adjunct while the underlying cause is addressed.

 

References

Polito NB, Fellows SE. Pharmacologic Interventions for Intractable and Persistent Hiccups: A Systematic Review. J Emerg Med. 2017 Oct;53(4):540-549. doi: 10.1016/j.jemermed.2017.05.033. PMID: 29079070.
Steger M, Schneemann M, Fox M. Systemic review: the pathogenesis and pharmacological treatment of hiccups. Aliment Pharmacol Ther. 2015 Nov;42(9):1037-50. doi: 10.1111/apt.13374. Epub 2015 Aug 25. PMID: 26307025.
Kocak AO, Akbas I, Betos Kocak M, Akgol Gur ST, Cakir Z. Intradermal injection for hiccup therapy in the Emergency Department. Am J Emerg Med. 2020 Sep;38(9):1935-1937. doi: 10.1016/j.ajem.2020.03.044. Epub 2020 Mar 25. PMID: 32245702.
Chang, F. Y., & Lu, C. L. (2012). Hiccup: mystery, nature and treatment. Journal of neurogastroenterology and motility, 18(2), 123–130. https://doi.org/10.5056/jnm.2012.18.2.123
Image of reflex arc: http://blog.clinicalmonster.com/2017/03/23/so-bored-i-hiccuped/
Marion, DW. Hiccups. In: UpToDate, Post, TW (Ed), UpToDate, Waltham, MA, 2020.

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