IDEA Series: DIY Suture Kit Station

laceration suture repair closure

In medical training there is a lack of simulation based activities including procedural labs. Suturing is a critical skill for trainees to master in the emergency department. However, supervised practice is needed prior to suturing a real patient for the first time. This innovation allows early trainees to master suturing while on shift, using easy to find materials, which increases procedural competency and confidence. This activity allows the teacher to assess and correct the trainees procedural skills prior to attempting to suture a real patient.

Name of innovation

  • This Do-It-Yourself Suture Kit Station incorporates easy to find materials available in every emergency department, allowing early trainees to master suturing prior to suturing real patients.

Learners targeted

  • Medical students and early trainees who need suture practice

General group size

  • One-on-one student training is ideal, but can have multiple students who can practice using multiple suturing stations
  • If teacher unable to instruct while on shift, trainees can be shown a suture training video and practice alongside the video

DIY suture training kit for laceration repair

Materials needed

  • Blue chuck pad
  • Paper/cloth tape
  • Scalpel
  • Suture material
  • Suture kit

More detailed description of the activity and how it was run

  • Make the DIY Suture Kit Station (see above video):
    • Place a thick chuck pad on a flat sturdy surface.
    • Apply cloth tape to the entire surface of the chuck, and tape over the chuck. This is now the suturing pad.
    • Use a scalpel to make an incision to the pad.
    • Use the back blunt end of the scalpel to ‘fluff’ up incision edges to make laceration.
  • Use a laceration repair kit and suture to close the laceration.
  • Instruct the trainee on proper suturing technique on the suture station (or show a suture training video)
  • Have the trainee continue practicing until adequate comfort and proficiency level is achieved
  • Suture real patient!

Lessons learned, especially with regard to increasing resident and program buy in

  • Procedural skills require much repetition to gain proficiency. This is best done with video tutorials, supervision, and deliberate practice.
  • Practicing in a simulated environment greatly improves skill and confidence in real clinical practice.

Educational theory behind the innovation including specifics/styles of teaching involved

  • Simulation practice increases procedural competency.
  • Practicing on shift allows trainees to reach the number of repetitions required to gain mastery in suturing, Routt [1] showed that the number of repetitions required to gain proficiency was 41 times.
  • Competency in suturing is required even when cases are low. Wongkietachorn et al. demonstrated that tutoring suturing improves the trainees’ skillset. A practice suture kit helps improve retention for real-life scenarios [2].

Pearls

  • This DIY suture pad station technique is easily available and inexpensive.
  • To improve suturing techniques and enhance skill retention, medical students and early trainees need to learn with guided supervision on simulated task trainers.

 

References

  1. Routt E, Mansouri Y, de Moll EH, Bernstein DM, Bernardo SG, Levitt J. Teaching the Simple Suture to Medical Students for Long-term Retention of Skill. JAMA Dermatol. 2015 Jul;151(7):761-5. doi: 10.1001/jamadermatol.2015.118. PMID: 25785695.
  2. Wongkietkachorn A, Rhunsiri P, Boonyawong P, Lawanprasert A, Tantiphlachiva K. Tutoring Trainees to Suture: An Alternative Method for Learning How to Suture and a Way to Compensate for a Lack of Suturing Cases. J Surg Educ. 2016 May-Jun;73(3):524-8. doi: 10.1016/j.jsurg.2015.12.004. Epub 2016 Feb 20. PMID: 26907573.
By |2021-10-08T10:19:05-07:00Oct 15, 2021|IDEA series, Trauma|

SplintER Series: Don’t Go Breaking My Heart

A 45-year-old man presents to the emergency department with chest pain after a high-speed motor vehicle accident where his sternum hit the steering wheel. You notice an area of ecchymosis noted over his sternum, so you decide to get a CT scan (Figure 1).

Figure 1. Case courtesy of Dr Henry Knipe, Radiopaedia.org, rID: 26332

 

(more…)

Stanford’s INFODEMIC Conference on COVID-19 Misinformation: Open-access podcasts

In July 2021, Dr. Vivek Murthy became the first U.S. Surgeon General to declare health misinformation a public health crisis. Specifically, COVID-19 vaccine misinformation and disinformation on social media greatly affects vaccination rates in certain populations. Rapid increases in reliable health information about COVID-19 can be overshadowed by the spread of even greater amounts of misinformation, leading to an ‘infodemic.’

The World Health Organization defines an infodemic as:

“… too much information including false or misleading information in digital and physical environments during a disease outbreak. It causes confusion and risk-taking behaviours that can harm health. It also leads to mistrust in health authorities and undermines the public health response. An infodemic can intensify or lengthen outbreaks when people are unsure about what they need to do to protect their health and the health of people around them.”

INFODEMIC Conference on Social Media and COVID-19 Misinformation

On August 26, 2021, Stanford University’s Department of Emergency Medicine and Ethics, Society, and Technology Hub co-sponsored a unique conference to address this issue, “INFODEMIC: A Stanford Conference on Social Media and COVID-19 Misinformation.” Speakers presented virtually from around the world including experts in social media, health policy, ethics, and medicine. The conference focused on the causes of COVID-19 misinformation and mitigation strategies. Vaccine Confidence, Vaccine Hesitancy, and Vaccine Equity were among the main topics of the meeting. INFODEMIC also featured representatives from Facebook, Google, and Twitter, as well as physician influencers, to discuss the role of social media companies to address misinformation online.

Below are recordings of each of the INFODEMIC conference presentations, presented as podcasts. Video recordings of these presentations are also available to view online. The conference agenda and featured speakers are listed on the Stanford INFODEMIC website.

Podcasts

By |2021-10-06T19:40:30-07:00Oct 8, 2021|Academic, COVID19|

SmilER 104: Pericoronitis and Dry Socket

This fourth and final installment in the SmilER series covers the diagnosis and management of 2 common dental conditions that present to the emergency department: pericoronitis and dry socket.

Author: Richard Ngo, DMD
Editors: Cameron Lee, DMD, MD; Andrew Eyre, MD, MS-HPEd
Series Editor: Chris Nash, MD

How well did you learn the material? Go to ALiEMU to take the multiple-choice quizzes to receive your badges and certificates.

Learning Objectives

  1. Understand diagnostic criteria of pericoronitis and alveolar osteitis (dry socket).
  2. Understand treatment modalities for patients with pericoronitis and alveolar osteitis (dry socket).
  3. Name some of the pharmacological adjuncts to aid in recovery.
  4. Review key points to include in discharge instructions.

Diagnosis

Patients may present to the ED with pericoronitis, an inflammation of the gingival soft tissue overlying a mandibular third molar. This soft tissue is subject to trauma from the patient biting down and may lead to pericoronitis due to normal oral flora. Patients with compromised host defenses may more easily develop pericoronitis. Repeated trauma to the operculum, the soft tissue overlying a partially erupted tooth, may lead to increased swelling more easily subject to subsequent trauma—a vicious cycle leading to worsening pain and erythematous swelling. Food may also become entrapped under the soft tissue due to difficulty maintaining oral hygiene.

Pericoronitis is a clinical diagnosis and does not require imaging.

Treatment, discharge, and follow up

  1. Irrigation: In the emergency department and as an outpatient, irrigation of food debris under the operculum using chlorhexidine or normal saline can acutely reduce bacterial counts.
  2. Antibiotics: The patient can be prescribed penicillin, or clindamycin if allergic to penicillin. If not treated, pericoronitis may result in a localized soft tissue infection (see SmilER 103).

The patient should follow-up with an outpatient dentist to prevent recurrent infections. This typically involves the patient undergoing definitive treatment, that is, extraction of the offending tooth.

Diagnosis

Dry socket, also known as alveolar osteitis, is moderate to severe pain experienced after dental extraction due to exposure of bony surfaces. The pain typically begins 3-5 days following a tooth extraction. Although the cause is unclear, it is thought to be related to fibrinolytic activity within the extraction socket, which leads to lysis of the developing blood clot. The subsequent exposure of bone leads to moderate to severe pain that may be dull and aching. This pain may radiate to the ipsilateral ear. Associated symptoms include a foul odor or taste. Although dry socket is rare (2%) following routine dental extractions, it is more commonly associated with extraction of the mandibular third molars.

Dry socket diagram

Dry socket illustration for exposed bone and nerve after a blood clot is dislodged

Treatment, discharge, and follow up

Treatment of a dry socket is relatively simple. The premise is to NOT dislodge any newly forming blood clot, which serves as a protective covering.

  1. Irrigate the socket with sterile saline
  2. Gently suction away the excess saline, but do not go too deep into the socket as to evacuate the developing blood clot. The area also should NOT be curetted, as this will often worsen and possibly dislodge beneficial blood clots.
  3. Insert a medicated dry socket dressing (iodoform gauze) into the socket. These may be available in your emergency department or, alternatively, can be obtained from the pharmacy or as a commercial preparation from a dental supply company. Ingredients in this dressing include: eugenol to help with pain, topical anesthetic such as benzocaine, and a carrying vehicle such as balsam of Peru. Upon application, the patient should experience immediate relief within 5 minutes. Unfortunately, many emergency departments do not stock dry socket paste or Dressol-X. An alternative is ribbon gauze or Gelfoam impregnated with eugenol, iodine, or oil of cloves.

The patient should follow-up with an outpatient dentist or oral surgeon within 2 days to have their dry socket dressing changed every other day for the next 3-5 days.

References

  1. Hupp J, Ellis E, Tucker M. Contemporary Oral and Maxillofacial Surgery. Elsevier; 2019. 
  2. Berman L, Blanco L, Cohen S. A Clinical Guide to Dental Traumatology. Mosby; 2006.
  3. Kademani Deepak. Atlas of Oral and Maxillofacial Surgery. Saunders; 2015.

By |2023-02-07T13:43:30-08:00Oct 6, 2021|ALiEMU, Dental, SmilER|

SAEM Clinical Image Series: Silver Scales

A 6-year-old otherwise healthy female presented to the emergency department (ED) with a rash across all four extremities. She has had seven months of pruritic, expanding lesions starting on her shins, now beginning to expand on her forearms. No history of allergies or irritant exposure. Due to Covid-19, she has been unable to see a provider before today’s ED visit.

Vitals: T 98.3°F; BP 96/72; HR 92; RR 24; O2 sat 100%

Skin: Numerous patchy red lesions scattered across bilateral upper and lower extremities with silver plaque accumulation. No nailbed involvement. No mucous membrane involvement.

Non-contributory

Psoriasis vulgaris, plaque subtype, is a common dermatologic condition often seen in the outpatient setting. Plaques are most commonly noted on the knees, elbows, and lower back. The silvery plaques in characteristic locations are a hallmark of this diagnosis but are rarely seen to this extent. Unfortunately for this patient, this was the initial presentation due to the inability to access care during the COVID-19 pandemic.

Initial management is with high-potency topical corticosteroids. Systemic steroids should be avoided to prevent exacerbation or eruption of pustular psoriatic lesions. In this case, given the patient’s age and disease severity, she was seen in the ED by Dermatology and initiated on corticosteroid topical therapy. She was encouraged to establish care with rheumatology to be routinely screened for associated life-altering pathologies including psoriatic arthritis and uveitis.

Take-Home Points

  • When making a visual diagnosis of plaque psoriasis, evaluate for erythema, edema, or signs of superinfection.
  • Avoid systemic steroids given the risk of rash exacerbation, especially upon withdrawal.
  • Younger patients and those with more than 10% body surface area involvement should be evaluated by a dermatologist for initiation of topical corticosteroids and possible escalation to phototherapy, methotrexate, retinoids, or biologic agents.
  1. Menter A, Cordoro KM, Davis DMR, Kroshinsky D, Paller AS, Armstrong AW, Connor C, Elewski BE, Gelfand JM, Gordon KB, Gottlieb AB, Kaplan DH, Kavanaugh A, Kiselica M, Kivelevitch D, Korman NJ, Lebwohl M, Leonardi CL, Lichten J, Lim HW, Mehta NN, Parra SL, Pathy AL, Farley Prater EA, Rupani RN, Siegel M, Stoff B, Strober BE, Wong EB, Wu JJ, Hariharan V, Elmets CA. Joint American Academy of Dermatology-National Psoriasis Foundation guidelines of care for the management and treatment of psoriasis in pediatric patients. J Am Acad Dermatol. 2020 Jan;82(1):161-201. doi: 10.1016/j.jaad.2019.08.049. Epub 2019 Nov 5. Erratum in: J Am Acad Dermatol. 2020 Mar;82(3):574. PMID: 31703821.

 

 

 

SmilER 103: Odontogenic Infections

This third module for the SmilER series covers the diagnosis and management of odontogenic infections seen in the emergency department (ED). What anatomical structures should be avoided? When is imaging necessary? What is the discharge plan?

Author: Richard Ngo, DMD
Editors: Cameron Lee, DMD, MD; Andrew Eyre, MD, MS-HPEd
Series Editor: Chris Nash, MD

How well did you learn the material? Go to ALiEMU to take the multiple-choice quizzes to receive your badges and certificates.

Learning Objectives

  1. Understand the major classifications and diagnostic criteria of odontogenic infections.
  2. Understand the indications and contraindications for computed tomographic (CT) imaging as well as incision and drainage (I&D).
    • List the materials that are required to perform an incision and drainage.
    • List some of the potential complications of incision and drainage.
  3. Name some of the pharmacological adjuncts to aid in recovery.
  4. Review key points to include in patient discharge instructions.
Diagram showing caries leading to abscess formation

Evolution of odontogenic infections, progressing from caries, pulp inflammation, to abscess formation

Odontogenic infections are infections that are dental in origin. Infections start as carious (cavitary) lesions of the dentition that spread through the pulpal tissue to develop an abscess, a purulent collection that begins at the tooth’s root. From here, the abscess may extend through the mandible or maxilla to other regions of the mouth, face, and the rest of the body through the fascial planes of the head and neck.

Diagram showing abscess formation around the roots of the maxillary incisors

(A) Periradicular (around the root) infection in a maxillary incisor with the root apex close to the facial aspect of the maxilla results in erosion of the facial cortex and an abscess in the vestibular space. (B) Maxillary incisor with the root apex closer to the palatal cortex, increasing the likelihood of palatal cortical erosion and palatal abscess. [1] 

Abscess vs Cellulitis

An abscess is a localized, fluctuant mass that can be palpated upon physical examination. In contrast, cellulitis is characterized by diffuse induration without purulence. In both cases, patients may be febrile and may exhibit erythema or warmth of the infected site. Abscesses benefit from incision and drainage treatment, while antibiotics alone are sufficient for cellulitis.

Incision and Drainage (I&D)

For abscesses, the most important therapeutic intervention is the I&D of purulent material. The technique and approach is similar to the I&D of skin and soft tissue abscesses in other parts of the body. For odontogenic infections, I&D also changes the previously anaerobic environment into an aerobic one, thus making it difficult for anaerobic microbes to survive. As with skin and soft tissue abscesses, antibiotic therapy is a necessary adjunct to proper drainage.

Buccal abscess

Buccal space abscess spontaneously draining through the skin of the cheek (path of least resistance) [1]

.

Fascial Planes

The head and neck regions have many fascial planes containing potential spaces by which pus or cellulitis from odontogenic infections may spread. Major anatomic groups include: the midface, cheek and lateral face, mandible and below, and pharyngeal and cervical areas. Once eroded through bone, an infection can express itself in various places depending on the the relationship of muscle attachments to the site of perforation. Regions beyond the local buccal and vestibular spaces of the oral cavity should be escalated to specialty care, given anatomy complexity and potential risk for airway compromise or irreversible damage to anatomic structures.

Masticator Space Abscess

One example of a deep space that may become infected and requires specialty consultation is the masticator space. The masticator space is a general term that includes the any of the following spaces:

  • Pterygomandibular space
  • Submasseteric space
  • Superficial temporal space
  • Deep temporal space

The boundaries of the masticator space consists of the muscles of mastication, which including the following:

  • Masseter muscle
  • Medial and lateral pterygoid muscles
  • Temporalis muscle

The superficial and deep temporal spaces are separated from each other by the temporalis muscle. The lateral pterygoid muscle divides the pterygomandibular space from the infratemporal portion of the deep temporal space. The zygomatic arch divides the submasseteric space from the superficial temporal space. Abscesses within any of the components of the masticator space will require surgical drainage in an operating room under general anesthesia and should not be attempted in the ED.

The above axial cross-section diagram marks other extraoral regions which require specialty consultation. The fascial planes of the head and neck region may serve as potential pathways for the spread of infection into deeper spaces. As an example, the retropharyngeal space (yellow area in diagram above) allows for the potentially dangerous extension of infection into the mediastinum.

Part 1: History

Proper diagnosis of odontogenic infection in the ED begins with a thorough medical and dental history (see the Oral Examination and Local Anesthesia course). Additionally, ask about the course and progression of the swelling, dysphagia, odynophagia, dyspnea, foul breath or taste, and any immunocompromising conditions.

Part 2: Examination

Suction, irrigate, and examine the oral cavity thoroughly. Palpate any intraoral or extraoral masses to assess fluctuance or induration. Also note the following:

  • Location of swelling and dental pain
  • Floor of mouth elevation or induration
  • Uvular deviation
  • Periorbital swelling
  • Orbital proptosis

Measure the maximal incisal opening by asking patients to open their mouths as wide as possible; this is the greatest distance between the incisal edge of the maxillary central incisor and the incisal edge of the mandibular central incisor. A normal adult mouth opening is between 30-40 mm. Trismus, or reduced mouth opening, should raise concern for a potential deep space infection.

Measuring the maximal incisal opening with a ruler, between the incisal edges of upper and lower central incisors.

Measuring the maximal incisal opening, between the incisal edges of upper and lower central incisors.

A crucial odontogenic infection-related physical exam finding includes blunting of the inferior border of the mandible at the body; this is significant facial swelling that prevents the provider from palpating the bony structures at the body of the mandible.

Mandibular Anatomy

Anatomy of the mandible. An important exam finding includes swelling of the soft tissues overlying the body of the mandible.

Part 3: Imaging

Computed tomography (CT) imaging is indicated if there is concern for an odontogenic infection involving a deep fascial space. Two physical exam findings help predict when CT imaging is warranted [2].

  1. Blunting of inferior border of the mandibular body
  2. Trismus, as determined by maximum incisal opening <25 mm
Algorithm to determine need for CT vs Radiographs

Algorithm to determine whether CT imaging for odontogenic infection is necessary

If CT is not indicated, a Panorex panoramic radiograph is sufficient.

It can be challenging to determine when a patient’s odontogenic infection warrants specialist consultation in the ED, operative treatment, or inpatient admission.

High risk odontogenic infections

The patient will require inpatient admission and likely operative treatment for these following conditions in the setting of an odontogenic infection:

  • Involvement of the airway or deeper fascial spaces
  • Rapid progression of the infection
  • Need for general anesthesia
  • Dehydration or the inability to take fluids orally
  • Trismus
  • Immunocompromised status
  • Lack of improvement on oral antibiotics

These patients should be monitored for progression of the infection, as cases may rapidly progress to life-threatening conditions. If the infection is evident on the skin, mark the edge of the erythematous regions of the infection to monitor spread.

Odontogenic infections which do NOT require specialty consultation

Intra-oral maxillary and mandibular vestibular and buccal space swellings are infections limited to relatively safe, low-risk areas. These abscesses are amenable to incision and drainage by the emergency physician under local anesthesia. These are fascial spaces that will not cause airway obstruction and generally do not require general anesthesia or extraoral incisions to achieve adequate drainage. In these cases, patients normally do not complain of trismus, difficulty breathing, or swallowing. CT imaging is usually unnecessary.

1. Vestibular Abscess

Vestibular abscesses are infections that spread through bone to buccal tissues when the apex of the involved tooth is within the confines of the buccinator muscle attachment. The infection remains between the oral mucosa and the nearby facial muscle.

2. Buccal Abscess

3. Buccal Space Abscess

The buccal space lies superficial to the buccinator muscle and deep to the overlying skin and subcutaneous tissue. In these cases, the involved tooth’s apex is either superior or inferior to the insertion of the buccinator muscle. This potential space may become involved via infection of maxillary or mandibular molars.

A) When the tooth root apex is within the confines of the attachment for the buccinator muscle (in red), a vestibular space abscess localized medial to the buccinator muscle results. 

B) When the tooth root apex is outside of the confines of the attachment for the buccinator muscle (in red), a buccal space abscess localized lateral to the buccinator muscle results.


Odontogenic infections which DO require specialty consultation

Progression of infections to deeper spaces beyond the vestibular and buccal spaces increases the severity of the infection and thus requires specialty consultation. Indications for specialty consultation include any of the following:

  • The spread of infection to potentially dangerous fascial spaces, potentially leading to airway compromise
  • Difficulty swallowing
  • Trismus
  • Systemic signs of infection, such as a toxic appearance, respiratory distress, or altered mental status

In these cases, CT imaging is usually needed to determine the location and extent of the infection.

What deep space areas are especially dangerous?

Dangerous fascial planes include infection which spread:

  • Beyond the alveolar process (such as to the submental, sublingual, or submandibular spaces)
  • To the palatal spaces (medial relative to the maxillary dentition)
  • To the masticator space involving the muscles of mastication
  • To the more posterior oropharyngeal/retropharyngeal spaces
  • To the superiorly-located sinuses or orbital spaces
  • To any nearby vital structures such as major nerves and arteries (mental, lingual, facial, and ophthalmic bundles).

When in doubt, CT imaging should be obtained to determine proximity to nearby vital structures. In more severe cases, odontogenic infections may potentially lead to but are not limited to cavernous sinus thrombosis, Ludwig’s angina (the bilateral involvement of the submandibular, sublingual, and submental spaces), sinusitis, brain abscess, or mediastinitis. These more severe cases often require airway management, CT imaging, IV antibiotics, or emergent I&D in the operating room by specialty surgical services.

Examples of High-Risk Cases

The following figures indicate common regions involved in odontogenic infections for which escalation of care with specialty consultation is recommended. These complex infections include: palatal space abscesses on the palate of the mouth medial to the maxillary dentition, sublingual and submandibular space abscesses inferior to the tongue and floor of mouth, and abscesses that extends superiorly to involve the sinuses or orbits. To reiterate, any abscess requiring an extra oral approach for management requires specialist consultation.

Abscesses in the Mandibular Premolar Region:

Abscesses located in the mandibular premolar region are located near the mental neurovascular bundle. Those that require I&D need a cautious approach to avoid this vital structure. These may be better served by drainage by a consulting dentist or oral surgeon. 

Palatal Space Abscesses:

Found medial to the maxillary dentition. I&D should be escalated to specialty care to avoid damaging the greater and lesser palatine neurovascular bundles.

Sublingual Abscesses:The sublingual space lies between the oral mucosa and the mylohyoid muscle and can become infected from the mandibular premolar and first molar teeth. I&D should be escalated to specialty care as abscesses in this space are at high risk for rapid spread and airway compromise.

Submandibular Abscesses:

The submandibular space lies between the mylohyoid muscle and anterior layer of the deep cervical fascia, just deep to platysma muscle. It includes the lingual and inferior surfaces of the mandible below the mylohyoid muscle attachment. I&D should be escalated to specialty care as abscesses in this space are at high risk for rapid spread and airway compromise.

Potential risks for incision and drainage (I&D) should be discussed with the patient and informed consent obtained. These risks include but may not be limited to pain, bleeding, swelling, scarring, damage to adjacent anatomic structures, nerve damage, and the need for additional procedures.

Steps

  1. Examine the oral cavity for any foreign material.
  2. Suction out any blood, saliva, and purulence.
  3. Irrigate the oral cavity with copious normal saline.
  4. Administer local anesthesia should be administered via a regional block and/or into the mucosa adjacent to the site of infection. Be careful not to pass the needle from infected to uninfected tissue to avoid the unintended inoculation of offending bacteria. Additional anesthesia may be required in the setting of infection. If the initial level of anesthesia is suboptimal, partially drain the abscess and irrigate to remove some of the pus. This can improve the acidic pH of the infection, allowing for additional local anesthetic to be more effective.
  5. Palpate the abscess to determine where the incision would obtain maximum drainage.
  6. Make a 1- to 2-cm incision perpendicular to the underlying bone at the height of fluctuance, while avoiding any major anatomical structures.
    • Maxillary vestibular abscesses: Placing the incision in a dependent (inferior) position prevents incomplete drainage. Upon evacuation of pus, a syringe can be used to collect cultures to be sent for sensitivity analysis. Submucosal spreading to break open any loculations with a curved hemostat should be performed. Finally, irrigate the surgical site copiously.
Maxillary Vestibular Abscess

For a maxillary vestibular abscess, an incision at a dependent, inferior position (green arrow) helps to prevent incomplete drainage from the pooling of the purulence on the inferior aspect of the abscess cavity. An incision at a non-dependent, superior position (red arrow) may lead to pooling of purulence and inadequate drainage.

I&D Technique

Incision and drainage technique for vestibular abscess. (A) Periapical infection of a mandibular premolar (note buccal cortical erosion superior to the buccinator muscle attachment). (B) Incision made into fluctuant swelling to the depth of the abscess cavity. (C) Curved hemostat used in opening motion in various directions to break loculations of purulence within the abscess cavity. (D) Optional: insertion of a Penrose drain (1 cm diameter) into the depth of the abscess cavity. (E) Optional: suturing of the drain with a single nonabsorbable suture (3-0 silk).

Oral Hygiene

Patients should be prescribed chlorhexidine 15 mL swish and spit, twice daily for 1 week.

Antibiotics

Mixed aerobic and anaerobic bacteria cause most odontogenic infections. Antibiotics are an adjunct but not a replacement for incision and drainage in odontogenic abscess management. Antibiotics are particularly important for immunocompromised patients.

  1. Oral amoxicillin 500 mg TID for 3-7 days
  2. Alternative: Oral penicillin V potassium 500 mg QID for 3-7 days
  3. If first-line treatment fails: Either broaden the antibiotic therapy by adding oral metronidazole 500 mg TID for 7 days, or discontinue first-line treatment and prescribe oral amoxicillin 500 mg and clavulanate 125 mg (Augmentin) TID for 7 days.

 What if the patient has a penicillin allergy?

  • Inquire whether the patient has a history of anaphylaxis, angioedema, or hives with penicillin, ampicillin, or amoxicillin.
  • If the patient does not have any history of these severe allergic reactions, prescribe oral cephalexin 500 mg QID for 3-7 days.
  • If the patient does have such an allergic history, then prescribe oral azithromycin with a loading dose of 500 mg for one day, followed by 250 mg for an additional 4 days. An alternative to this would be oral clindamycin 300 mg QID for 3-7 days. If first-line treatment fails, then broaden antibiotic therapy to by adding oral metronidazole 500 mg TID for 7 days.

Pain Management

Postoperative pain can be managed with ibuprofen and/or acetaminophen. Peak swelling and inflammation is expected roughly 48 hours post-procedurally.

Follow-up

The patient must be instructed to follow up with an outpatient dentist as soon as possible to address the underlying cause of the infection. A root canal treatment or extraction of the offending tooth will likely be necessary to achieve source control of the infection. Failing this, the patient is likely to return to the ED with a recurring infection. Reasons for return to the hospital may include but are not limited to inadequate drainage with residual undrained loculations, spread of infection to deeper fascial planes, inappropriate antibiotic choice or dosage, or issues related to patient compliance.

References

  1. Hupp J, Ellis E, Tucker M. Contemporary Oral and Maxillofacial Surgery. Elsevier; 2019.
  2. Christensen BJ, Park EP, Suau S, Beran D, King BJ. Evidence-Based Clinical Criteria for Computed Tomography Imaging in Odontogenic Infections. J Oral Maxillofac Surg. 2019;77(2):299-306. PMID: 30347202
  3. Berman L, Blanco L, Cohen S. A Clinical Guide to Dental Traumatology. Mosby; 2006.
  4. Kademani D. Atlas of Oral and Maxillofacial Surgery. Saunders; 2015.

By |2022-09-22T06:43:34-07:00Sep 30, 2021|ALiEMU, Dental, SmilER|

ED Management of Cannabinoid Hyperemesis Syndrome: Breaking the Cycle

cannabis cannabinoid hyperemesis syndrome

What is cannabinoid hyperemesis syndrome?

Cannabinoid hyperemesis syndrome (CHS) is a condition in which patients who have been using cannabis or synthetic cannabinoids for a prolonged period of time develop a pattern of episodic, severe vomiting (usually accompanied by abdominal pain) interspersed with prolonged asymptomatic periods.

When should you consider cannabinoid hyperemesis syndrome as a diagnosis?

The diagnostic criteria for CHS require evidence of relief of symptoms with sustained cessation from cannabis, which makes them of limited utility in the Emergency Department (ED) [1]. However, a number of ED-based diagnostic criteria have been proposed with overlapping features [1,2]. There are 3 key components to assess for when making a presumed diagnosis:

  1. An episodic pattern of vomiting
    • Episodes of vomiting should last < 7 consecutive days
    • Asymptomatic periods often last > 1 month between episodes
  2. Prolonged cannabis use
    • Criteria vary: normally >1 time per week (often daily) for at least 1 year
    • Importantly, this is not an intoxication effect from a single large ingestion
  3. Exclusion of alternative diagnoses
    • Look for atypical features on history & exam including abnormal vital signs, diarrhea, focal abdominal pain, peritonitis, and jaundice
    • It is important to exclude pregnancy in all female patients
    • If a patient has never had an esophagogastroduodenoscopy (EGD), it is reasonable to refer newly diagnosed patients to gastroenterology for a non-emergent EGD to assess for a structural cause of the patient’s symptoms

What causes cannabinoid hyperemesis syndrome?

There is no singular theory that fully explains CHS. Importantly, the pattern of illness does not correlate well with the amount of cannabis consumed acutely, suggesting it is not related to a direct effect of the delta-9-tetrahydrocannabinol (THC) or a withdrawal effect. There are two prevailing theories related to changes in neuro-signaling and receptor expression with chronic THC exposure:

Theory #1: Downregulation of the cannabinoid receptor type 1 (CB-1) receptor which occurs with chronic THC use causing dysregulation of the hypothalamic-pituitary-adrenal stress axis. This theory supports why medications that have sedative or anxiolytic properties, such as haloperidol and benzodiazepines, have reported efficacy.

Theory #2: Changes in central nervous system dopamine signaling pathways with chronic THC exposure leading to a hypersensitive emesis response to dopamine. This theory is less well supported but has been used to explain the beneficial effects of dopamine antagonists such as haloperidol, droperidol, and olanzapine.

How should we treat cannabinoid hyperemesis syndrome in the ED?

Ondansetron, Metoclopramide, and Antihistamines

Traditional antiemetics have had low rates of success in treating CHS based on reported cases (ondansetron = 1.75%, metoclopramide = 4.35%) [3]. Antihistamines such as dimenhydrinate, diphenhydramine, and meclizine have no studies supporting their use, and the limited case reports available suggest they are ineffective [3]. While cases of treatment failure are more likely to be published which contributes to a reporting bias, clinical experience supports that CHS often does not respond well to these antiemetics. These medications may still have a role as an adjunct for patients who are refractory to other treatments, but given the evidence available supporting other agents, they can no longer be recommended as first-line therapy. Drawbacks to using a “traditional antiemetics first” strategies include a delay to effective treatment, prolonged ED length of stay, and prolongation of the QT interval.

Haloperidol

The HaVOC trial showed haloperidol was twice as effective as ondansetron at reducing nausea (change from baseline = -5.0 vs. -2.4) and abdominal pain (change from baseline = -4.3 vs. -2.1). Haloperidol also decreased rescue medication use (31% vs. 76%) and time from medication administration to ED discharge (3.1 hours vs. 5.6 hours) [4].

Lower doses of haloperidol were recommended (0.05 mg/kg) due to higher rates of adverse reactions with larger doses. Weight-band based dosing may be a more practical approach:

  • Haloperidol 2.5 mg IV for adults < 80 kg
  • Haloperidol 5 mg IV for adults > 80 kg

Olanzapine

There is very limited evidence supporting olanzapine specifically in CHS (6 reported cases) [3]. However, olanzapine has strong evidence supporting its antiemetic properties in oncology literature [5,6]. Unlike haloperidol, olanzapine does not prolong the QT interval and it has much lower rates of extrapyramidal side effects. Therefore, olanzapine may be a reasonable substitution for haloperidol in the following cases: documented allergy to haloperidol, prolonged QT interval, or previous extrapyramidal effects with haloperidol.

Capsaicin

While capsaicin is often discussed as a treatment [ALiEM trick of the trade], the evidence supporting its use is limited to a small case series and a small RCT with some significant limitations. The small RCT published in support of capsaicin had large baseline differences between the capsaicin and placebo groups. The placebo group was “more sick”, having higher baseline nausea which was not corrected for in the analysis [7].

The trial reported a significant reduction in nausea scores with capsaicin (60-minute nausea score: Placebo = 6.4 vs. Capsaicin = 3.2, p = 0.007) which looks impressive, but the change in nausea from baseline was much less substantial (change in nausea: Placebo = -2.1 vs. Capsaicin = -2.8). Overall, the evidence supporting capsaicin is limited, so its use should be a shared decision.

Benzodiazepines

Lorazepam has no studies assessing its utility in CHS, but a summary of case reports suggests an efficacy of 58.3% in 19 patients [3]. Despite the lack of evidence, clinical experience has led to lorazepam being recommended as an adjunct in recent cyclic vomiting syndrome guidelines for patients who have an anxiety component to their presentation [8]. Since 40-50% of traditional cyclic vomiting syndrome patients were chronic cannabis users, it is reasonable to extrapolate these guidelines to CHS until more specific literature is published.

Overall Approach to Treatment

Based on the currently available research outlined above and clinical experience, the following is a reasonable approach to acute symptomatic management of CHS in the ED:

What should we be considering at the time of discharge?

Like other chronic episodic illnesses (eg. migraines) the long-term management of CHS can be conceptualized to have three components: avoidance of triggers, management of acute episodes, and episode prevention (prophylaxis).

Avoidance of Triggers

  • The only cure for CHS is the prolonged cessation of cannabis. It is important to emphasize that it may take 6 months of cannabis cessation before symptoms improve, and to recognize that the challenges in stopping cannabis use are often underestimated. Professional addictions support is encouraged.

Management of Acute Episodes

  • Medications at home to abort acute episodes are a logical management strategy and may be a safe option to reduce recurrent ED visits in some patients. This will depend on which medications work for the patient, their comorbidities, and the patient’s access to reliable follow-up.
  • There is no current evidence to guide outpatient treatment. Traditionally, many gastroenterologists have used a combination of sublingual lorazepam and ondansetron which may be reasonable if a patient has responded to these medications in the ED.
  • The use of oral haloperidol at home is currently being studied, but there are no good protocols published to guide practice.

Episode Prevention

  • There have been no studies on using medications to reduce the frequency of CHS episodes. However, amitriptyline is recommended as a first-line prophylactic treatment for adults with cyclic vomiting syndrome as it reduces subjective symptoms scores, episode frequency, and ED utilization [9,10].
  • Using amitriptyline for CHS would be considered experimental and amitriptyline has several well-recognized side effects, requires slow up-titrated, and necessitates close follow-up. It may be reasonable for a patient to discuss with their primary care provider.

 

References

  1. Venkatesan T, Levinthal DJ, Li BUK, et al. Role of chronic cannabis use: cyclic vomiting syndrome vs cannabinoid hyperemesis syndrome. Neurogastroenterology & Motility. 2019 Jun;31(Suppl 2):e13606.
  2. Sorensen CJ, DeSanto K, Borgelt L, Phillips KT. Cannabinoid hyperemesis syndrome: diagnosis, pathophysiology, and treatment – a systematic review. Journal of Medical Toxicology. 2017;13:71-87.
  3. Richards JR, Gordon BK, Danielson AR, Moulin AK. Pharmacologic treatment of cannabinoid hyperemesis syndrome: a systematic review. Pharmacotherapy. 2017;37(6):725-34.
  4. Ruberto AJ, Sivilotti ML, Forrester S, et al. Intravenous haloperidol versus ondansetron for cannabis hyperemesis syndrome (HaVOC): a randomized, controlled trial. Annals of Emergency Medicine. 202 Nov;S0196-0644(20)30666-1.
  5. Hashimoto H, Abe M, Tokuyama O, Mizutani H, Uchitomi Y, Yamaguchi T, Hoshina Y, Sakata Y, Takahashi TY, Nakashima K, Nakao M, et al. Olanzapine 5 mg plus standard antiemetic therapy for the prevention of chemotherapy-induced nausea and vomiting (J-FORCE): a multicentre, randomised, double-blind, placebo-controlled, phase 3 trial. Lancet Oncology. 2020;21:242-49.
  6. Naravi RM, Qin R, Ruddy KJ, et al. Olanzapine for the prevention of chemotherapy-induced nausea and vomiting. New England Journal of Medicine. 2016 Jul;375(2):134-42.
  7. Dean DJ, Sabagha N, Rose K, et al. A pilot trial of topical capsaicin cream for treatment of cannabinoid hyperemesis syndrome. Academic Emergency Medicine. 2020;27:1166-72.
  8. Venkatesan T, Levinthal DJ, Tarbell SE, et al. Guidelines on management of cyclic vomiting syndrome in adults by the American neurogastroenterology and motility society and the cyclic vomiting syndrome association. Neurogastroenterology & Motility. 2019;31(Supp 2):e13604.
  9. Hejazi RA, Reddymasu SC, Namin F, et al. Efficacy of tricyclic antidepressant therapy in adults with cyclic vomiting syndrome: a two year follow up study. Journal of Clinical Gastroenterology. 2010;44:18-21.
  10. Namin F, Patel J, Lin Z, et al. Clinical, psychiatric and manometric profile of cyclic vomiting syndrome in adults and response to tricyclic therapy. Neurogastroenterology & Motility. 2007;19:196-202.
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