Nursemaid’s Elbow

Nursemaid’s Elbow

Medical Student Pearl

 

Erika Maxwell

@ErikaMaxwell

Memorial University Class of 2023

Reviewed by: Dr. David Lewis


Case

A 10-month-old female is brought into the Emergency Department by her mother with a left arm injury. The infant had a fall from standing and the mother reached out to grab her and caught her left forearm. After the incident, the patient’s mother noticed that the infant was no longer using the arm. The child has no medical history and is not taking any medications. She is vitally stable.

On exam, the child’s left arm is limp and extended at her side. She is using her right arm and hand exclusively, including to grasp for items on the left side of her body (pseudoparalysis). There is no deformity, erythema, edema, or ecchymosis. The arm and hand are neurovascularly intact (strong brachial pulse, pink and warm).


Differential Diagnosis

  • Nursemaid’s elbow/pulled elbow/radial head subluxation
  • Elbow fracture
  • Wrist fracture or soft tissue injury
  • Shoulder dislocation

Background

A pulled elbow occurs most frequently in young children with the median age for presentation being 2 years [1]. The reason for this is debated in the literature with some sources saying that the annular ligament is weaker in children [2] and others saying that the radial head is smaller [1], both resulting in a less stable joint.

The most common mechanism of injury is axial traction (i.e. pulling on the arm or hand), but falls or rough play may also be responsible [2].


Anatomical Context

The annular ligament holds the radial head in place next to the ulna. When axial traction is applied by pulling the forearm or hand, the radial head may move underneath the annular ligament and trap it in the radiohumeral joint, against the capitellum [1].

Figure 1: The arm on the left displays a normal elbow, whereas on the right the radius is subluxated and trapping the annular ligament against the capitellum [3].


Signs and Symptoms [3]

  • Pain at elbow
  • Pseudoparalysis of injured arm
  • Extension or light flexion of injured arm, often pronated

Diagnosis and Management

A full examination of the upper limb is required. Leave obviously swollen or deformed areas until the end. Palpate the clavicle, humerus, forearm and gently move the joints (shoulder, wrist, and lastly elbow). Pulled elbows rarely result in joint swelling. If this is present an alternative diagnosis should be considered (e.g., supracondylar fracture).

If a pulled elbow is the only likely diagnosis, then it may be reasonable to proceed to a subluxated radial head reduction manoeuvre. However, when the history is not clear (e.g., unwitnessed mechanism involving siblings or a fall), then it is much safer to perform further diagnostic tests prior to manipulation. These include radiograph of the elbow to rule out fracture or elbow ultrasound to rule out joint effusion [4].


Reduction Technique

 This is done by supporting the elbow with one hand and using your other hand to move the patient’s arm through the recommended maneuvers. There are 2 different maneuvers to try, and they may be used alone or in combination [1-3,5].

  • Supinate the child’s forearm with your hand and flex the elbow

 

Figure 2: Demonstration of the supination/flexion maneuver [5]

  • Hyperpronate the child’s forearm

Figure 3: Demonstration of the hyperpronation maneuver [5]

Some research has indicated that the hyperpronation maneuver may be more effective and less painful for the patient [2,6], so it may be worth attempting this maneuver first.

If the maneuvers are successful, you may hear a click from the radial head as it moves back into place. The child may briefly cry as the subluxation is reduced. Movement recovery can take anywhere from a few minutes to several hours, but usually occurs within 30 minutes. The greater the delay from injury to presentation and subsequent reduction, the longer it will take for post reduction return to normal movement [2].

If a click is heard or felt during the manoeuvre it can usually be assumed that reduction has occurred. Ideally, it is recommended that the child remain under observation until normal movement returns. However, if delayed, it is reasonable to discharge the child with advice to return.

In any case where an x-ray or ultrasound has not been performed and the child does not rapidly start using their arm post manoeuvre, then imaging is required prior to any further manipulation.


Prognosis

Although a pulled elbow does not result in a permanent injury, it is important to inform the family that their child will be vulnerable to recurrent pulled elbows in the affected arm. Up to 27% of patients with a pulled elbow may experience a recurrence [7-8].


Case continued:

Based on the patient’s history and physical exam, she was diagnosed with a pulled elbow. Using the supination and flexion maneuver followed by the hyperpronation maneuver, an audible click was elicited from the patient’s elbow. Shortly thereafter, she began using the arm again as if no injury had occurred and was discharged home.


Key points:

 

  1. A pulled elbow is a common upper limb injury in young children presenting to the Emergency Department
  2. Careful assessment may preclude the need for diagnostic imaging however if in any doubt further investigation should be performed prior to manipulation. Many physicians will never forget the time they used a pulled elbow reduction technique in a child with an unexpected supracondylar fracture
  3. HYPERPRONATE and/or SUPINATE & FLEX!
  4. Recurrence is common

References

  1. Aylor, M., Anderson, J., Vanderford, P., Halsey, M., Lai, S., & Braner, D. A. (2014). Reduction of pulled elbow. New England Journal of Medicine, 371(21), e32.
  2. Wolfram, W., Boss, D., & Panetta, M. (2018, December 18). Nursemaid Elbow. Medscape. Retrieved September 6, 2022, from https://emedicine.medscape.com/article/803026-overview#a5
  3. Boston Children’s Hospital. (2021). Nursemaid’s elbow. Retrieved September 6, 2022, from https://www.childrenshospital.org/conditions/nursemaids-elbow
  4. Varga, M., Papp, S., Kassai, T., Bodzay, T., Gáti, N., & Pintér, S. (2021). Two- plane point of care ultrasonography helps in the differential diagnosis of pulled elbow. Injury, 52(1), S21-24.
  5. Kilgore, K., & Henry, K. (2021). Nursemaid’s elbow. Society for Academic Emergency Medicine – Clerkship Directors in Emergency Medicine. Retrieved September 6, 2022, from https://www.saem.org/about-saem/academies-interest-groups-affiliates2/cdem/for-students/online-education/peds-em-curriculum/nursemaid%27s-elbow
  6. Lewis, D., Argall, J., & Mackway-Jones, K. (2003). Reduction of pulled elbows. Emergency Medicine Journal, 20, 61-62.
  7. Schunk, J. F. (1990). Radial head subluxation: epidemiology and treatment of 87 episodes. Annals of emergency medicine, 19(9), 1019-1023.
  8. Teach, S. J., & Schutzman, S. A. (1996). Prospective study of recurrent radial head subluxation. Archives of pediatrics & adolescent medicine, 150(2), 164-166.
Continue Reading

Bicuspid Aortic Valve – An important incidental PoCUS finding?

Bicuspid Aortic Valve – An important incidental PoCUS finding?

Medical Student Pearl

 

Khoi Thien Dao

MD Candidate – Class of 2023

Dalhousie Medicine New Brunswick

Reviewed by: Dr. David Lewis


Case:

A 58-year-old male presents to Emergency Department with sudden onset of chest pain that is radiating to the back. He was also having shortness of breath at the same time of chest pain. The patient later reveals that his past medical history only consists of “bicuspid valve”, and he takes no medication. On examination, he was uncomfortable, but no signs of acute distress. His respiratory and cardiac exam were unremarkable for reduced air sound, adventitious sound, heart murmur, or extra heart sound. ECG was normal and initial cardiac markers were within normal range. His chest x-ray is normal.

You are aware that with his medical presentation and a history of bicuspid aortic valve, you need to consider associated concerning diagnosis (aortic root aneurysm and aortic dissection) within the differential (myocardial infarct, congestive heart failure, pneumonia, etc.).


Bicuspid Aortic Valve

Bicuspid aortic valve is one of the most common types of congenital heart disease that affects approximately one percent of population. There is a strong heritable component to the disease. Bicuspid aortic valve occurs when two leaflets fused (commonly right and left coronary leaflets) and form a raphe, a fibrous ridge1. The fusion of the leaflets can be partial, or complete, with the presence or absence of a raphe1. Bicuspid aortic valve disease is associated with increasing risks for valve calcification, which lead to aortic stenosis or regurgitation secondary to premature degeneration1. This congenital heart defect is also a well-known risks factor for aortic dissection and aortic dilatation. Reports have estimated prevalence of aortic dilation in patients with bicuspid aortic valve ranging between 20 to 80 percent, and that the risks of aortic dilation increase with age2. Increases risk of aortic dilatation in bicuspid valve disease also leads to a significantly greater risk for aortic dissection2.3.

The majority of patients with bicuspid aortic valve are asymptomatic with relatively normal valve function and therefore can remain undiagnosed for many years. However, most patients with bicuspid aortic valve will develop complications and eventually require valve surgery within their lifetime. Early diagnosis, while asymptomatic, can enable close follow-up for complications and early intervention with better outcomes. However, asymptomatic individuals are rarely referred for echocardiography.

With increasing use of cardiac PoCUS by Emergency Physicians, there are two scenarios where increased awareness of the appearance of bicuspid aortic valve and its complications may be of benefit.

  1. Known bicuspid aortic valve patients presenting with possible associated complications
  2. Undiagnosed bicuspid aortic valve patients presenting with unrelated symptoms undergoing routine cardiac PoCUS

This clinical pearl provides a review of the clinical approach to bicuspid aortic valve and its associated complications and provides guide to enhancing clinical assessment with PoCUS.


Clinical Approach:

Although bicuspid aortic valve commonly presents as asymptomatic, a detailed focused cardiac history can assess for clinical signs and symptoms related to valve dysfunction and its associated disease, such as reduced exercise capacity, angina, syncope, or exertional dizziness1. Information about family history with relation to cardiac disease is essential for a clinician’s suspicion of heritable cardiovascular disease. Red flag symptoms that shouldn’t be missed such as chest pain, back pain, hypertensive crisis, etc. should be specifically identified. They are indicators for possible emergent pathologies that should not be missed (for example: acute MI, aortic dissection, ruptured aortic aneurysm, etc.)

Physical examination findings in patients with bicuspid aortic valve include, but not limited to, ejection sound or click at cardiac apex/base, murmurs that have features of crescendo-decrescendo or holosystolic. Clinical signs of congestive heart failure such as dyspnea, abnormal JVP elevation, and peripheral edema may also be present.


Core Cardiac PoCUS:

With cardiac PoCUS, it is important to obtain images from different planes and windows to increase the complexity of the exam and to be able to be confidently interpreting the exam. There are four standard cardiac view that can be obtained: parasternal short axis (PSSA), parasternal long axis (PSLA), subxiphoid (sub-X), and apical 4-chamber view (A4C). Each cardiac view has specific benefits.

Parasternal Long Axis

With the PSLA, the phased-array transducer is placed to the left sternum at 3rd or 4th intercostal with transducer orientation pointing toward patient’s right shoulder. Key structures that should be seen are Aortic Valve (AV), Mitral Valve (MV), Left Ventricle (LV), pericardium, Right Ventricle (RV), Left Ventricular Outflow Tract (LVOT), and portion of ascending and descending aorta8. It is primarily used to assess left ventricular size and function, aortic and mitral valves, left atrial size8. Furthermore, pericardial effusions and left ventricular systolic function can be assessed.

Parasternal Long Axis

 

Parasternal Short Axis

Using the same transducer position as the PSLA the transducer can be centered to the mitral valve and rotated 90 degrees clockwise to a point where the transducer marker points to patient’s left shoulder to obtain the PSSA. With this orientation, one can assess for global LV function and LV wall motion8. Furthermore, with five different imaging planes that can be utilized with this view, aortic valve can be visualized in specific clinical contexts.

Parasternal Short Axis

 

Apical 4-Chamber

The apical 4-chamber view is generated by placing the transducer at the apex, which is landmarked just inferolateral to left nipple in men and underneath inferolateral of left breast in women. This view helps the clinician to assess RV systolic function and size relative to the LV8.

Apical 4-Chamber

 

Subxiphoid

The subxiphoid view can be visualized by placing a transducer (phased-array or curvilinear) immediately below the xiphoid process with the transducer marker points to patient’s right. The movements of rocking, tilting, and rotation are required to generate an optimal 4-chamber subcostal view. A “7” sign, which consists of visualizing the border between liver and pericardium, the septum, and the RV and LV that looks like number 7. This view allows user to assess RV functions, pericardial effusion, and valve functions8. In emergency setting, it can be used for rapid assessments in cardiac arrest, cardiac tamponade, and global LV dysfunction8.

From –  the PoCUS Atlas

Subxiphoid labelled

 

7 Sign


PoCUS Views for Aortic Valve Assessment

In assessing the aortic valve, the PSSA and PSLA can be best used to obtain different information, depending on clinical indications. Both views can be used to assess blood flows to assess stenosis or regurgitation. However, the PSLA view includes the aorta where clinician can look for aortic valve prolapse or doming as signs of stenosis and its complications, like aortic dilatation. On the other hand, PSSA are beneficial when assessing the aortic valve anatomy.

Parasternal Long Axis

From PoCUS 101

Parasternal Short Axis

From – the PoCUS Atlas


PoCUS Appearance of Normal Aortic Valve (Tricuspid) vs Bicuspid Aortic Valve

With PSSA view, the normal aortic valve will have three uniformly leaflets that open and form a circular orifice during most of systole. During diastole, it will form a three point stars with slight thickening at central closing point. The normal aortic valve is commonly referred to as the Mercedes Benz sign.

Parasternal Short Axis – Normal Tricuspid AV – Mercedes Benz Sign and 3 cusp opening

Pitfall

However, the Mercedes Benz Sign sign can be misleading bicuspid valve disease when three commissure lines are misinterpreted due to the presence of a raphe. A raphe is a fibrous band formed when two leaflets are fused together. It is therefore important to visualize the aortic valve when closed and during opening, to ensure all 3 cusps are mobile. Visualization of The Mercedes Benz sign is not enough on its own to exclude Bicuspid Aortic Valve.

Apparent Mercedes sign when AV closed due to presence of raphe. Fish mouth appearance of the same valve when open confirming bicuspid aortic valve

Bicuspid Aortic Valve

Identification requires optimal valve visualization during opening (systole). Appearance will depend on the degree of cusp fusion. In general a ‘fish mouth’ appearance is typical for bicuspid aortic valve.

Parasternal Short Axis – Fish Mouth Opening – Fusion L & R Coronary Cusps – Bicuspid Aortic Valve

In the parasternal long axis view the aortic valve can form a dome shape during systole, and prolapse during diastole, rather than opening parallel to the aorta. This is called systolic doming. Another sign that can be seen in PSLA view is valve prolapse, when either right or non-coronary aortic valve cusps showed backward bowing towards the left ventricle beyond the attachment of the aortic valve leaflets to the annulus. This can be estimated by drawing a line joining the points of the attachment.

Systolic doming

 

Diastolic prolapse and systolic doming

 

 

 


PoCUS Appearance of the Complications of Bicuspid Valve Disease

In patients presenting with chest/back pain, shock or severe dyspnea who have either known or newly diagnosed bicuspid valve disease, PoCUS assessment for potential complications can be helpful in guiding subsequent management.

Complications of bicuspid aortic valve include aortic dilatation at root or ascending (above 3.8cm) and aortic dissection 5-9.

Dilated aortic root, from – sonomojo.com

Aortic root dilatation – Normal maximum = 40mm

 

Aortic root dilatation with dissection

Valve vegetations or signs of infective endocarditis are among the complications of severe bicuspid valve5-9

Aortic valve vegetations


General Management of Patients with Bicuspid Valve in the Emergency Department

Management of bicuspid aortic valve disease is dependent on the severity of the disease and associated findings.

For a patient with suspicious diagnosis of bicuspid valve disease, a further evaluation of echocardiography should be arranged, and patient should be monitored for progressive aortic valve dysfunction as well as risk of aortic aneurysm and dissection. Surgical intervention is indicated with evidence of severe aortic stenosis, regurgitation, aneurysm that is > 5.5cm, or dissection1.


How accurate is PoCUS for Aortic Valve assessment?

Bicuspid aortic valve disease is usually diagnosed with transthoracic echocardiography, when physical examination has revealed cardiac murmurs that prompt for further investigation. However, patients with bicuspid valve disease frequently remain asymptomatic for a prolonged periods. Michelena et al. (2014) suggested that auscultatory abnormalities account for 60 to 70% diagnostic echocardiograms for BAV in community10.

While there are no published studies on the utility of PoCUS for the diagnosis of bicuspid aortic valve, there are studies on the use of PoCUS as part of the general cardiac exam. Kimura (2017) published a review that reported early detection of cardiac pathology when PoCUS was used as part of the physical exam 9. Abe et al. (2013) found that PoCUS operated by expert sonographer to screen for aortic stenosis has a sensitivity of 84% and a specificity of 90% in 130 patients 11. In another study by Kobal et al. (2004), they found that PoCUS has a specificity of 93% and sensitivity of 82% in diagnosing mild regurgitation12.

There are also limitations of using PoCUS to assess for bicuspid aortic valve disease, or valve disease in general. Obtaining images from ultrasound and interpretation are highly dependent on user’s experiences to assess for the valve9. Furthermore, research is needed to investigate the use of PoCUS in lesser valvular pathology.

 

When a new diagnosis of bicuspid aortic valve is suspected, a formal echocardiogram should be arranged, and follow-up is recommended.


Summary 

  • Bicuspid aortic valve is often asymptomatic and undiagnosed until later in life
  • Patients with known bicuspid aortic valve disease are closely followed and may require surgical intervention in the event of complications
  • Diagnosis of bicuspid aortic valve requires careful visualization of valve closing and opening during diastole and systole
  • The increased use of PoCUS by Emergency Physicians as an adjunct to cardiac examination may result in increased diagnosis of bicuspid  aortic valve. These may be related to the presentation or incidental findings
  • In patients presenting to the Emergency Department with known or newly diagnosed bicuspid aortic valve disease, consider if a complication is related to their presentation
  • In patient with incidental finding of bicuspid aortic valve disease refer for cardiology follow up

 


References

  1. Braverman, A. C., & Cheng, A. (2013). The bicuspid aortic valve and associated aortic disease. Valvular heart disease. Philadelphia: Elsevier, 179-218.
  2. Verma, S., & Siu, S. C. (2014). Aortic dilatation in patients with bicuspid aortic valve. N Engl J Med370, 1920-1929.
  3. Della Corte, A., Bancone, C., Quarto, C., Dialetto, G., Covino, F. E., Scardone, M., … & Cotrufo, M. (2007). Predictors of ascending aortic dilatation with bicuspid aortic valve: a wide spectrum of disease expression. European Journal of Cardio-Thoracic Surgery31(3), 397-405.
  4. Tirrito, S. J., & Kerut, E. K. (2005). How not to miss a bicuspid aortic valve in the echocardiography laboratory. Echocardiography: A Journal of Cardiovascular Ultrasound and Allied Techniques22(1), 53-55.
  5. Baumgartner, H., Donal, E., Orwat, S., Schmermund, A., Rosenhek, R., & Maintz, D. (2015). Chapter 10: Aortic valve stenosis. The ESC textbook of cardiovascular imaging. European Society of Cardiology.
  6. Fowles, R. E., Martin, R. P., Abrams, J. M., Schapira, J. N., French, J. W., & Popp, R. L. (1979). Two-dimensional echocardiographic features of bicuspid aortic valve. Chest75(4), 434-440.
  7. Shapiro, L. M., Thwaites, B., Westgate, C., & Donaldson, R. (1985). Prevalence and clinical significance of aortic valve prolapse. Heart54(2), 179-183.
  8. Gebhardt, C., Hegazy, A.F., Arntfield, R. (2015). Chapter 16: Valves. Point-of-Care Ultrasound. Philadelphia: Elsevier, 119-125.
  9. Kimura, B. J. (2017). Point-of-care cardiac ultrasound techniques in the physical examination: better at the bedside. Heart103(13), 987-994.
  10. Michelena, H. I., Prakash, S. K., Della Corte, A., Bissell, M. M., Anavekar, N., Mathieu, P., … & Body, S. C. (2014). Bicuspid aortic valve: identifying knowledge gaps and rising to the challenge from the International Bicuspid Aortic Valve Consortium (BAVCon). Circulation129(25), 2691-2704.
  11. Abe, Y., Ito, M., Tanaka, C., Ito, K., Naruko, T., Itoh, A., … & Yoshikawa, J. (2013). A novel and simple method using pocket-sized echocardiography to screen for aortic stenosis. Journal of the American Society of Echocardiography26(6), 589-596.
  12. Kobal, S. L., Tolstrup, K., Luo, H., Neuman, Y., Miyamoto, T., Mirocha, J., … & Siegel, R. J. (2004). Usefulness of a hand-carried cardiac ultrasound device to detect clinically significant valvular regurgitation in hospitalized patients. The American journal of cardiology93(8), 1069-1072.
  13. Le Polain De Waroux, J. B., Pouleur, A. C., Goffinet, C., Vancraeynest, D., Van Dyck, M., Robert, A., … & Vanoverschelde, J. L. J. (2007). Functional anatomy of aortic regurgitation: accuracy, prediction of surgical repairability, and outcome implications of transesophageal echocardiography. Circulation116(11_supplement), I-264.
Continue Reading

Drop it like it’s Hot – Tetracaine eye drops following corneal abrasion?

Drop it like it’s Hot- A case presentation and critical appraisal on the use of tetracaine eye drops following corneal abrasion: A Medical Student Pearl

Claudia Cullinan

DMNB, Med 3

Reviewed by Dr. Kavish Chandra


Case:

It’s a sunny July afternoon and you are just starting your shift in the ED when a 25-year-old male presents with sudden onset of severe right eye pain. You bring him into the exam room, and he explains he ran into a tree branch. He is reluctant to open his eye due to the pain and his eye is watering uncontrollably. He also keeps his sunglasses on while you talk because his eye is now extremely sensitive to the bright ED lights.

The patient is visibly in a lot of distress, so you do a quick penlight exam and attempt to assess visual acuity to confirm there is no evidence of penetrating trauma.

At this point you suspect a corneal abrasion, so you move onto a slit lamp and fluorescein examination and add a tetracaine 0.5% (topical anesthetic) to the affected eye. The patient appears more comfortable within seconds. You are able to complete the exam with the patient sitting comfortably in the exam chair. There is no evidence of Seidel sign (streaming fluorescein caused by leaking aqueous humor) and no visible foreign body in the eye. You can visualise a linear yellow lesion along the lateral cornea when viewed with fluorescein under cobalt blue light and you are confident this is a simple corneal abrasion.


Figure 1. Corneal abrasion viewed with cobalt blue light after fluorescein staining. Accessed from DFOptometrists.com


You explain to the patient that he has a corneal abrasion, prescribe him erythromycin 0.5% ophthalmic ointment to be inserted into the affected eye QID for 5 days and encourage him to avoid rubbing his eyes. He can also take PRN ibuprofen if needed. He asks “That one eye drop made my eye feel so much better, can I have a bottle of that to bring home?”

You know he is talking about Tetracaine, and you remember learning about the controversy of using topical anesthetics for the outpatient treatment of corneal abrasions….what do you tell him?


Critical Appraisal : Short-term topical tetracaine is highly efficacious for the treatment of pain caused by corneal abrasions: a double-blind, randomized clinical trial. (2020)

Background:

Corneal abrasions are among the most common ophthalmic presentations to the emergency department (ED). They occur when the corneal epithermal becomes disrupted, such as when tiny foreign bodies land in your eye or when your new puppy accidentally scratches the surface of your eye.  Although corneal abrasions typically heal rapidly with minimal risk of complication, they are often VERY painful and can be extremely debilitating. There has been controversy on whether patients should be discharged home with topical anesthetics for short term management of corneal abrasions because of previously described safety concerns regarding toxicity. However, recent literature is beginning to surface suggesting there may be a role for short term topical analgesia following simple corneal abrasion, with appropriate follow up.

Figure 2. Anatomy of the cornea. Accessed form AAFP.org

Clinical Question:

How effective is the home use of topical tetracaine every 30 minutes PRN pain for 24 hours following corneal abrasion?

Reference

Shipman, S., Painter, K., Keuchel, M., & Bogie, C. (2021). Short-Term Topical Tetracaine Is Highly Efficacious for the Treatment of Pain Caused by Corneal Abrasions: A Double-Blind, Randomized Clinical Trial. Annals of Emergency Medicine, 77(3), 338–344.       https://doi.org/10.1016/j.annemergmed.2020.08.036


Study Overview:

Population: Patients 18-80 years old presenting to an urban ED in Oklahoma City with suspected acute corneal abrasion.

Intervention: 2mL bottle of Tetracaine 0.5% one drop applied q30 minutes PRN pain for a maximum of 24 hours + antibiotic ophthalmic solution (polymyxin B sulfate/ trimethoprim sulfate) 2 drops to affected eye q4h.

Control: 4 separate 0.5mL ampules of artificial tears (Systane) one drop applied q30 minutes PRN pain for a maximum of 24 hours + antibiotic ophthalmic solution (polymyxin B sulfate/ trimethoprim sulfate) 2 drops to affected eye q4h.

Outcome: Pain rating at 24-48h follow up.

Methods:

  • Prospective, double blind, randomised control trial of topical tetracaine vs control (artificial tears) in the ED following diagnosis of corneal abrasion in the ED.
  • Took place in an urban Oklahoma ED from 2015 to 2017.
  • One hundred and eleven patients were included and were randomly assigned to the treatment or control group.
  • The patients in both groups had similar baseline characteristics and baseline numeric rating scale (NRS) pain scores (0-10, 10 being the most pain).

Inclusion criteria:

Patients 18 to 80 years old, presenting to the ED with suspected acute corneal abrasion, and gave written informed consent.

Exclusion criteria:

Contact lens wearers, previous corneal surgery or transplant in the affected eye, presented more than 36 hours after their injury, had a grossly contaminated foreign body, had coexisting ocular infection, currently pregnant, retained foreign body, penetrating eye injury, receiving immunosuppression, allergy to study medication, unable to attend follow-up, unable to fluently read and speak English or Spanish, and any injury requiring urgent ophthalmologic evaluation.

Results:

Main outcomes at the 24-48hr follow up appointment:

  • The overall numeric rating scale (NRS) pain score was significantly lower in the tetracaine group compared to the control group (1 versus 8, P<0.001).
  • The number of patients found to have a small residual corneal abrasion on their follow up slit-lamp examination was similar between groups (18% in the tetracaine group and 11% in the control group).
  • There were only two complications in the tetracaine group (versus 6 in the control group), with similar rates of worsening corneal abrasions in both groups. All patients had normal healing after 10 days. No serious adverse outcomes were encountered.

Table 1. Patient baseline demographics and 24-48hr follow up data points.

Group Tetracaine (n=59) Control (n=59)
Age, y 35 (28-43) 38 (27-47)
Male patients, No. (%) 36 (61) 34 (58)
Baseline pain rating 7 (6-7.5) 7 (6-8)
24-48hr pain rating 1 (1-2) 8 (7-8)
No. of hydrocodone tablets recorded 1 7
Adverse Events, No (%) 2 (3.6) 6 (11)

Limitations and suggestions for future studies:

  • Although this was a double-blind study, there are two things that could have made patients aware of their treatment group. First, the control was packaged in 4 ampules and the treatment was packaged in a single bottle. Second, Tetracaine burns when administered to the eye and Systane (control) does not.
  • The study was slightly underpowered for the primary outcome of efficacy and certainly not powered to determine safety for rare adverse events associated with topical anesthetics. That being said, there are more patients in this trial demonstrating short term safety than previous care reports and series demonstrating tetracaine harm.
  • There was an extensive exclusion criterion, including patients who wear contacts (which are a common cause of corneal abrasions). By broadening the inclusion criteria, the results could be applied to a greater number of patients.
  • Patients were required to return for follow up at which time they were required to return their “study drops” so the drops cannot be abused. It would be more feasible to limit the amount of eye drops in the bottle so the patient does not have to return to the ED for bottle disposal.

Our conclusions:

Short term topical tetracaine is an efficacious analgesic for acute corneal abrasions, is associated with less hydrocodone use compared to control, and appears to be safe.

 


Case

Back to our original question…what do we tell our patient?

Provide him with a limited number of tetracaine drops and administer one drop in affected eye q30 minutes PRN pain for a maximum of 24 hours. Advise him to return to ED if his symptoms persist beyond 48 hours or get worse.


References

McGee, H. T., & Fraunfelder, F. (2007). Toxicities of topical ophthalmic anesthetics. Expert Opinion    on Drug Safety, 6(6), 637–640. https://doi.org/10.1517/14740338.6.6.637

Shipman, S., Painter, K., Keuchel, M., & Bogie, C. (2021). Short-Term Topical Tetracaine Is Highly        Efficacious for the Treatment of Pain Caused by Corneal Abrasions: A Double-Blind, Randomized             Clinical Trial. Annals of Emergency Medicine, 77(3), 338–344.       https://doi.org/10.1016/j.annemergmed.2020.08.036

Wipperman, J. L., & Dorsch, J. N. (2013). Evaluation and management of corneal abrasions.    American Family Physician, 87(2), 114–120.

Yu, C. W., Kirubarajan, A., Yau, M., Armstrong, D., & Johnson, D. E. (2021). Topical pain control for     corneal abrasions: A systematic review and meta-analysis. Academic Emergency Medicine, 28(8), 890–908. https://doi.org/10.1111/acem.14222

Continue Reading

SHC – EM Reflections

Thanks to Dr. Paul Frankish for leading SHC EM Reflection rounds today.

Key Learning Points

 


Case 1:

Polytrauma patient with fluctuant GCS, tenuous airway in prehospital phase of care, transient hypotension in ED.

 

Learning Points:

  1. Rocuronium has slower onset than Succinylcholine.
  2. Consider redosing of sedation agent for intubation if significant time has passed since the last induction dose.
  3. Ongoing paralysis is rarely if ever indicated for transport, particularly if adequate sedation and analgesia have been accomplished.

Rapid Sequence Intubation

 


Case 2:

Polytrauma patient with severe agitation, hypoxia, and significant chest injuries.

 

Learning Points:

  1. Hypoxia and hypotension should be avoided if at all possible, in neurotrauma patients
  2. Chest tube pearls
    1. Obtain a cooperative patient (ie. pain control, sedation)
    2. Measure out depth of chest wall and diaphragm position with POCUS
    3. Large incision as needed
    4. Consider a “twisting screwdriver” motion on insertion (avoids fissure)
    5. Confirm placement in thoracic cavity by feeling chest tube alongside finger thru the intercostal space

Tube Thoracostomy

 


Case 3:

Patient with severe necrotizing infection and septic shock.

 

Learning Points:

  1. Consider using POCUS for rapid evaluation of shock patient
  2. Paralytic only intubation should be reserved for peri-arrest patients
  3. Beware subtle presentations of necrotizing infection in immunocompromised patients (Diabetes, immunosuppressants, neutropenia)


Case 4:

Pediatric septic shock

 

Learning Points:

  1. Differential diagnosis for a sick neonate is broad (THEMISFITS mnemonic) but sepsis is generally always at the top of the list
  2. Bradycardia in a severely ill neonate is generally a pre-terminal event
  3. If possible intravenous/intraosseous administration of antibiotics is preferred to the IM route
  4. Oxygenation of a spontaneously breathing patient with a BVM device requires several things to be successful:
    1. Adequate seal
    2. Adequate respiratory effort to open valve component
    3. PEEP valve to close off exhalation port preventing entrainment of room air

Continue Reading

Academic Emergency Physician – New opportunities for a great work/life balance, based in a centre of academic excellence…

The Department of Emergency Medicine, Saint John is recruiting! We are seeking Emergency Physicians who want to deliver clinical excellence within a thriving collegial academic environment.

 

Do you want to provide high-quality emergency medicine in the leading regional emergency department?

Are you interested in joining a team with an established research group that is internationally recognized, multi award winning and prolifically published? – Dal-EM New Brunswick Research Program

Do you have a passion for Point-of-care Ultrasound? Do you want to join the teaching faculty for our hugely popular PoCUS courses and conferences? – SJRHEM PoCUS Program

Are you a potential simulation expert or do you want to develop simulation in medical education skills and help grow our successful local and regional simulation program?

Are you an enthusiastic medical educator? Do you want to teach medical students at one of Canada’s newest medical school campuses?

Do you want to help train future Emergency Medicine physicians by joining our innovative Post Grad Education Program?

And do you want to do all this while living in Atlantic Canada’s natural playground surrounded by fresh waterways on one side and the ocean on the other, all in close proximity to a thriving historic uptown scene

 

Apply here:

Assistant Academic Head

Director of Continuing Professional Development

Communications Director

Emergency Medicine Physician

 

bay-of-fundy-city-of-saint-john-bay-of-fundy-hopewell-rocks-new-brunswick-canada-217-dfde

2

150899_i_dsj_website-banner_urban_en

 

Download (PDF, 376KB)

 

Continue Reading

Pediatric Appendicitis PoCUS – Deep Dive – Don’t Dive Deep

PoCUS Fellow Pearl

Dr. Rawan Alrashed 

Pediatric Emergency Physician

Dalhousie PoCUS Fellow

Dalhousie University Department of Emergency Medicine

@Loolla1988

 

Reviewed & Edited by Dr David Lewis (@e_med_doc)

All case histories are illustrative and not based on any individual

 


Case:

12 years old female, previously healthy, presented to the ED with 1 day history of abdominal pain persistent, mainly in the lower abdomen, nauseated, with loss of appetite, no vomiting, no bowel motion, low grade fever, by exam she was distress in pain with tachycardia abdominal exam showed periumbilical and RLQ tenderness. Labs requested.

Awaiting the results, thinking of differential diagnosis and best imaging study….

Would POCUS help in the diagnostic process??

 


Background:

In children, acute appendicitis constitutes 1-8% of the abdominal pain diagnosis and is the most common condition requiring emergency surgery. The potential for morbidity and mortality from perforation of the appendix necessitates prompt diagnosis. Although a variety of clinical scoring systems have been developed, there is still no consensus on clinical, laboratory, and imaging criteria for diagnosing appendicitis, which poses a dilemma for the emergency clinician (1). The clinical presentation of children with appendicitis varies from that of adults which makes it more difficult to diagnose it. Multiple scoring systems (Pediatric Appendicitis score, Alvarado score, Pediatric Appendicitis risk calculator) were developed and externally validated with varying degree of sensitivity and specificity (2).

 


Anatomy:

The appendix is a blind-ended tubular structure that arises from the posteromedial aspect of the cecum, proximal to the ileocecal valve. The average length of the appendix varies from neonates to adults, ranging from 4.5 mm to 9.5 mm. The orientation of the appendix can be retrocecal, subcecal, preileal, retroileal, or in a pelvic site (1).

 

From Wikipedia

Pathology:

Appendicitis is a result of obstruction of the appendiceal lumen. Obstruction can occur secondary to stones, fecaliths, or other processes that inflame the lymphoid tissue. 

Pathology review


Diagnostic Imaging

Imaging Study

Sensitivity

Specificity

US

88%

94%

CT

94%

95%

MRI

96%

96%

 (Benabbas, 2017 (2))                                                                                 


PoCUS Anatomy

Cecum (C) is the most lateral structure in the RLQ, it’s a gas-fecal filled (dirty shadow) identified by following the haustra on the ascending colon caudally

Terminal ileum (TI) is a smooth wall that is fluid filled showing peristaltic movement and demonstrates valvulae conniventes.

(Ref – 9,12)

 

Cecum and terminal Ileum – Radiology Assistant
Colon – haustra
Small bowel – valvulae conniventes
Ileocecal valve (long arrow), Appendix (short arrow) (Jeffery,2018)
P-Psoas, Iv/a-Iliac vein and artery, Ap – Appendix From The PoCUS Atlas

Gongidi,2017

Normal 5 layers of the Appendix 

a) echogenic mucosa

b) hypoechoic muscularis mucosa

c) echogenic submucosa

d) hypoechoic muscularis propria

e) echogenic serosa


PoCUS Technique 

Use the LINEAR Probe (Curvilinear might be needed in large habitus people)

  • Analgesia First – Start with controlling the PAIN before starting the scan
  • Start by scanning the Maximum point of tenderness at the RLQ
  • Use the GRADED COMPRESSION as a technique to remove bowel gas
  • Scan in both planes (Longitudinal and Transverse) the entire length of appendix
  • Utilize the psoas muscle, iliac vessels and caecum as landmarks by:
    • Identify the iliac vessels
    • Identify the ileum above them then ileocecal junction
    • Scan inferiorly to the base of the caecum (appendix should be seen here)

If appendix is not visualized use the systematic approach (suggested by Sivitiz et al)

  • Move the probe laterally, until identify the ascending colon and lateral abdominal wall 
  • Move the transducer on the lateral border of the cecum.
  • Then, move the transducer medially, across the psoas and iliac vessels.
  • With the psoas muscle and iliac vessels kept in view, move the transducer down into the pelvis and towards the umbilicus at the border of the cecum.
  • If the appendix is not yet visualized, put the probe in the sagittal position, identifying the cecum in the long axis and move the transducer (sweep medially) compressing the cecum against the psoas muscle.

(Ref – 3,5,8)

Adaptations

Retrocecal Appendix

Consider applying pressure dorsally on the patient RLQ from the back. Scan while the patient on left posterior oblique position and scan parasagittal through the right flank in a coronal plane parallel to long axis of the psoas muscle; the appendix will appear anterior to the psoas muscle.  

Pelvic Appendix

Consider using curvilinear transducer. Scan deeper and use the bladder as a window

(Ref 5)


Core Ultrasound  – 5 Min Sono – Appendicitis


PoCUS Findings

Normal Appendix

Primary signs of Appendicitis

Secondary signs

Tubular blind ended structure arising from base of the Caecum

a non compressible appendix

(Target sign)

free Fluid in the right lower quadrant

No peristalsis

appendix wall diameter > 3 mm

echogenic edematous mesenteric fat stranding

Anteroposterior diameter

overall appendiceal diameter

> 6 mm (some reported 7mm)

appendiceal wall hyperemia (ring of fire)

Compressible target sign

ultrasound McBurney’s sign 

abnormal lymph nodes

 

presence of appendicolith

abnormal adjacent bowel, and bowel wall edema

(Ref 4,11)


Normal Appendix


Primary Signs of Appendicitis

 

Non-compressible, Thickened wall, Diameter >6mm
Superficial to Iliac vessels, Non-compressible, Thickened wall
Appendicolith

Secondary Signs of Appendicitis

 

Periappendicular Fluid
Ring of Fire

PoCUS Appendicitis – Evidence

  • A systematic review by Benabbas et al concluded that ED POCUS had 86% sensitivity and 91% specificity which was similar to RUS with sensitivity of 88% and specificity of 94%. POCUS reported as having a positive likelihood ratio of 9.24% and a negative likelihood ratio of 0.17. (2)

  • The American College of Radiology issued appropriateness criteria for imaging in RLQ pain recommending ultrasound as the first line option in children. (4)
  • The utilization of staged imaging approach has led to reduction of CT by 55-63% in different studies considering US (POCUS+ RUS) as first line image and CT used in equivocal cases or non visualized appendix. (6)
  • Elikashvili et al. demonstrated a significantly decreased length of stay for patients with disposition by POCUS compared to radiology (154–288 min) without any cases of missed appendicitis. (14)
  • Abnormal echogenicity or so-called infiltration of peri appendiceal fat has been found to be a particularly useful sign of appendicitis on US. Trout et al. found it to be the only independent statistically significant parameter to predict appendicitis, with a positive odds ratio of greater than 60. (3)

 


Limitations and Pitfalls

  • Operator dependent (level of experience with POCUS determines test acuracy).
  • The duration since the onset of symptoms (around 48 hours was found to be the optimal time to diagnose appendicitis by POCUS)
  • Misidentification of small bowel as the appendix (confirm a blind ended structure to prevent this)
  • Visualization of only the normal portion of a diseased appendix, where inflammation is isolated to the tip (false negative) scan the entire appendix.
  • Misdiagnosing a normal appendix as inflamed secondary to other intra-abdominal processes, such as Crohn’s disease or pelvic inflammatory disease (false positive).
  • Misdiagnosing acute appendicitis based on a diameter greater than 6 mm in an ovoid appearing compressible appendix and/or without any secondary signs of inflammation.
  • It can be difficult to visualize a perforated appendix due to the inability to perform a graded compression exam on a patient with peritonitis. (7)

 


Case Conclusion

PoCUS was performed. The images strongly suggested a diagnosis of appendicitis. A consultative ultrasound was performed in Diagnostic Imaging which confirmed our findings. After surgical consultation the child had an appendectomy and discharged the next day.


Bottom Line

  • Follow a Bayesian approach when using PoCUS to support your diagnosis of appendicitis. Pre-test probability will influence  your staged approach to a child with RLQ pain.
  • Utilize PoCUS and consultative DI Ultrasound to minimize radiation exposure with CT.
  • Review the proposed algorithm as an approach to suspected pediatric appendicitis.
  • Always consider appendicitis mimics in pediatrics (intussusception, IBD, ovarian torsion etc..) – don’t miss these!

 

Adapted from Pediatric Emergency Practice, 2019


References

1) Becker C, Kharbanda A. Acute appendicitis in pediatric patients: an evidence-based review. Pediatr Emerg Med Pract. 2019;16(9):1-20.
2) Benabbas, R., Hanna, M., Shah, J., & Sinert, R. (2017). Diagnostic Accuracy of History, Physical Examination, Laboratory Tests, and Point-of-care Ultrasound for Pediatric Acute Appendicitis in the Emergency Department: A Systematic Review and Meta-analysis. Academic Emergency Medicine, 24(5), 523–551.
3) Swenson DW, Ayyala RS, Sams C, Lee EY. Practical Imaging Strategies for Acute Appendicitis in Children. AJR Am J Roentgenol. 2018;211(4):901-909.
4) Lawton B, Goldstein H, Davis T, Tagg A. Diagnosis of appendicitis in the paediatric emergency department: an update. Curr Opin Pediatr. 2019;31(3):312-316.
5) Berghea-Neamţu, C. T. (2019). The Ultrasonographic Exam for Acute Appendicitis at Patient’s Bed. Acta Medica Transilvanica, 24(4), 48–50.
6) Doniger SJ, Kornblith A. Point-of-Care Ultrasound Integrated Into a Staged Diagnostic Algorithm for Pediatric Appendicitis. Pediatr Emerg Care. 2018;34(2):109-115.
7) Marin JR, Abo AM, Arroyo AC, et al. Pediatric emergency medicine point-of-care ultrasound: summary of the evidence [published correction appears in Crit Ultrasound J. 2017 Dec;9(1):3]. Crit Ultrasound J. 2016;8(1):16.
8) Sivitz AB, Cohen SG, Tejani C. Evaluation of acute appendicitis by pediatric emergency physician sonography. Ann Emerg Med. 2014;64(4):358-364.
9) “US of the GI Tract – Normal Anatomy.” The Radiology Assistant : US of the GI Tract – Normal Anatomy, https://radiologyassistant.nl/abdomen/ultrasound/lk-jg-1-1.
10) Riscinti, Matthew. “Bedside Ultrasound for Acute Appendicitis – Featuring Colorized Images.” TPA, TPA, 10 Jan. 2021, https://www.thepocusatlas.com/new-blog/appendicitis.
11) Gongidi P, Bellah RD. Ultrasound of the pediatric appendix. Pediatr Radiol. 2017;47(9):1091-1100.
12) Jeffrey RB, Wentland AL, Olcott EW. Sonography of the Cecum: Gateway to the Right Lower Quadrant. Ultrasound Q. 2018;34(3):133-140.
13) US probe: Ultrasound for small bowel obstruction. emDOCs.net – Emergency Medicine Education. (2018, March 27), http://www.emdocs.net/us-probe-ultrasound-for-small-bowel-obstruction.
14) Elikashvili I, Tay ET, Tsung JW. The effect of point-of-care ultrasonography on emergency department length of stay and computed tomography utilization in children with suspected appendicitis. Acad Emerg Med. 2014 Feb;21(2):163-70.

Continue Reading

COVID-19 Airway Rounds – Dr. George Kovacs

Thanks to Dr. George Kovacs at DalEM for providing this link to his recent COVID-19 Airway Rounds. This presentation is informative, evidence-based and highly entertaining. SJEM is proud to be part of DalEM and associated with so many great educators.

Supporting material is available here


AIME Airway

Canada’s premium Airway Management course. Visit the website for access to free airway resources and also registration for the courses.

Continue Reading

Recognizing and Treating Cannabinoid Hyperemesis Syndrome

Cannabinoid Hyperemesis Syndrome – Med Student Pearl

Eric Plant, Med II, Class 2024

Dalhousie Medicine New Brunswick, Saint John

Reviewed and copyedited by Dr. David Lewis @e_med_doc


Quick Summary: The Pearls You Came Here For

  • Cannabis hyperemesis syndrome (CHS) is a subtype of cyclic vomiting syndrome (CVS). While initially a novelty condition worthy of case reports, CHS has become more widely accepted and has since received a ROME criteria. To fulfil the criteria for cannabinoid hyperemesis syndrome, there must be all the features of cyclic vomiting syndrome as well as chronic cannabis use (>4 times per week for about a year).
  • CGS is under recognized and commonly not treated appropriately. This results in unnecessary suffering for the patient as well as numerous avoidable emergency department visits and investigations.
  • CHS should be considered in all patients who have episodic vomiting and chronic cannabis use.
  • Identifying CHS involves taking a history of the patients hyperemetic episodes and pattern of cannabis use. Given the vast differential diagnosis of acute nausea and vomiting the history should be very thorough.
  • Differentiating between CVS and CHS is useful because the treatment is different.
  • First line treatment for abdominal pain and hyperemesis during the hyperemetic phase should be IV benzodiazepines and topical capsaicin.
  • Second line therapies can be haloperidol, ondansetron, and metoclopramide but traditional antiemetic regimes are not usually effective.
  • The only definitive treatment for CHS is cessation of cannabis use and patients will likely benefit from an addictions specialist in the ED and/or outpatient setting.

Useful Links


Case

You are a med 2 working on your second shift in the ED. You are asked to see a 26-year-old male who was just brought in from triage with a chief complaint of persistent vomiting. The patient does not look happy to see you and between episodes of wrenching gives short, irritated answers to your questions. The patient states that he has no recent illnesses and has IBS which he typically self-medicates with cannabis. His girlfriend states that they recently moved here from Ontario and several times a year they would have to visit the local emergency department due to 24 hours periods of constant vomiting. She said the visits to emergency were not very helpful in stopping the vomiting and the only thing that seemed to help was taking a hot shower. You recall talking to a classmate recently who said that chronic cannabis use can cause profuse vomiting, but you are confused because you also recall that cannabis can be used to treat nausea in oncology patients. Before you report to your preceptor you frantically search the internet for some advice on what to report.

Initial Presentation Summary:

ID: 24 M
Chief Complaint:
  • Acute undifferentiated vomiting
History of Present Illness:
  • Persistent nausea and vomiting for 4 hours
  • No recent illnesses
  • Profuse vomiting all afternoon only relieved by compulsive desire for a hot shower
  • Bowel habits are inconsistent due to irritable bowel syndrome but have been “normal for him”
Medications
  • Pantoprazole
Allergies:
  • None known
Past Medical History:
  • Irritable bowel syndrome diagnosed after many presentations to numerous providers and several referrals
Social
  • No tobacco use
  • Long history of using cannabis products. Now primarily uses cannabis oil vape “pen”
  • Infrequent alcohol use and no other recreational drugs
Family Medical History
  • Paternal: alive and healthy with hypertension
  • Maternal: alive and healthy with occasional migraines

 


 

Introduction to CVS vs CHS

Any discussion of an approach to undifferentiated nausea and vomiting cannot begin without admitting that this presentation has a vast differential diagnosis. A more recent addition to this wide differential, cannabinoid hyperemesis syndrome (CHS), was first identified in 2004 and is categorized by most as a subtype of cyclic vomiting syndrome (CVS) which occurs in the setting of chronic cannabis use.17 With cannabis being legalized or decriminalized in many regions, there has been increasing attention paid to potential harms of cannabis use including CHS which has since received a ROME criteria. Despite recent academic interest in this disorder over the past 20 years, many physicians are still unaware of this diagnosis resulting in a mean time to diagnosis of 4 years for patients with many recurrent ED visits in that period.5 Since recent initiatives have moved towards classifying CHS as a subtype of CVS, we will start with an explanation of the parent disorder.

From Gajendran, M., Sifuentes, J., Bashashati, M., & McCallum, R. (2020). Cannabinoid hyperemesis syndrome: Definition, pathophysiology, clinical spectrum, insights into acute and long-term management. Journal of Investigative Medicine, 68(8), 1309-1316. doi:10.1136/jim-2020-001564


 

Overview of CVS

Definition and Diagnosis

CVS is a functional gastrointestinal disorder defined by recurrent episodes (5-12 cycles per year depending on age) of severe nausea and vomiting separated by long periods of relief. “Severe nausea and vomiting” typically manifest as about 4-8 episodes of vomiting constantly for a matter of hours to days. There are distinct Rome IV criteria for adult and pediatric forms of this condition.

 

Rome IV Criteria for CVS

Pediatric Criteria (all conditions must be met)

  • Occurrence of two or more periods of intense, unremitting nausea and paroxysmal vomiting, lasting hours to days within a 6-month period
  • Episodes are stereotypical in each patient
  • Episodes are separated by weeks to months with return to baseline health between episodes
  • After appropriate medical evaluation, the symptoms cannot be attribute to another condition

 

Adult Criteria (all conditions must be met)

  • Stereotypical episodes of acute vomiting lasting for less than one week
  • 3 or more discrete episodes in the prior year and 2 episodes in the past 6 months, occurring at least 1 week apart
  • Absence of vomiting between episodes, but other milder symptoms can be present between cycles

Note that the pediatric criteria allow for more cycles in a shorter period of time and require a return to baseline between the episodes. These differences are reflected in the natural history of either variety of the condition.

Natural History:

Cyclic vomiting syndrome can have either a pediatric or adult onset. While the pediatric onset has been studied more than the adult onset, most studies were small with even smaller numbers of patients who were followed up longitudinally. However, these studies suggest that about 60% of pediatric patients who were diagnosed at a mean age of 5.8 had their symptoms resolve by age 12.6 The natural history of adult onset cyclic vomiting syndrome has not been well studied with different sources claiming the mean age of diagnosis to be between 25 and 32.2, 22 Studies do agree that there is a significant delay between the initial presentation of the disease with one study suggesting that there were an average of 15 ED visits prior to diagnosis.2

The typical course of this disorder can be separated into four phases although some resources do not list the inter-episodic phase.7 The vast majority of patients will present to the ED during the vomiting phase.

Prodrome
  • Lasts for minutes to days but most commonly a matter of hours
  • Symptoms of panic, profuse sweating, cold/hot flashes, rising nausea, and sometimes diarrhea
Vomiting or Hyperemesis
  • Can last for hours to days but typically resolves in 48 hours
  • 4-8 episodes of vomiting and retching per hour
  • Associated symptoms of abdominal pain, lethargy, pallor, sometimes fever, and least commonly, diarrhea.
  • One third of patients experience migraine-like symptoms including headache, photophobia, and/or vertigo
  • Compulsive use of hot water showers or bathing to relieve symptoms is seen is greater than 50% adult patients and some adolescent patients as well.
Recovery
  • Characterized by dehydration and lethargy but cessation of episodic vomiting
Inter-Episodic or Asymptomatic period
  • Patterns of cycles and symptoms between episodes differ between adults and children:
  • Children:
    • Mean duration of 12 cycles per year with a mean duration of 2 days
    • Chronic nausea between cycles is rare (12%)
    • Triggering events have been identified in 70% of children
  • Triggers are most commonly infection, psychological stress, dietary, and least commonly menstrual
  • Adults
    • Mean of 4 cycles per year with a mean duration of 6 days
    • Chronic nausea between events is common (40-60%)
    • Can be associated with a triggering event but less commonly.

Adapted from UpToDate2, 6, 20

Epidemiology

The epidemiology of CVS is complicated by delayed and missed diagnoses but the difference between pediatric and adult populations is significant. Generally, the prevalence of CVS to be between 1.9 and 2.3% with an incidence of 3.2 per 100,000.4 The data on adult onset is much less robust.

  • Pediatric onset2, 4
    • Average age of symptom onset of 5.8 years
    • Average age of diagnosis of 9.6 years
    • 86% female sex predominance
  • Adult onset2
    • Average age of symptom onset of 32 years
    • Average age of diagnosis 41
    • 57% female sex predominance

Overview of CHS

Definition and Diagnosis

Requires that the cyclic pattern and character of the hyperemesis phase be consistent with CVS with the addition that it must occur after prolonged, excessive cannabis use. Additionally, some resources suggest that resolution of symptoms after cannabis cessation (from between 7 days to 6 months) is diagnostic for this condition but at patient presentation in the emergency department (ED), this is obviously not useful for diagnosis. Therefore, in the ED we will rely on the Rome IV diagnostic criteria which are clinical and listed below:

 

Rome IV Criteria for CHS

All three criteria must have been present for the last three months with symptoms onset at least 6 months before diagnosis

·     Stereotypical episodic vomiting resembling cyclical vomiting syndrome in onset, duration, and frequency

·     Presentation after prolonged, excessive cannabis use

·     Relief of vomiting by a sustained cessation of cannabis use

 

From: https://cvsanordic.net/wp-content/uploads/CHS-table.jpg

The Rome IV criteria also notes that the palliative behaviour of prolonged hot baths or showers is often present and is a useful distinguishing feature from other diagnoses. However, it must be noted that CVS also commonly presents with this feature, so the primary distinguishing feature between CHS and CVS is chronic cannabis use. Most recent reviews of the literature have also suggested that epigastric pain which radiates diffusely typically accompanies the onset of the vomiting and is an important feature of CHS which should be added to the Rome criteria.18

“… the primary distinguishing feature between CHS and CVS is chronic cannabis use.”

Natural History

As stated above in the definition, the natural history is very similar to that of cyclic vomiting syndrome with the added distinction that it is dependent on the patient’s chronic cannabis use. However, poor definition of chronic or “excessive cannabis use” is one of the primary criticisms limitations of the Rome Criteria. Most resources define cannabis use of greater than 4 times per week for at least 1 year meets the criteria of ‘excessive cannabis use’ and ‘sustained cessation of cannabis use’ should mean the patient abstains for at least 6 months.22 Unfortunately, a study by Venkatesan et al published in 2020 complicated the picture between CHS and CVS further by finding that about 20% of people with CVS use cannabis > 4 times per week but did not have relief from symptoms after 1 month of cessation. This all means that further research is still needed to better understand the amount of cannabis use required for a diagnosis of CVS and how long a person must abstain before their symptoms are likely to disappear.

It is also important to note the delay in diagnosis that most patients with CHS experience. Some evidence shows that most patients had symptom 4-10 years prior to diagnosis with 10% of patients experiences symptoms for 10 years or longer.18 A systematic review from 2017 found that on average patients had 7.1 emergency department visits, 3.1 hospitalizations, and 5.0 clinic visits prior to diagnosis.20

“…cannabis use of greater than 4 times per week for at least 1 year meets the criteria of ‘excessive cannabis use’ and ‘sustained cessation of cannabis use’ should mean the patient abstains for at least 6 months.”

From Zhu, J. W., Gonsalves, C. L., Issenman, R. M., & Kam, A. J. (2021). Diagnosis and acute management of adolescent cannabinoid hyperemesis syndrome: A systematic review. Journal of Adolescent Health, 68(2), 246-254. doi:10.1016/j.jadohealth.2020.07.035

Epidemiology

Unfortunately, the epidemiology of CHS is not well understood as the diagnostic criteria have been challenging as well as continually evolving since its discovery in 2004. Perhaps more importantly, patients have historically been hesitant to disclose their cannabis use to providers and providers have often chartered cannabis use as either positive or negative rather than obtaining a detailed history of the pattern of use. However, visits to the ED for cannabis related problems is increasing and these patients typically presents numerous times per year to the emergency department.11

  • While CVS has a slight female predominance, different sources suggest that CHS is evenly distributed between the sexes or has a male predominance of up to 72%.2, 5, 16, 19, 20
  • Most common between the ages of 18—397, 19
  • In the “Western world” the prevalence is thought to be 0.1% but it is very difficult to calculate, and the lack of recent Canadian data is particularly important in this case due to Canada’s legalization of recreational marijuana being still relatively unique.7

While chronic use of cannabis is critical for the diagnosis of CHS, individual susceptibility is difficult to determine. Some suggest that cytochrome P450 polymorphisms, the type of marijuana used, and levels of psychological stress have all been implicated as potential predisposing factors.1

Finally, it is important to note that CHS is commonly identified in patients with certain functional disorders such as migraine, irritable bowel syndrome, affective disorders, anxiety, and depression. Once again, it shares these associations with CVS.23


 

Physiology of Nausea and Vomiting

As a quick reminder to prime a better understanding of the proposed pathophysiology and treatment, it is worth reviewing the physiology of nausea and vomiting. Emesis can be triggered from one of four places: GI tract, vestibular system, corticothalamic tracts, and the area postrema which is probably of the most important in CHS.9 The area postrema (commonly called the chemoreceptor trigger zone) is a portion of the caudal wall of the fourth ventricle.13 Unlike most of the brain, there is no blood brain barrier so it is able to monitor the blood and trigger emesis and/or the sensation of nausea. This area is known to contain receptors for specific varieties of dopamine, neurokinin, serotonin, opioid, and histamine.13 When stimulated, the area postrema signals to the nucleus tractus solitarius (solitary nucleus) which is another central node in the emesis reflex. Although it is widely stated that there is a well-localized “vomiting center,” more recent physiology suggests that the activation of the vomiting reflex is done by a more complex neural circuit known as a central pattern generator that is composed of poorly localized nuclei throughout the medulla.9, 15 This is important for a discussion of CHS because some of the best treatments for CHS have more systemic effects that affect areas throughout the brain7, 15


 

Pathophysiology of CVS and CHS

The pathophysiology of CHS is still not well understood and many of the theories are beyond the scope of this page. Endocannabinoids can stimulate cannabinoid receptors directly on vagal nerve afferents in the GI tract or through the enteric nervous system.1, 10, 11 However, cannabinoid receptors are found throughout many other parts of the body including the areas of medulla and cortex and given the complexity of signals which can trigger emesis, it is difficult to determine a single isolated pathway that is dysregulated1, 5, 11.  What is paradoxical about CHS is that the tetrahydrocannabinol (THC) in cannabis is known to inhibit serotonin release in the medulla and therefore is used as an antiemetic.2 Currently it is thought that it is the THC which results in the mechanism of CHS as there have been no reports of CHS in patients who use cannabidiol (CBD) products.22  Some theories suggest that mechanism is due to the fact that cannabinoid receptors are downregulated and desensitized due to chronic cannabis use.11, 15 Others suggest accumulation of lipophilic cannabinoids over a longer period of time can be suddenly released due to lipolysis during times of stress or dysfunction in the HPA axis.15 However, the cannabis plant contains more than 400 chemicals that accumulate in the body over time causing the pathophysiology to be pervasively elusive.

From Richards, J. R. (2018). Cannabinoid hyperemesis syndrome: Pathophysiology and treatment in the emergency department. The Journal of Emergency Medicine, 54(3), 354-363. doi:10.1016/j.jemermed.2017.12.010


 

Assessment

Differential Diagnosis:2, 3, 20, 21, 24

  • Cyclic vomiting syndrome
  • Gastroparesis
  • Peptic ulcer disease
  • Gastrointestinal reflux disease
  • Acute cannabis toxicity
  • Bowel obstruction or sigmoid volvulus
  • Gastritis
  • Biliary colic
  • Renal colic
  • Pancreatitis
  • Appendicitis
  • Diverticulitis
  • Ectopic pregnancy
  • Ovarian torsion
  • Morning sickness of pregnancy
  • Opioid withdrawal
  • Abdominal aortic aneurysm
  • Acute coronary syndrome

 

Emergent Complications of CHS15

  • Acute renal failure
  • Hypokalemia
  • Esophageal injury especially cautious for Mallory Weiss tear
  • Pneumomediastinum

History

  • It is important to establish a history of a cyclic pattern of episodes of hyperemesis: 4-8 episodes of wrenching and vomiting per hour, for less than 24 hours, happening 4-8 times per year. Cycles are more often but less severe in adolescents and children.20, 24
  • To distinguish between CVS and CHS it is important to establish a history of chronic cannabis (at least 4 times per week for about a year). Infrequent cannabis use leans more towards a diagnosis of CVS
    • One recent study (2020) suggested that due to the high frequency of cannabis use in patients with CVS, using a tool such as CUDIT-R to screen for cannabis use disorder may be more specific for identifying CHS, but this was a small study.22
    • It is also important to note that CHS has been observed in people who take their cannabis products in a variety of ways: smoke, vaporize, or in oil or wax form. According to a article from 2018, no cases have been associated with edible marijuana as the only route of administration.11 It has also been observed in patients taking synthetic cannabis or “spice”11, 14
  • Acute cannabis toxicity, particularly with edible or high-potency cannabis can be associated with isolated episodes of hyperemesis but will be easy to distinguish from CHS which requires chronic cannabis use.21
  • Abdominal pain is typically diffuse and generalized in nature.
  • Travel history is important to screen for infectious etiologies. Infectious etiologies are also more likely to occur with tardive increase in abdominal pain, myalgias, fever, and other signs of infection which are not common CHS.
  • A good history of bowel habits should be obtained as most patients with CHS report normal bowel habits and constipation or diarrhea can suggest other conditions on the differential.
    • Younger patients with changes in bowel habits should be considered for cannabis-induced acute pancreatitis.14
  • Weak evidence suggests that CHS symptoms more commonly present in the morning.24
  • Mild hematemesis is common, especially after prolonged vomiting, but the presence of increasing frank blood should prompt emergent evaluation for upper GI bleed.

 

Physical Exam

  • The physical exam is largely unremarkable for patients with CHS and none of the guidelines for CHS suggest any special tests to help guide diagnosis.
  • A good screening neurological examination would be important to ensure that there are no associated focal neurological symptoms which may prompt a change in the differential diagnosis and CT scan.9
  • Abdominal pain is typically diffuse but if distention or focal points of tenderness are identified abdominal imaging should be considered to rule out an obstruction.9
  • Dehydration can be detected with poor skin turgor or (tenting), dry axillae, and xerostomia or ridges in on the tongue.

 

Investigations

  • Blood work2, 3
    • CBC – Evaluating for blood loss and leukocytosis
    • Electrolytes – Important due to likely dehydration
    • Renal studies – Acute kidney injury is a concern for patients with CHS.
    • Blood glucose – High blood glucose levels should prompt a more through investigation for diabetic gastroparesis.
    • Pregnancy test
  • Electrocardiogram3
    • Important screen for an atypical presentation of ischemic cardiac etiology
    • Assess the QT interval, especially those who are on antipsychotic medications who you plan to give ondansetron. Additionally, chronic cannabis use has been associated with prolonged QT interval in a small subset of people.
  • Imaging3
    • Abdominal imaging is typically unremarkable. Decision for imaging should be guided by the history and may be important to rule out other conditions on the differential diagnosis.
    • Focal neurological findings should prompt a brain CT scan and a diagnosis other than CHS.
  • Toxicology screening
    • Establishing a patient’s blood concentration of COOH-THC has been suggested by some to affirm the patient’s history, however given the unknown pathophysiology of CHS and our current difficulties with correlating COOH-THC level with clinical outcomes, it is not recommended.14
    • Urine toxicology screening may be helpful in ruling out the use of other recreational drugs but do not give very much information about the pattern of use and will not be useful if the patient admits plainly to being a chronic cannabis user.14

A systematic review form 2020 found the following criteria most commonly used to identify patients of CHS. Their frequencies as they were used to identify patients in these studies are listed next to each criteria. It is important to note that the GRADE (Grading and Recommendations Assessment, Development, and Evaluation) of these studies was either “Low” or “Very Low” for each criteria and the total number of patients included was 500.24

  1. Recurrent vomiting (100%)
  2. Age < 50 at evaluation (100%)
  3. Resolution of symptoms with cannabis use (100%)
  4. Severe nausea and vomiting (99.4%)
  5. History of chronic cannabis use (99.2%)
  6. Abdominal pain (99%)
  7. Normal bowel habits (97.2%)
  8. Normal laboratory, radiographic, and endoscopic results (96.5%)
  9. Morning predominance of symptoms (77.5%)
  10. Compulsive bathing to produce symptom relief (23%)
  11. Male predominance (19.6%)
  12. At least one discrete episode in the prior year and two episodes in the past 6 months occurring at least 1 week apart (insufficient evidence)
  13. No evidence of gallbladder or pancreatic inflammation (insufficient evidence)
  14. Weight loss > 5kg (insufficient evidence)

Note that this list does not show the frequency with which these symptoms present in patients with CHS, but rather the frequency with which experts use each of the criteria to help identify CHS. Note that while compulsive bathing to produce symptom relief is a memorable feature of CHS, it is not pathognomonic for CHS and therefore is not frequently used as a criterion for identifying it.23

“Note that while compulsive bathing to produce symptom relief is a memorable feature of CHS, it is not pathognomonic for CHS and therefore is not frequently used as a criterion for identifying it.”


 

Treatment

Treatment in the ED centers around initial resuscitation of electrolyte abnormalities, antiemetics, and treatment of associated symptoms like abdominal pain and anxiety. Treatment of CHS is complicated by the unknown and potential multifactorial etiology of CHS and therefore it is unsurprising that traditional antiemetic therapy alone is commonly not sufficient. Benzodiazepines, and antipsychotics like haloperidol and olanzapine have shown to be more effective than with typical nausea and vomiting and there is some speculation that its because these therapies treat the nausea, anxiety, abdominal pain, while also acting as antiemetics.

It is also important to note that most of the treatments suggested have been studied in adult populations with little data present on pediatric or adolescent populations.24 CHS has presented in adolescents and so far many of the following treatments appear about as effective or ineffective as they are in adults.24

Treatment in the ED

  • Fluid resuscitation and correction of electrolyte abnormalities
  • ED substance use counselling
    • It is especially important for the ED physician to inform the patient that their cannabis use is likely the cause of these episodes and that cessation of us is the only known means of definitive treatment.10, 11 Many patients find relief after 1 month, but some take up for 3-6 months.14
    • If an emergency department has on site addictions specialists, they were shown to be effective in aiding cessation of cannabis in a small case series.14
    • Regular users are less likely to abstain even if told it was the cause of their issue as they perceive that it makes their symptoms better so providing time for explanation and using a non-judgemental attitude is critical in these conversations.
  • Benzodiazepines
    • The mechanism of action of benzodiazepines involves crossing the blood brain barrier and acting on GABA receptors but there are also GABA receptors in the GI tract.16 Therefore, their mechanism is more global than the other conventional antiemetics. As they are a blunter tool which affects numerous regions of the brain, this may explain why they have shown to more effective given the unknown pathophysiology of CHS.15, 23
    • Intravenous benzodiazepines have better efficacy than ondansetron and metoclopramide15, 16
    • Suggested dose: Lorazepam IV 1-2mg every 4-6 hours PRN11
  • Capsaicin
    • Topical capsaicin cream has been studied as a therapy given that it stimulates some of the same receptors (TRPV1) activated by high temperatures (> 41°C) in hot water bathing.11 Additionally, these receptors are often near cannabinoid receptors (CB1) which may imply a functional relationship.17
    • It is important to note that hot water bathing is also seen in CVS and that capsaicin has not been studied for patients with CVS without cannabis exposure so the specificity of capsaicin for CHS is uncertain.17, 23
    • Some guidelines suggest it as a first-line treatment11 but it is important to note the evidence is not strong and that some patients find it uncomfortable. It has also been associated with blisters, and severe skin irritation.17
    • It must be applied on in-tact skin, away from face, eyes, nipples, and perineum.
    • Gloves must be used during application and hands must be washed thoroughly.
    • It must not be covered by an occlusive dressing.
    • Apply capsaicin 0.025% to 0.075% to areas where the patient has stated that hot water bathing provides relief (often the abdomen and backs of arms)11
  • Haloperidol
    • Given that haloperidol is a dopamine antagonist and cannabis is known to increase dopamine activity, some believe this is why it has shown dramatic effect in small case studies.10, 20
    • Suggested dose: 5mg IV11
  • Ondansetron
    • A serotonin antagonist is thought to act on a couple of the theorized pathophysiologies, both in the gastrointestinal tract and in the chemoreceptor trigger zone, however as it does not easily cross the blood brain barrier it does not have any impact on potential etiologies in the medulla or cortex which may explain why it has not been found to be as effective as benzodiazepines or some antipsychotics.
    • Given that the evidence is still weak, it is reasonable to attempt a trial of ondansetron although conventional antiemetics are usually ineffective. They are still often administered prior to or in conjunction with other therapies.
    • Ensure to check the QTC interval which can be prolonged with chronic cannabis use.
    • Suggested dose: 4-8mg IV11
  • Metoclopramide was specifically noted not to be effective in a 2017 systematic review.16
  • Opioids
    • Not appropriate for patients suspected of CHS, despite the severe abdominal pain they may experience. It has been shown to worsen nausea and vomiting in patents with CHS and should be avoided until other treatments fail.20 (3,
    • If opioids significantly improve symptoms the patient should be screened for an opioid use disorder.

 

Summary of Recommendations for Treatment in the ED

  • Fluid resuscitation and correction of electrolyte or metabolic abnormalities
  • Discussion on the importance of cessation of cannabis use and referral to addictions supports.
  • 1st line treatments for hyperemesis and abdominal pain
    • Benzodiazepine IV
    • Topical capsaicin or allow patient to perform hot water bathing.
  • 2nd line treatments for hyperemesis and abdominal pain
    • If initial therapy with benzodiazepine and capsaicin are not effective, move to haloperidol, or ondansetron.

 

Definitive Treatment and Counselling

  • Outpatient addictions management is ideal to aid patients in cessation of their cannabis use.14
  • Outpatient prophylactic pharmacological management is controversial and has not well been studied. Patients with CVS are commonly started on treatments of tricyclic antidepressants (TCA) which have shown some benefit.6 If there is difficulty differentiating between a diagnosis CVS and CHS due to frequent but not “chronic” cannabis use, it is reasonable to attempt TCA therapy while also counselling for cessation of cannabis use.7, 23

 

Case Conclusion

After finding a useful resource on the website for a local emergency department, the student confidently suggested that cannabinoid hyperemesis syndrome should be considered likely. After a thorough history it was decided that abdominal imaging was not required and the patient responded well to benzodiazepines, IV rehydration, and topical capsaicin. Prior to discharge the patient stated they would try for cessation of cannabis use of the next few weeks and knew how to contact local addictions resources if they were struggling. They appreciated the advice from the department and stated they would share their experience as well as the following infographic with their friend from home who has had similar symptoms for years.

Infographic for patients on CHS from Institute of Safe Medication Practices Canada

https://www.ccsa.ca/public-education

Download (PDF, 702KB)


 

References

  1. Galli, J., Andari Sawaya, R., & K. Friedenberg, F. (2011). Cannabinoid hyperemesis syndrome. Current Drug Abuse Reviewse, 4(4), 241-249. doi:10.2174/1874473711104040241
  2. B, L. U., Patterson, M. C., Heyman, M. B., & Hoppin, A. G. (2020). Cyclic vomiting syndrome (T. W. Post, Eds.). In UpToDate. Waltham, MA: UpToDate.
  3. Chu F, Cascella M. Cannabinoid Hyperemesis Syndrome. [Updated 2020 Jul 4]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK549915/
  4. Davis, A., Nichols, C. J., & Bryant, J. H. (2020, September 07). Cyclic vomiting syndrome. Retrieved February 10, 2021, from https://www.ncbi.nlm.nih.gov/books/NBK500018/
  5. Deceuninck, E., & Jacques, D. (2019). Cannabinoid Hyperemesis Syndrome: A Review of the Literature. Psychiatria Danubina, 29(3), 390-394.
  6. Fitzpatrick, E., Bourke, B., Drumm, B., & Rowland, M. (2007). Outcome for children with cyclical vomiting syndrome. Archives of Disease in Childhood, 92(11), 1001-1004. doi:10.1136/adc.2007.116608
  7. Gajendran, M., Sifuentes, J., Bashashati, M., & McCallum, R. (2020). Cannabinoid hyperemesis syndrome: Definition, pathophysiology, clinical spectrum, insights into acute and long-term management. Journal of Investigative Medicine, 68(8), 1309-1316. doi:10.1136/jim-2020-001564
  8. Hayes, W., VanGilder, D., Berendse, J., Lemon, M., & Kappes, J. (2018). Cyclic vomiting syndrome: Diagnostic approach and current management strategies. Clinical and Experimental Gastroenterology, Volume 11, 77-84. doi:10.2147/ceg.s136420
  9. Hornby, P. J. (2001). Central neurocircuitry associated with emesis. The American Journal of Medicine, 111(8), 106-112. doi:10.1016/s0002-9343(01)00849-x
  10. Knowlton, M. C. (2019). Cannabinoid hyperemesis syndrome. Nursing, 49(10), 42-45. doi:10.1097/01.nurse.0000577992.82047.67
  11. Lapoint, J., Meyer, S., Yu, C., Koenig, K., Lev, R., Thihalolipavan, S., . . . Kahn, C. (2018). Cannabinoid hyperemesis syndrome: Public health implications and a novel model treatment guideline. Western Journal of Emergency Medicine, 19(2), 380-386. doi:10.5811/westjem.2017.11.36368
  12. Longstreth, G. F., & Grover, S. (2021). Approach to the adult with nausea and vomiting (1202794849 897533483 T. W. Post & 1202794850 897533483 N. J. Talley, Eds.). In UpToDate. Waltham, MA: UpToDate.
  13. MacDougall, M. (2020, September 27). Physiology, chemoreceptor Trigger Zone. Retrieved April 28, 2021, from https://www.ncbi.nlm.nih.gov/books/NBK537133/
  14. Pélissier, F., Claudet, I., Gandia-Mailly, P., Benyamina, A., & Franchitto, N. (2016). Cannabis Hyperemesis syndrome in the Emergency Department: How can a Specialized addiction team be Useful? A pilot study. The Journal of Emergency Medicine, 51(5), 544-551. doi:10.1016/j.jemermed.2016.06.009
  15. Richards, J. R. (2018). Cannabinoid hyperemesis syndrome: Pathophysiology and treatment in the emergency department. The Journal of Emergency Medicine, 54(3), 354-363. doi:10.1016/j.jemermed.2017.12.010
  16. Richards, J. R., Gordon, B. K., Danielson, A. R., & Moulin, A. K. (2017). Pharmacologic treatment of Cannabinoid HYPEREMESIS Syndrome: A systematic review. Pharmacotherapy: The Journal of Human Pharmacology and Drug Therapy, 37(6), 725-734. doi:10.1002/phar.1931
  17. Richards, J. R., Lapoint, J. M., & Burillo-Putze, G. (2017). Cannabinoid hyperemesis syndrome: Potential mechanisms for the benefit of capsaicin and hot water hydrotherapy in treatment. Clinical Toxicology, 56(1), 15-24. doi:10.1080/15563650.2017.1349910
  18. Schey, R. (2020). Cannabinoid hyperemesis syndrome: The conundrum is here to stay. Journal of Investigative Medicine, 68(8), 1303-1304. doi:10.1136/jim-2020-001669
  19. Simonetto, D. A., Oxentenko, A. S., Herman, M. L., & Szostek, J. H. (2012). Cannabinoid HYPEREMESIS: A case series of 98 Patients. SciVee. doi:10.4016/39227.01
  20. Sorensen, C. J., DeSanto, K., Borgelt, L., Phillips, K. T., & Monte, A. A. (2016). Cannabinoid hyperemesis syndrome: Diagnosis, pathophysiology, and treatment—a systematic review. Journal of Medical Toxicology, 13(1), 71-87. doi:10.1007/s13181-016-0595-z
  21. Turner, A. (2020, July 19). Marijuana toxicity. Retrieved May 06, 2021, from https://www.ncbi.nlm.nih.gov/books/NBK430823/
  22. Venkatesan, T., Hillard, C. J., Rein, L., Banerjee, A., & Lisdahl, K. (2020). Patterns of cannabis use in patients with cyclic vomiting syndrome. Clinical Gastroenterology and Hepatology, 18(5). doi:10.1016/j.cgh.2019.07.039
  23. Venkatesan, T., Levinthal, D. J., Li, B. U., Tarbell, S. E., Adams, K. A., Issenman, R. M., . . . Hasler, W. L. (2019). Role of chronic cannabis use: Cyclic vomiting syndrome vs cannabinoid hyperemesis syndrome. Neurogastroenterology & Motility, 31(S2). doi:10.1111/nmo.13606
  24. Zhu, J. W., Gonsalves, C. L., Issenman, R. M., & Kam, A. J. (2021). Diagnosis and acute management of adolescent cannabinoid hyperemesis syndrome: A systematic review. Journal of Adolescent Health, 68(2), 246-254. doi:10.1016/j.jadohealth.2020.07.035
Continue Reading

Rib Fractures and Serratus Anterior Plane Block

Continue Reading