Dr. Rawan Makhdom
DalEMSJ PoCUS Fellow
Consultant Emergency Medicine
King Fahad Hospital of the University, Al Khobar KSA
DalEMSJ PoCUS Fellow
Consultant Emergency Medicine
King Fahad Hospital of the University, Al Khobar KSA
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).
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].
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].
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].
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].
Figure 2: Demonstration of the supination/flexion maneuver [5]
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.
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].
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.
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 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.
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.
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.
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.
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.
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.
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.
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
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.
From – the PoCUS Atlas
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.
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
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.
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.
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.
Valve vegetations or signs of infective endocarditis are among the complications of severe bicuspid valve5-9
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.
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.
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?
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
How effective is the home use of topical tetracaine every 30 minutes PRN pain for 24 hours following corneal abrasion?
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
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.
Patients 18 to 80 years old, presenting to the ED with suspected acute corneal abrasion, and gave written informed consent.
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.
Main outcomes at the 24-48hr follow up appointment:
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) |
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.
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.
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
Thanks to Dr. Paul Frankish for leading SHC EM Reflection rounds today.
Polytrauma patient with fluctuant GCS, tenuous airway in prehospital phase of care, transient hypotension in ED.
Polytrauma patient with severe agitation, hypoxia, and significant chest injuries.
Patient with severe necrotizing infection and septic shock.
Pediatric septic shock
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Dr. Rawan Alrashed
Pediatric Emergency Physician
Dalhousie PoCUS Fellow
Dalhousie University Department of Emergency Medicine
Reviewed & Edited by Dr David Lewis (@e_med_doc)
All case histories are illustrative and not based on any individual
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??
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).
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).
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.
Imaging Study |
Sensitivity |
Specificity |
US |
88% |
94% |
CT |
94% |
95% |
MRI |
96% |
96% |
(Benabbas, 2017 (2))
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)
a) echogenic mucosa
b) hypoechoic muscularis mucosa
c) echogenic submucosa
d) hypoechoic muscularis propria
e) echogenic serosa
Use the LINEAR Probe (Curvilinear might be needed in large habitus people)
If appendix is not visualized use the systematic approach (suggested by Sivitiz et al)
(Ref – 3,5,8)
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)
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)
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.
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.
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
Canada’s premium Airway Management course. Visit the website for access to free airway resources and also registration for the courses.
Eric Plant, Med II, Class 2024
Dalhousie Medicine New Brunswick, Saint John
Reviewed and copyedited by Dr. David Lewis @e_med_doc
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.
ID: | 24 M |
Chief Complaint: |
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History of Present Illness: |
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Medications |
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Allergies: |
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Past Medical History: |
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Social |
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Family Medical History |
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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
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.
Pediatric Criteria (all conditions must be met)
Adult Criteria (all conditions must be met)
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.
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 |
|
Vomiting or Hyperemesis |
|
Recovery |
|
Inter-Episodic or Asymptomatic period |
|
Adapted from UpToDate2, 6, 20
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.
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:
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.”
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
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 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
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
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
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
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 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
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