Polymyalgia Rheumatica

Polymyalgia Rheumatica – A Medical Student Clinical Pearl

Alexis Lamontagne

MD Candidate, Class of 2022

DMNB, Dalhousie University


A 73 y/o M presents with a 1 week history of proximal muscle aches and stiffness including his hips, shoulders and neck. He describes the stiffness as worse in the morning, recently he has had trouble getting out of bed at all. He finds that the stiffness is relieved and regains function as he begins to move around. He also notes increased stiffness after periods of immobility. It has become progressively worse over the past week which lead to seeking medical help in the emergency department.

There are no other associated symptoms including jaw claudication, headache, weight loss, fevers, chills, night-sweats, vision changes, paresthesias, or preceding cold or illness.

The patient has no significant past medical history. His only regular medication is omeprazole. He does not smoke, consumes 4 alcoholic drinks per day, and uses no other recreational drugs. He lives at home with his wife and they are both retired.

While asking about whether there are any rheumatological conditions that run in the family you learn that his older brother has Polymyalgia Rheumatica (PMR).


Polymyalgia Rheumatica:

The clinical syndrome of PMR should be considered in those aged over 50 presenting with pain and stiffness of the neck, shoulders and hips that is typically worst in the early hours of the morning or on waking, and tends to improve over the course of the day. Inflammatory markers (ESR/CRP) are typically elevated and anaemia may be present due to inflammation. Symptoms of PMR should resolve rapidly with low-dose glucocorticoids.


Although weight loss, fever and synovitis/tenosynovitis have all been described in PMR, they should raise suspicion of :

  • malignancy,
  • deep-seated or disseminated infection (such as endocarditis or osteomyelitis),
  • inflammatory arthritides such as rheumatoid arthritis (RA), spondyloarthropathy, or crystal arthropathy.



Bloodwork reveals a normal CBC and an elevated CRP at 108.



Prednisone is initiated at 15mg PO daily. If the initial dose of 15mg does not demonstrate clinical improvement in one week, this can be increased to 20mg or a maximum dose of 25mg.

Once symptoms are controlled for 2 to 4 weeks the dose of prednisone can be tapered. Prednisone can be reduced by 2.5mg every 2 to 4 weeks until 10 mg daily is reached. The dose can then be further tapered by 1 mg per month until cessation or symptoms flare. There is no consensus regarding an optimal tapering regime.

Should a flare occur during the taper, a CRP should be measured and prednisone increased to the lowest dose that relieves symptoms. If a patient relapses several times during the taper, dose reductions can be lengthened to six to eight weeks. If a relapse occurs after the cessation of glucocorticoid use, a CRP should be obtained and prednisone can be initiated at the original dose which managed symptoms.

CRP should be measured again 2 months after the initiation of glucocorticoid therapy and 3 to 6 months thereafter during the course of treatment. Monitoring for symptoms of PMR and Giant Cell Arteritis (GCA) should also take place throughout treatment.



The cause of polymyalgia rheumatica (PMR) is unknown.

The strongest risk factor for PMR is increasing age. It is unheard of in those under 50 years old and incidence increases with each decade, peaking around 75 years. Proposed mechanisms include ageing of the immune system (immunosenescence), ageing of the tissues, and ageing of neurohumoral regulatory systems. Based on the clustering of cases in space and time, it has been proposed that PMR may be triggered by infection. This could lead to persistent inflammation on a background of chronic low-grade inflammation secondary to decline in adaptive immunity and a compensatory increase in innate immune mechanisms. (Mackie 2013)


Relationship to Giant Cell Arteritis:

There is a well-known association between PMR and giant cell arteritis (GCA). Many patients with GCA also have polymyalgic symptoms and some patients with PMR subsequently develop GCA (Mackie 2010). There is some discussion as to whether PMR and GCA are separate disease entities or two conditions on a single pathophysiological spectrum. For the practising clinician it is important to realise that PMR and GCA are treated with different doses of glucocorticoids and that treatment of GCA is a medical emergency, whereas the immediate priority with PMR is to exclude other conditions before starting treatment. All patients with PMR should be assessed for signs and symptoms of GCA at diagnosis and screened for underlying GCA at follow-up visits. These symptoms include constitutional symptoms, headache, jaw claudication, ocular involvement, large vessel involvement, and anemia.



With a prescription for prednisone, a follow up was arranged with the patient’s family doctor in one week. The patient was advised that the family doctor would taper his prednisone, monitor CRP, and screen for symptoms of PMR and GCA. Additionally, monitoring for the adverse effects of glucocorticoids, including osteoporosis, glucose intolerance, and hypertension would take place.



Mackie SL. Polymyalgia rheumatica: pathogenesis and management. Clin Med (Lond). 2013;13(4):398-400.

Mackie SL. Et al. Can the prognosis of polymyalgia rheumatica be predicted at disease onset? Results from a 5-year prospective study. Rheumatology (Oxford). 2010 Apr; 49(4):716-22.


Continue Reading

It’s Not Over Till It’s Over – ECMO Resuscitation in the ED

It’s Not Over Till It’s Over – ECMO Resuscitation in the ED: A Medical Student Clinical Pearl

Ryan Buyting

Med III, Class of 2022

Dalhousie Medicine New Brunswick (DMNB)

Reviewed by Dr. Luke Taylor

Copyedited by Dr. Mandy Peach

Extracorporeal Membrane Oxygenation (ECMO), also sometimes referred to as extracorporeal life support (ECLS), employs components from traditional cardiopulmonary bypass machines to augment a patient’s heart and/or lung capacity for a prolonged duration of days to weeks. Importantly, ECMO is not a treatment but a bridge to native heart/lung recovery or durable organ replacement. 1


ECMO has been a hot topic of discussion over the past year based on its role in supporting patients with severe COVID-19 infections. The Extracorporeal Life Support Organization (ELSO), the World Health Organization and the Surviving Sepsis Campaign (SSC) Guidelines recommend considering ECMO, in specialized centers, for patients with COVID-19 who develop severe acute respiratory distress syndrome (ARDS). 2 Many of these cases made use of veno-venous ECMO, which exclusively provides pulmonary bypass for severe respiratory failure.


This article will focus on veno-arterial ECMO (which provides both cardiac and pulmonary bypass) and seeks to provide readers with an overview of the following:

  • What is an Extracorporeal Cardiopulmonary Resuscitation (ECPR) code?
  • Which patients should be considered for acute ECMO initiation?
  • What care will patients need in the ED post-circuit initiation?
  • What is the evidence for the use of ECPR?



Calling an ECPR Code and Patient Selection

An ECPR code essentially mobilizes the cannulation team to initiate an ECMO circuit in a previously high-functioning patient. The goal is to restore end-organ perfusion, buying time to investigate the underlying causative pathology, with hopes of improving long-term survival and neurological outcomes. Emergency physicians should consider calling an ECPR code for severe cardiac and/or pulmonary failure deemed refractory to conventional therapies. 3 Patients in cardiac arrest are potential candidates for ECPR if they meet the following:

  • reversible cause of arrest
  • witnessed arrest with bystander CPR
  • total chest compression time < 60 minutes
  • no known preexisting terminal illnesses


Review the reversible causes of cardiac arrest or see the image below outlining the “Hs and Ts” mnemonic.

Figure 1: The Hs and Ts / Reversible Causes of Cardiac Arrest 4

The timing at which an ECPR code should be initiated is (at present) left to physician discretion, but often depends on the availability of the cannulation team. ECMO as an option for a given patient should be anticipated and considered early amid a code to allow the team and equipment to be assembled. Most often the procedure is performed by a cardiac surgeon, however there is growing interest and involvement from vascular, general, and trauma surgeons. 5


The initiation of ECMO is divided into 3 stages:

(1) vascular access,

(2) insertion of ECMO cannulas and connection to the circuit once the patient is determined to be an ECMO candidate,

(3) pump initiation.


In emergent situations, unilateral peripheral cannulation is the preferred and most expedient method. 6 This approach also allows for the continuation of high-quality CPR while access is obtained. Either through surgical exposure or under ultrasound guidance, a venous drainage cannula is placed in the femoral vein. Blood is returned from the machine through a similarly placed cannula in the adjacent femoral artery. Several alternative circuits are possible in extenuating circumstances depending upon patient injuries or characteristics. 1

Figure 2: Veno-arterial peripheral ECMO via unilateral femoral-arterial and femoral-venous cannulation. 7


Post-Circuit Initiation Critical Care

After the circuit has been initiated, the lines should be closely examined; the venous drainage blood should be dark red and the arterial return blood should be bright red. Given the proximity of the vessels and the fact that these procedures are often done with ongoing CPR, this confirmation of placement is crucial.


Next, it is important to reassess the patient’s rhythm; if the patient is in VFIB, defibrillation should be repeated after a few minutes on circuit as it is important to have an ejecting left ventricle on ECMO to prevent distention. 8


At this point, the team should obtain a right radial arterial line (for accurate measurement of the MAP) and an ABG (to assess for adequate oxygenation and the need for setting adjustments). Vasopressors and/or inotropes should be initiated as required to meet a target MAP of 60-80mmHg. If LV distention (as assessed based on arterial line pulsatility >10mmHg or POCUS) is not improved with these medications on board, an LV vent (such as an Impella or intra-aortic balloon pump) may be needed. 8


Important next steps in the process include the initiation of therapeutic hypothermia, planning for the placement of a distal perfusion catheter to prevent leg ischemia, and, based on the etiology of the arrest, any other appropriate treatment (such as transfer to the cardiac catheterization laboratory for acute coronary syndrome).


Current Evidence for ECPR

No randomized trials concerning the use of ECPR have been published to date. Sonneville and Schmidt recently summarized the four most robust observational studies comparing the use of ECPR versus conventional CPR in patients with out-of-hospital cardiac arrest. 9 They describe a large study that reported similar low survival rates between 525 patients managed with ECPR and 12,666 patients with conventional CPR, with no significant effect of ECPR on outcomes after adjusting for confounders. 10 However, more recently, after instituting very strict patient selection criteria, Bartos et al. reported a relative risk reduction of 29% for death or poor neurological outcome (95% CI, 18%–41%) for patients receiving between 20 and 59 minutes of CPR and 19% (95% CI, 10%–27%) for patients receiving more than 60 minutes of CPR. 11 This group has since published the University of Minnesota ECPR Protocol here. 12


Until results from randomized trials become available, it is likely that difficult continuation decisions will need to be made on a case-by-case basis at physician discretion. Protocols requiring objective data input such as specific time periods, lactate level and oxygenation status upon arrival, may help ease this burden in the meantime, if only marginally.



  1. Badulak JH, Shinar Z. Extracorporeal Membrane Oxygenation in the Emergency Department. Emerg Med Clin North Am. 2020;38(4):945-959. doi:10.1016/j.emc.2020.06.015
  2. Ramanathan K, Shekar K, Ling RR, et al. Extracorporeal membrane oxygenation for COVID-19: a systematic review and meta-analysis. Crit Care. 2021;25(1):211. doi:10.1186/s13054-021-03634-1
  3. Extracorporeal Life Support Organization (ELSO). Guidelines. Accessed August 29, 2021. https://www.elso.org/Portals/0/ELSO%20Guidelines%20General%20All%20ECLS%20Version%201_4.pdf
  4. @lightssirensaction. Hs and Ts. Accessed August 28, 2021. https://www.instagram.com/p/CA4MMdVBy8V/
  5. McCallister D, Pilon L, Forrester J, et al. Clinical and Administrative Steps to the ECMO Program Development. IntechOpen; 2019. doi:10.5772/intechopen.84838
  6. Stoecklein H, Slack S, Tonna JE, Youngquist ST. ECMO & ECPR. JEMS. Published December 2, 2017. Accessed August 28, 2021. https://www.jems.com/patient-care/ecmo-ecpr/
  7. Lawler PR, Silver DA, Scirica BM, Couper GS, Weinhouse GL, Camp PC. Extracorporeal Membrane Oxygenation in Adults With Cardiogenic Shock. Circulation. 2015;131(7):676-680. doi:10.1161/CIRCULATIONAHA.114.006647
  8. Cevasco M, Takayama H, Ando M, Garan AR, Naka Y, Takeda K. Left ventricular distension and venting strategies for patients on venoarterial extracorporeal membrane oxygenation. J Thorac Dis. 2019;11(4):1676-1683. doi:10.21037/jtd.2019.03.29
  9. Sonneville R, Schmidt M. Extracorporeal Cardiopulmonary Resuscitation for Adults With Refractory Out-of-Hospital Cardiac Arrest. Circulation. 2020;141(11):887-890. doi:10.1161/CIRCULATIONAHA.119.044969
  10. Bougouin W, Dumas F, Lamhaut L, et al. Extracorporeal cardiopulmonary resuscitation in out-of-hospital cardiac arrest: a registry study. Eur Heart J. 2020;41(21):1961-1971. doi:10.1093/eurheartj/ehz753
  11. Bartos JA, Grunau B, Carlson C, et al. Improved Survival With Extracorporeal Cardiopulmonary Resuscitation Despite Progressive Metabolic Derangement Associated With Prolonged Resuscitation. Circulation. 2020;141(11):877-886. doi:10.1161/CIRCULATIONAHA.119.042173
  12. Yannopoulos D, Bartos JA, Martin C, et al. Minnesota Resuscitation Consortium’s Advanced Perfusion and Reperfusion Cardiac Life Support Strategy for Out‐of‐Hospital Refractory Ventricular Fibrillation. J Am Heart Assoc. 5(6):e003732. doi:10.1161/JAHA.116.003732
Continue Reading

Bell’s Palsy or Stroke?

Bell’s Palsy or Stroke? A Medical Student Clinical Pearl

Alicia Synette, Med III

Class of 2022 MUN

Reviewed by Dr. Jeremy Gross

Copyedited by Dr. Mandy Peach


A 48M presented to the Emergency Department with right sided facial droop and altered facial sensation for two days.

He woke up one morning and described the right side of his face as feeling “saggy”. At this time, he assumed that he had slept funny. The facial droop progressed that day until it became noticeable by his wife. Two days later, he decided to go to the ER when his symptoms did not resolve. At this time, he described altered sensation at the right side of the face and tongue, which he compared to the feeling of local anesthetic after dental work. His smile was “crooked”, he was unable to purse his lips, and he could not completely close his right eye. The affected eye was also red and irritated. Taste and hearing were unchanged. Review of systems was otherwise unremarkable.

PMH: T2DM, HTN, hyperlipidemia

Medications: Ramipril, Fenofibrate, Janumet, Rosuvastatin, ASA, Lantus, Humalog

On exam, he appeared well, he was afebrile, and vital signs were stable. Pupils were equal and reactive to light. Conjunctival injection was present at the right eye with increased tearing. Mild facial droop was apparent. The right eyelid was droopy and he was unable to keep it closed against resistance. Facial movements on the right side were also weak (smile, purse lips, puff cheeks, close eyes tight), however, weakness of the forehead muscles could not be appreciated when asked to raise his eyebrows. Sensation to light touch was altered at V1. Pinprick touch was normal. There was no deviation of the tongue. He had 5/5 strength and normal sensation bilaterally at the extremities. Normal rapid alternating movements and normal heel to shin test. Normal hearing bilaterally and no hyperacusis.

Accessed from grepmed – https://www.grepmed.com/

Differential Diagnosis for Facial Nerve Palsy

Table 1: differential diagnosis for facial nerve palsy.6


Lab results were unremarkable aside from an elevated random blood glucose. HbA1C level from one month prior to the ER visit was 11.1%.

CBC – LKC 8.2, Hgb 137, PLT 213

Electrolytes – Na 140, K 3.9, Cl 103

Glucose (random) 9.9

Urea 5.4, Ca+ 2.45, Mg 0.87, TSH 1.33

CT head showed no evidence of mass lesion, hemorrhage, hydrocephalus, subacute or chronic infarct.


Bell’s Palsy

Bell’s palsy is an isolated CNVII (facial nerve) paresis/paralysis as a result of acute inflammation and/or edema of the nerve. The onset is typically acute and progresses within hours, and while the cause is unknown, it is thought that the most likely etiology is viral (HSV, CMV, EBV).5


The facial nerve innervates the facial muscles, therefore, CNVII palsy presents with sudden onset unilateral facial paralysis, which can include: 1

  • Eyebrow sagging.
  • Inability to close the eye.
  • Disappearance of the nasolabial fold.
  • Drooping at the affected corner of the mouth, which is drawn to the unaffected side.2


CNVII also innervates the lacrimal glands, salivary glands, stapedius muscle, and taste fibres on the tongue, therefore, other associated features can include:1

  • Decreased tearing.
  • Hyperacusis
  • Loss of taste sensation on the anterior 2/3 of the tongue. 2

Figure 1: Anatomy of the facial nerve. 6


Risk Factors5

  • Pregnancy
  • Severe pre-eclampsia
  • Obesity
  • Hypertension
  • Diabetes
  • Upper respiratory illnesses

House-Brackmann Classification

The House-Brackmann classification seen below is used to determine severity of facial nerve dysfunction and has prognostic value. The lower the grade, the more likely a patient is to make a full recovery.7

Table 2: House-Brackmann classification of facial nerve dysfunction.3



Diagnosis of Bell’s Palsy is considered a clinical diagnosis so there is no gold standard test, however, other causes of facial nerve palsies tend to have associated features and can be ruled out clinically. Most significantly, it is important to rule out life-threatening central lesions, such as ischemic/hemorrhagic stroke.4

Central vs. Peripheral Lesions

Central lesions – result in forehead sparing, as the facial nerve is innervated by ipsilateral and contralateral fibres from the motor cortex. Patients with forehead sparing need a head CT to rule out a central cause such as a stroke or mass!5

Peripheral lesions – the lesion is below the nucleus, and all the fibres innervating the facial nerve will be affected. Results in no forehead sparing.5

Figure 2: facial nerve lesion vs. supranuclear lesion with forehead sparing. 6

Other pertinent findings on history can include: rashes, arthralgias, or fevers, exposure to ticks (Lyme disease), and vesicular eruption (Ramsay Hunt Syndrome). In addition to a full cranial nerve and peripheral nerve exam, physical examination should involve assessment of the ear, tympanic membrane, and parotid gland for signs of AOM, cholesteatoma, or parotid tumor.6

Further investigations6

  • Lyme serology: if clinical suspicion for Lyme disease
  • Head CT: gradual onset of symptoms or forehead sparing
  • Neurology referral: bilateral palsies or no improvement



Corticosteroids +/- antiviral is the choice of treatment for Bell’s Palsy. Studies have demonstrated that antivirals alone have no benefit, but in combination with corticosteroids there is a significantly increased benefit compared to corticosteroids alone. Patients should be started on corticosteroids within 72 hours of presentation for a course of at least 7 days. Physicians can also discuss with patients the potential benefit of adding an anti-viral.8

Eye care is an important consideration in these patients as a proportion will have incomplete eye closure, putting them at risk of corneal injury. Artificial tears during the day are recommended as well as taping the eyelid closed to prevent excessive dryness or trauma.9

With treatment, patients will see improvement within weeks and most experience full recovery within 3-4 months. 5


Case Conclusion

Our patient was started on valacyclovir 100mg TID x7 days and prednisone 60mg daily x 7 days for suspected Bell’s Palsy. Despite a normal CT, which helped to rule out central causes of facial paresis (stroke, subdural hematoma, brain tumor), the potential forehead sparing of the patient’s presentation presented concern for stroke. He was referred to Stroke Prevention Clinic and was seen the following day.

Neurology assessed the patient and appreciated that there was mild weakness in the forehead noted as a “reduction of wrinkles”, therefore, the diagnosis of Bell’s Palsy was confirmed. It was recommended that he continue the valacyclovir and prednisone course. It was also recommended that he patch the eye in the evenings and continue to use lubricating eye drops in the affected eye to prevent exposure keratitis.

Key Points

  1. Bell’s palsy results in unilateral facial nerve paresis/paralysis, without forehead sparing
  2. Associated symptoms may include: decreased tearing, hyperacusis, loss of taste
  3. No investigations are required; however, patients with true forehead sparing need a head CT as this finding is suggestive of a central lesion
  4. Patients with systemic symptoms, gradual onset, or bilateral symptoms should have further work-up
  5. Most cases will resolve in 3-4 months with treatment
  6. Treatment with corticosteroids +/- an antiviral for 7 days should be initiated within 72 hours of symptom onset




  1. Baugh, R., et al. 2013. Clinical Practice Guideline. Otolaryngology–Head and Neck Surgery, 149(3_suppl), pp.S1-S27. Retrieved from: https://journals.sagepub.com/doi/10.1177/0194599813505967?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmed
  2. 2021. CRACKCast E105 – Brain and Cranial Nerve Disorders – CanadiEM. Retrieved from: https://canadiem.org/crackcast-e105-brain-cranial-nerve-disorders/
  3. House, J. and Brackmann, D., 1985. Facial Nerve Grading System. Otolaryngology–Head and Neck Surgery, 93(2), pp.146-147. Retrieved from: https://pubmed.ncbi.nlm.nih.gov/3921901/
  4. McCaul, J., Cascarini, L., Godden, D., Coombes, D., Brennan, P. and Kerawala, C., 2014. Evidence based management of Bell’s palsy. British Journal of Oral and Maxillofacial Surgery, 52(5), pp.387-391. Retrieved from: https://pubmed.ncbi.nlm.nih.gov/24685475/
  5. org.au. 2021. RACGP – A general practice approach to Bell’s palsy. Retrieved from: https://www.racgp.org.au/afp/2016/november/a-general-practice-approach-to-bell%E2%80%99s-palsy/#1
  6. Tiemstra JD, Khatkhate N. Bell’s palsy: diagnosis and management. Am Fam Physician. 2007 Oct 1;76(7):997-1002. PMID: 17956069. Retrieved from: https://pubmed.ncbi.nlm.nih.gov/17956069/
  7. Yoo, M., et al. 2020. Evaluation of Factors Associated With Favorable Outcomes in Adults With Bell Palsy. JAMA Otolaryngology–Head & Neck Surgery, 146(3), p.256. Retrieved from: https://pubmed.ncbi.nlm.nih.gov/31971554/
  8. Hato, N., et al. Efficacy of early treatment of Bell’s palsy with oral acyclovir and prednisolone. Otol Neurotol. 2003 Nov;24(6):948-51. Retrieved from: https://pubmed.ncbi.nlm.nih.gov/14600480/
  9. Ronthal, M. Greenstein, P. 2021. Bell’s palsy: Treatment and prognosis in adults. Retrieved from Uptodate October 26, 2021 from https://www.uptodate.com/contents/bells-palsy-pathogenesis-clinical-features-and-diagnosis-in-adults?search=bells%20palsy%20management&topicRef=5286&source=see_link






Continue Reading

Vertigo Makes the World Go Round – A Case of BPPV

Vertigo Makes the World Go Round – A Case of BPPV: Medical Student Clinical Pearl

Johnathan Rose, Med III

Class of 2022

Dalhousie Medical School New Brunswick (DMNB)

Reviewed by Dr. Maria Kovalik

Copyedited by Dr. Mandy Peach


A 73-year-old female presented to the emergency department via EMS with a three-day history of dizziness and associated nausea. On further questioning she stated that the dizziness began suddenly when she awoke three days prior. It felt like her environment was spinning and was made worse with movements. Episodes lasted about 30-60 seconds and would resolve if she stayed still. Her mobility was impaired due to feeling unsteady on her feet. She felt nauseous when dizzy but had no emesis; Gravol provided mild relief. She denied any headaches, vision/hearing changes, chest pain, shortness of breath, bowel/bladder changes, recent infections, muscle weakness, paresthesia, or constitutional symptoms.


She was an otherwise healthy 73-year-old with no past medical or surgical history. She was taking no medications. She did not smoke, drink alcohol, or use any recreational drugs.


Physical Exam:


The patient’s vital signs were all within normal limits and stable. Upon inspection, she appeared her stated age, was well kempt, and was laying very still with her eyes closed. She was alert and oriented x3. Her cranial nerve exam II-XII was normal. She had 5/5 strength in upper and lower limbs bilaterally. Tympanic membranes were normal bilaterally.


Upon sitting up, she had mixed horizontal and torsional nystagmus in her eyes bilaterally, as well as when she laid back down (Figure 1). When performing the Dix-Hallpike manoeuvre, she had mixed horizontal and torsional nystagmus when her head was tilted both left and right.

From: https://icrcat.com/en/nystagmus/

Figure 1. Types of Nystagmus. Diagram showing the 3 major forms of nystagmus: horizontal, vertical, and rotary.



What is vertigo?


There are four main types of dizziness: vertigo, light-headedness, presyncope, and disequilibrium. Vertigo is the most common, accounting for 54% of presentations1. Vertigo is the sensation of dizziness or illusory movement. Some people may perceive it as the environment moving while others perceive self-motion. It is often caused because of asymmetry in the vestibular system or dysfunction of the labyrinth, vestibular nerve, or central vestibular structures located in the brainstem2. Vertigo is a symptom, not a diagnosis, and the causes can be broken into two broad categories: central and peripheral3.



Does this patient have a central or peripheral cause of vertigo?


The history alone from a patient presenting with vertigo is able to correctly reveal the diagnosis in ¾ patients1. Therefore, it is necessary to ask questions that will help differentiate the causes of vertigo, as further investigations may not be helpful in doing so (Table 1).


Table 1. Distinguishing features between central and peripheral causes of vertigo1, 4.

Peripheral Central
Onset Sudden Gradual
Intensity Severe Mild
Duration Seconds Continuous
Nystagmus Horizontal and torsional; can be inhibited by fixation of gaze Purely vertical, horizontal, or torsional; cannot be inhibited by fixation of gaze
Associated neuro findings Rare Common
Tinnitus Common Rare
Nausea/Vomitting Frequent, severe Infrequent, mild


Physical exam for differentiating between central and peripheral vertigo should include a HINTS exam

Interpretation of the HINTS

“A benign HINTS exam is defined as abnormal HIT + direction-fixed horizontal nystagmus + absent skew.

dangerous HINTS exam is defined as any one of:

  • Normal/untestable HIT
  • or direction-changing horizontal nystagmus present/untestable
  • or skew deviation present/untestable

(Untestable refers to those patients with obvious oculomotor pathology or lethargy in whom the tests were unable to be completed).


The acronym INFARCT can be used to remember what constitutes a dangerous HINTS exam:

Impulse Normal

Fast-phase Alternating

Refixation on Cover Test.”8


Based on her history and physical exam findings, it is likely that our patient has peripheral vertigo.


What is the differential diagnosis for central vertigo1?

  • Multiple sclerosis
  • Migraine
  • Transient ischemic attack or stroke
  • Brain tumor


What is the differential diagnosis for peripheral vertigo1?

  • Benign positional paroxysmal vertigo (BPPV)
  • Ménière’s disease
  • Vestibular neuronitis
  • Acute labyrinthitis
  • Otosclerosis


What type of peripheral vertigo does our patient have?

The most common causes of peripheral vertigo are BPPV, Ménière’s disease, and vestibular neuronitis5. Table 2 illustrates some of the features that can be used to distinguish the causes of peripheral vertigo.

Table 2. Distinguishing features between common causes of peripheral vertigo5.

Ddx Duration Provoking Factors Special features Physical exam findings
Labyrinthitis Seconds – Minutes Change in position Hearing loss and tinnitus Hearing loss
Vestibular neuronitis Seconds – Minutes URTI Imbalance Normal hearing
BPPV Seconds – Minutes Change in position Positional Positive Dix-Hallpike
Ménière’s disease Hours Spontaneous Hearing loss and tinnitus Hearing loss




Taking into account both the history and physical exam, our patient has clear case of BPPV. She had a sudden onset of dizziness that is worse with changes in position and lasts 30-60 seconds before resolving if still. She had associated nausea and no other neurological signs. This, along with a positive Dix-Hallpike, is enough to secure the diagnosis.


BPPV Pathophysiology

BPPV is caused by canalithiasis, often calcium carbonate crystals, within the semicircular canals (Figure 2). The semicircular canals normally function to detect angular movements of the head. However, these heavy stones can cause inappropriate movement of the endolymph within the canals during times of linear accelerations, such as with gravity. Ultimately, this causes the improper sensation of spinning when the head shifts with respect to gravity6.

From: https://balanceanddizziness.org/disorders/vestibular-disorders/bppv/

Figure 2. Mechanism of BPPV. Calcium crystals normally found within the utricular cavity are displaced and fall into the semicircular canals. Once displaced, they then cause the erroneous sensation of spinning when the head moves6.



 Although episodes of dizziness last seconds to minutes, the symptoms may persist for up to two weeks, and will often resolve spontaneously6. Symptoms may recur after remission5.

Treatment options are limited for those with BPPV. Medications are often not helpful, and treatment with vestibular suppressant medications such as antihistamines and/or benzodiazepines should be avoided7. For those who find the symptoms to be too distressing, the Epley maneuver may be performed to try and dislodge the otoliths from the semicircular canals (Figure 3)6. This maneuver has roughly a 77% success rate in the literature, but anecdotally seems to be less while also making patients more nauseous5.

Figure 3. Epley Maneuver. Steps involved in trying to reposition the calcium debris within the semicircular canals to migrate toward the common crus and exit into the utricular cavity6.


Our Case

Our patient ended up having BPPV that would likely resolve on its own within 2 weeks. No further diagnostic workup was required. Treatment options were limited; she was disappointed when she learned we had no medications that would provide her relief of her spinning world. The Epley maneuver was offered with the premise that it may or may not help relieve symptoms but will likely make her more nauseous, which she declined.


Clinical Pearls


  • Vertigo is a symptom, not a diagnosis.
  • A detailed history is required to elicit features of central or peripheral causes of vertigo.
  • Serious causes of central vertigo need to be considered.
  • Physical examination should include a neurological, cardiovascular, eye, and ear exam.
  • Rule out orthostatic hypotension by seeing if the patient feels dizzy when they sit up as well as when they lay down.
  • Treatment with vestibular suppressant medications such as antihistamines and/or benzodiazepines should be avoided7.
  • The Epley maneuver may be useful in some patients but will likely increase their nausea.



  1. Labuguen RH. Initial Evaluation of Vertigo. Am Fam Physician. 2006;73(2):244-251.
  2. Evaluation of the patient with vertigo. https://www.uptodate.com/contents/evaluation-of-the-patient-with-vertigo?search=vertigo&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1#H1
  3. Baumgartner B, Taylor RS. Peripheral Vertigo. StatPearls. 2020. Available from: https://www.ncbi.nlm.nih.gov/books/NBK430797/
  4. Chang AK. Dizziness and vertigo. In: Mahadevan SV, Garmel GM, editors. An Introduction to Clinical Emergency Medicine. 2nd ed. Cambridge: Cambridge University Press; 2012. p. 289–300.
  5. Dommaraju S, Perea E. An approach to vertigo in general practice. Australian Family Physician. 2016;45(4):190-194.
  6. Benign paroxysmal positional vertigo. https://www.uptodate.com/contents/benign-paroxysmal-positional-vertigo?search=vertigo&source=search_result&selectedTitle=5~150&usage_type=default&display_rank=5#H4
  7. Stanton M, Freeman AM. Vertigo. StatPearls. 2021. Available from: https://www.ncbi.nlm.nih.gov/books/NBK482356/
  8. MacKay, J. HINTS exam in Acute Vestibular Syndrome. 2016. Retrieved Oct 26, 2021 from https://sjrhem.ca/resident-clinical-pearl-hints-exam-in-acute-vestibular-syndrome/
Continue Reading

A Case of Post-traumatic Delayed Facial Nerve Palsy in a Child

A Case of Post-traumatic Delayed Facial Nerve Palsy in a Child – A Medical Student Clinical Pearl

Jacqueline Mincer, BSc, MSc

Dalhousie Medicine New Brunswick Class of 2022, Med III

Reviewed by: Dr. Erin Slaunwhite

Copyedited by: Dr. Mandy Peach

History of Presenting Illness:

A 10-year-old girl presented to the emergency department (ED) one week after a bike accident with left-sided hemifacial palsy. The patient was biking down a hill without a helmet when she fell onto her left side. Emergency medical services (EMS) brought the patient to the ED with a Glasgow Coma Scale (GCS) score of 15. The patient denied loss of consciousness, nausea, vomiting or headache. Small amounts of blood were noted around her left tragus; however, the patient denied any hearing impairments at the time. She was otherwise healthy with no prior surgeries, no allergies, and no medications.


CT head, CT cervical spine, and shoulder XR were ordered. Imaging revealed a transverse fracture through the distal third of the clavicle with 100% displacement (Figure 1). CT head and cervical spine were both reported as normal, with no significant post-traumatic abnormalities detected.

Figure 1: L clavicle fracture

The clavicle fracture was treated non-operatively. The patient was discharged home with a sling to immobilize the shoulder and was provided with an outpatient follow-up appointment with orthopedics.


Four days after the accident, left-sided facial changes were first noticed and had been progressively worsening. The patient complained of left-sided numbness, photosensitivity, difficulty blinking, and lip palsy (Figures 2a, 2b). There was ongoing bloody drainage and intermittent hearing difficulties from the left ear.

Figure 2: L sided facial nerve palsy*:

2a) incomplete closure of the left eye

2b) limited ability to open mouth/smile on the left side; decreased movement of the upper left eyebrow

*photos taken with consent of patient and parent


To build a complete differential diagnosis, let’s first review the anatomy of the facial nerve as it enters and exits the skull:

  • The facial nerve is the 7th paired cranial nerve.
  • It arises in the pons and travels through the temporal bone via the internal acoustic meatus then travels through the “Z” shaped facial canal exiting the skull via the stylomastoid foramen (Figure 5).
  • Upon exiting the skull, the facial nerve runs anteriorly to the outer ear and gives rise to the posterior auricular nerve branch. The main motor root of the facial nerve passes through the parotid gland, ultimately splitting into 5 terminal branches: the temporal, zygomatic, buccal, marginal mandibular and cervical branches (Figure 6).

Figure 5: Pathway of facial nerve through skull. 

Dalhousie Medicine neuroanatomy lab manual.

Figure 6. Branches of the facial nerve (VII)

The facial nerve is a mixed nerve, containing motor, sensory and parasympathetic fibers.(1)

  • Motor: innervates muscles of facial expression.
  • Sensory: taste sensation from anterior 2/3 of the tongue (via chorda tympani, a branch of the mandibular nerve, V3).
  • Parasympathetic: supplies glands of the head and neck
    • Lacrimal gland (tearing), sublingual and submandibular glands (salivary).




  • Onset and progression (gradual onset more suggestive of mass lesion)
  • Recent rashes, arthralgias, fevers or other illnesses
  • Tick exposure, recent trauma, or prior history of peripheral nerve palsy



  • Head & Neck: inspect external ear, ear canal, tympanic membrane, oropharynx. Palpate parotid gland.
  • Neurologic exam: cranial nerve exam (Figure 8) and full neuro exam. Differentiate between upper motor neuron and lower motor neuron lesions by assessing forehead involvement. Forehead paralysis on affected side is suggestive of a lower motor neuron (peripheral) lesion. While no forehead paralysis on the affected side is suggestive of an upper motor neuron (central) lesion. This is due to bilateral innervation of the forehead from the central nervous system.
  • Skin: inspect for lesions suggestive of herpes zoster, Lyme disease or dysmorphic features


Figure 8: Cranial nerve function and testing


Pediatric facial nerve palsy can be congenital, acquired, or idiopathic.


Congenital: secondary to delivery trauma, genetic causes, or may make up one feature of a broader syndromic malformation.(2)

Acquired: resulting from infection or damage/trauma to nearby structures.

  • Infectious pathogens include Borrelia Burgdorferi, Herpes Varicella-Zoster (most common), Epstein-Barr virus, Haemophilus influenza, Tuberculosis, CMV, Adenovirus, Rubella, Mumps, Mycoplasma pneumoniae, and HIV.
  • Disease to neighbouring structures (Figure 7) include Otitis media, Cholesteatoma, Mastoiditis, and Meningitis.



Figure 7: neighbouring structures to facial nerve

  • Trauma/injury to the facial nerve from temporal bone fractures (at the basilar level)
  • Iatrogenic paralysis (surgical complication) from procedures involving the parotid gland, middle ear or mastoid.

Less common, acquired etiologies:

  • Inflammatory: vasculitis, HSP, or Kawasaki disease.
  • Neoplasm: schwannoma, hemangioma, bone tumor (rhabdomyosarcoma, histiocytosis), leukemia, parotid gland tumors.

Idiopathic: In approximately 50% of cases, the etiology remains unknown. Idiopathic facial paralysis is commonly referred to as “Bell’s Palsy”



Investigations, prognosis and treatment are all highly dependent on the overall clinical picture, including underlying etiology and severity of palsy.(3)



  • Imaging is warranted in patients who present with atypical signs, such as involvement of neighbouring cranial nerves, chronic otitis media, acute mastoiditis, temporal bone trauma, suspected malignancy, slow onset (>3 weeks), or no improvement at 6 months.
  • In “typical” incomplete facial palsy with good recovery, imaging may not be necessary.
  • Consider serologic testing to rule out Lyme disease if warranted.
  • Consider EEG, neuroimaging, lumbar puncture based on history and physical exam. (3)



  • Prognosis will vary depending on cause and mechanism of injury.
  • Most children with Bell’s palsy recover well and regain most if not all of their function. (3)



  • If applicable, treat the underlying disorder (e.g. Lyme disease, acute otitis media).
  • Bell’s Palsy:
    • Early treatment (within 3 days of symptom onset) with oral glucocorticoids. (2)
    • Prednisone 1-2mg/kg daily (up to 60-80mg) x 5 days, then a five-day taper by 10mg per day. (3)
  • Congenital or permanent acquired facial palsy: consider surgical consult
  • All patients will require supportive care:
    • Artificial tears to protect the cornea of the affected eye.
    • Taping of the eyelid shut overnight in patients unable to completely close the eye.


Case Conclusion:

The ED physician consulted the on-call radiologist and neurosurgeon. The CT-head from the day of the accident was revisited, detecting a 4cm basilar skull fracture to the left temporal bone (Figure 10).

Figure 10: Basal skull fracture

Delayed hearing loss and bloody drainage from the left ear was suggestive of a trauma-induced tympanic membrane perforation.

Inflammation from the basilar skull fracture and/or ruptured tympanic membrane likely explains compression of the facial nerve. In this case, the delayed presentation of left-sided facial palsy is a reassuring prognosis. It points towards inflammatory compression of the nerve as opposed to complete laceration of the nerve at the time of trauma.

She was discharged home with a two-day prescription for Dexamethasone 10mg PO once daily. A plan was made for a repeat CT head in 6-8 weeks as well as outpatient follow up with orthopedic surgery, neurosurgery, and pediatric neurology.

Take Home Points:

o Facial nerve palsy in children can be classified as congenital, acquired or idiopathic in nature.
o The case presented here was an acquired facial nerve palsy, following a traumatic basilar skull fracture.
o Investigations, prognosis and treatment are highly dependent on underlying etiology and severity
o If known, it is important to treat the underlying etiology.
o Consider glucocorticoids at early onset (within 3 days of presentation) as well as supportive management (artificial tears, eyelid taping).

1. The Facial Nerve (CN VII) – Course – Functions – TeachMeAnatomy [Internet]. [cited 2021 Jun 14]. Available from: https://teachmeanatomy.info/head/cranial-nerves/facial-nerve/
2. Ciorba A, Corazzi V, Conz V, Bianchini C, Aimoni C. Facial nerve paralysis in children. World J Clin Cases. 2015 Dec 16;3(12):973–9.
3. Facial nerve palsy in children – UpToDate [Internet]. [cited 2021 Jun 14]. Available from: https://www.uptodate.com/contents/facial-nerve-palsy-in-children?search=-%09Facial%20nerve%20grading%20(House-Brackman&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1#H4519763


Continue Reading

Approach to Biliary Pain

Approach to Biliary Pain – A Medical Student Clinical Pearl

Katie Oxford, Med III

Reviewed by: Dr. Colin Rouse

Copyedited by: Dr. Mandy Peach


Mr. X is a 20-year-old male, who has presented to the ER on multiple occasions with RUQ pain. This pain was constant, severe (8/10), and was exacerbated by eating. This pain started a few months ago, is not radiating, and is variable in duration. The patient had become increasingly frustrated due to multiple trips to the ER.

The patient has had no vomiting or nausea, no change in bowel movements. On review of systems, no abnormalities are noted. Vitals are stable.


On ultrasound and CT done during prior visits no gallstones were present within the gallbladder or within the biliary tree, but the common bile duct was dilated. The gallbladder appears normal on all imaging studies performed thus far, however the patient continues to have pain.

On physical exam, there were no concerns on inspection (no scars, visible masses, signs of liver disease, ascites). Normal bowel sounds were heard, and the abdomen was soft and non-tender on palpation. Murphy’s sign was negative. LFT’s, amylase and lipase studies were normal.

Sphincter of Oddi Dysfunction

Sphincter of Oddi dysfunction (SOD) is within the differential diagnosis for patients who present with recurrent biliary pain, with no apparent source 1. This disease process can present with biliary as well as pancreatic obstructive symptoms 2. There are multiple propositions as to the pathogenesis of this disease; it may be due to stenosis at the ampulla, or it could be caused by sphincter of oddi hypertension (either due to hypertrophy, or increased smooth muscle response to stimuli) 2.

Rome IV criteria for functional biliary sphincter of Oddi disorder5:

●Criteria for biliary pain are fulfilled

●Absence of bile duct stones or other structural abnormalities

●Elevated liver enzymes or dilated bile duct, but not both


Supportive criteria include

●Normal amylase/lipase

●Abnormal sphincter of Oddi manometry

●Abnormal hepatobiliary scintigraphy


It is important to avoid invasive testing in patients with suspected SOD, as their risk for post-ERCP pancreatitis is high 2.

There are several methods that can be used to assess patients for SOD:

Endoscopic ultrasound
Transabdominal ultrasound
Hepatobiliary Scintigraphy (HIDA) can be used to evaluate patients for SOD. 2

Additionally, cholecystokinin or secretin can be used in conjunction with the above tests in order to provoke the dysfunction 2

Back to our case:
In a case of RUQ pain, there are a few disease processes to keep in mind 3:

Differential Diagnoses:
• Cholecystitis
• Cholelithiasis
• Cholangitis
• Colitis
• Diverticulitis
• Abscess
• Hepatitis
• Mass
• Pneumonia
• Functional Gallbladder Disorder
• Abscess
• Embolus
• Nephrolithiasis
• Pyelonephritis

Because Mr. X had pain that resembled biliary colic very closely, yet multiple previous imaging studies and lab studies showed no signs of acute cholecystitis,  cholelithiasis, pancreatitis, or liver disease, it was thought that perhaps sphincter dysfunction could be the root cause of the problem.

HIDA Scans:

Hepatobiliary Scintigraphy (HIDA) is a nuclear medicine procedure involved IV injection of a radiotracer which is excreted into the biliary system. This allows for the visualization of the bilirubin metabolic pathway and can be used to diagnose various biliary pathologies 4

After discussion with the patient and reassurance, a HIDA scan was ordered in order that confirmed suspicions of SOD.

Management 6:

The goal is to relieve pain. There are 3 main approaches:

  1. pharmacological: calcium channel blocker and nitrates to reduce basal sphincter of oddi pressure and relaxation of the sphincter.
  2. endoscopic sphincterotomy: particularly beneficial in those with elevated sphincter of oddi pressure
  3. surgical sphincterotomy

The patient was referred to gastroenterology and initiated on a calcium channel blocker in the interim.



  1. Bistritz L, Bain VG. Sphincter of Oddi dysfunction: Managing the patient with chronic biliary pain [Internet]. Vol. 12, World Journal of Gastroenterology. WJG Press; 2006. p. 3793–802.
  2. Small AJ, Kozarek RA. Sphincter of Oddi Dysfunction. Vol. 25, Gastrointestinal Endoscopy Clinics of North America. W.B. Saunders; 2015. p. 749–63.
  3. Cartwright SL, Knudson MP. Evaluation of Acute Abdominal Pain in Adults [Internet]. Vol. 77, American Family Physician. 2008 Apr.
  4. Snyder E, Kashyap S, Lopez PP. Hepatobiliary Iminodiacetic Acid Scan [Internet]. StatPearls. StatPearls Publishing; 2021.
  5. Cotton, P. B., Elta, G. H., Carter, C. R., Pasricha, P. J., & Corazziari, E. S. (2016). Rome IV. Gallbladder and Sphincter of Oddi Disorders. Gastroenterology, S0016-5085(16)00224-9. Advance online publication. https://doi.org/10.1053/j.gastro.2016.02.033
  6. Catalano, M. F, Thosani, N. (2021). Treatment of Sphincter of Oddi Dysfunction. Retrieved from UptoDate https://www.uptodate.com/contents/treatment-of-sphincter-of-oddi-dysfunction?search=sphincter%20of%20oddi%20dysfunction%20treatment&source=search_result&selectedTitle=1~136&usage_type=default&display_rank=1


Continue Reading

Alternative Rib Fracture Management in the ED

Alternative Rib Fracture Management in the ED – A Medical Student Clinical Pearl

Victoria Mercer, Clinical Clerk 3, DMNB

Reviewed and Copyedited by Dr. Mandy Peach

Rib fractures are a frequent presentation in the ED, occuring in approximately 10% of all injured patients with the primary causes being blunt chest trauma and MVAs(1,2).  The mainstay of treatment for rib fractures is analgesic control(1). When pain cannot be adequately managed, the patient is at a heightened risk of hypoventilation due to decreased thoracic mobility and secretion clearance, predisposing the patient to significant atelectasis(1,2).

Historically the pain from rib fractures has been managed with acetaminophen or NSAIDS and if these do not sufficiently alleviate the pain, opioids are used(1,3). Unfortunately, these methods often do not provide adequate pain control or in the case of opioids, come with a myriad of side effects such as nausea, vomiting, constipation, respiratory depression and the potential for dependency and abuse (1,4).

An alternative to traditional methods include regional techniques such as paravertebral or epidural nerve blocks. These interventions have been shown to effectively control pain in rib fractures(3,4). The downside to these interventions include being technically challenging and time consuming with significant complication risks and contraindications such as coagulation disorders (1,3).

The solution? A serratus anterior block 

An ultrasound guided blockade of the lateral cutaneous branches of the thoracic intercostal nerves was first described by Blanco et al. in 2013 for patients following breast surgery to manage their postoperative pain(5). This procedure has been adopted by many emergency departments for its convenience and practicality compared to epidural or paravertebral nerve blocks(3).

Serratus anterior blocks are less invasive and considerably more practical in the ED setting, providing paresthesia to the ipsilateral hemithorax for 12-36 hours (6).

The only absolute contraindications are patient refusal, allergy to local anesthetic and local infection(1).

Complications of a serratus anterior block include pneumothorax, vascular puncture, nerve damage, failure/inadequate block, local anesthetic toxicity and infection(1).

Serratus anterior blocks are only effective for the anterior two-thirds of the chest wall (3).


Figure 1. Ultrasound image of serratus anterior muscle and surrounding tissues with superficial or deep needle guides. Image from Thiruvenkatarajan V, Cruz Eng H, Adhikary SD. An update on regional analgesia for rib fractures. Current Opinion in Anaesthesiology. 2018;31(5):601–607.

How do you do it?

The procedure is usually performed with the patient laying supine however the patient could also lay in a lateral decubitus position (1,3). Using a high frequency linear ultrasound probe (6-13MHz), identify the serratus anterior and latissimus dorsi muscles over the fifth rib in the mid-axillary line(1,3). Using an in-plane approach, insert the needle either superficial or deep to the serratus anterior and confirm correct needle placement by visualizing anaesthetic spread via ultrasound(1,3). According to May et al., superficial spreading tends to have a longer lasting analgesic effect(1). Place and secure a catheter to infuse the remainder of the bolus(1,3). Thiruvenkatarajan et al. recommend a bolus of 40ml of 0.25% levobupivacaine and a 50mm 18G Tuohy catheter needle(3).

See this excellent review by Dr. David Lewis on identifying rib fractures and their complications using ultrasound (start 3:08) as well as a review of the block and procedure (start 8:00)

Rib Fractures and Serratus Anterior Plane Block


  1.         May L, Hillermann C, Patil S. Rib fracture management. BJA Education. 2016 Jan 1;16(1):26–32.
  2.         Malekpour M, Hashmi A, Dove J, Torres D, Wild J. Analgesic choice in management of rib fractures: Paravertebral block or epidural analgesia? Anesthesia and Analgesia. 2017 Jun 1;124(6):1906–11.
  3.         Thiruvenkatarajan V, Cruz Eng H, Adhikary S das. An update on regional analgesia for rib fractures. Vol. 31, Current opinion in anaesthesiology. 2018. p. 601–7.
  4.         Tekşen Ş, Öksüz G, Öksüz H, Sayan M, Arslan M, Urfalıoğlu A, et al. Analgesic efficacy of the serratus anterior plane block in rib fractures pain: A randomized controlled trial. American Journal of Emergency Medicine. 2021 Mar 1;41:16–20.
  5.         Blanco R, Parras T, McDonnell JG, Prats-Galino A. Serratus plane block: A novel ultrasound-guided thoracic wall nerve block. Anaesthesia. 2013 Nov;68(11):1107–13.
  6.         Mayes J, Davison E, Panahi P, Patten D, Eljelani F, Womack J, et al. An anatomical evaluation of the serratus anterior plane block. Anaesthesia [Internet]. 2016 Sep 1 [cited 2021 Apr 18];71(9):1064–9. Available from: http://doi.wiley.com/10.1111/anae.13549



Continue Reading

A Biopsychosocial Approach to Epigastric Pain

A Biopsychosocial Approach to Epigastric Pain – A Medical Student Clinical Pearl

Gabrielle Hibbert, Med III

Dalhousie Medicine New Brunswick

Reviewed by Dr. Jay Hannigan

Copyedited by Dr. Mandy Peach


A 22 year old male presented to the ER with a 6-week history of epigastric pain. The patient described the pain as a burning sensation radiating to his throat and RUQ. The pain was constant, exacerbated post-prandially, and associated with nausea and vomiting. He denied any hemoptysis, hematochezia, melena, dysphagia, odynophagia, symptoms of extra-esophageal reflux, or dyspepsia. He reported having a poor appetite associated with a twenty-pound weight loss. Review of systems was otherwise negative. Pantoprazole recently prescribed by his GP had not improved his symptoms. He denied using NSAIDs. He reported experiencing a lot of anxiety recently due to relationship conflicts with his partner and inability to access counselling services. He was scheduled to have an outpatient ultrasound of his gallbladder.

Past medical history: bipolar disorder, general anxiety disorder, depression, and tonsillectomy

Medications: olanzapine odt, citalopram, lamotrigine, and pantoprazole

Social: The patient worked at American Eagle, and he lived with his partner, his partner’s parents, and their 18-month-old son. He smoked one gram of Marijuana per day, vaped daily, and occasionally consumed alcohol. He was an ex-smoker and had a history of abusing cocaine, LSD, and crystal meth but had not used in three years.

Physical exam: The patient was afebrile, and his other vitals were within normal limits. He looked well and was in no visible distress. He had some mild epigastric tenderness to palpation. Cardiac, respiratory, and abdominal exam were unremarkable.


CBC, electrolytes, LFTs, and TSH recently ordered by his GP were within normal limits. Serology testing for celiac disease was negative. CRP was <0.6.

The Biopsychosocial model

The biopsychosocial model illustrated in Figure 1 was introduced in 1977 by the American Psychiatrist George Engel1. He stated that “to provide a basis for understanding the determinants of disease… a medical model must also take into account the patient, the social context in which he lives, and the complementary system devised by society to deal with the disruptive effects of illness”1.

Figure 1. The Biopsychosocial model. Figure modified from 2.

The diathesis-stress model, proposed by Spielman and colleagues in 1987, illustrates how psychological, biological, and social factors contribute to the development and maintenance of disease3. An example of this model is shown in Figure 2.

Figure 2. Summary of potential predisposing, precipitating, and perpetuating factors across biopsychosocial domains3


Gastroesophageal Reflux Disease (GERD)

Gastroesophageal reflux occurs when there is inappropriate relaxation of the lower esophageal sphincter (LES) or delayed gastric emptying4. Multiple factors such as hiatal hernias, increased intraabdominal pressure, and certain drugs can contribute to this pathogenesis5. Altered processing of signals from the esophagus leading to hypersensitivity has also been linked to the pathogenesis of reflux6.

As illustrated in Figure 3, the bidirectional communication between the enteric nervous system and central nervous system is termed the “brain–gut axis” 7. Neurotransmitters involved include endogenous opioids, endocannabinoids, and serotonin6. These neurotransmitters are affected by stress and anxiety6. Dysregulation of the brain-gut-axis has been proposed to play a role in physical symptoms commonly reported by individuals with anxiety such as nausea, diarrhea, and abdominal pain7.

Figure 3. The brain gut axis. Figure modified from8.


Typical symptoms of gastroesophageal reflux include regurgitation and pyrosis4. Lifestyle modifications listed in Figure 4 and/or a short trial of a medication such as a proton pump inhibitor as illustrated in Figure 5 are reasonable first step in the management of patients with typical symptoms9.

Figure 4. Lifestyle modifications for GERD 11

Figure 5. Pharmacological therapy of GERD10


Atypical symptoms of gastroesophageal reflux include chest or epigastric pain, water brash, satiety, burping or hiccups, bloating as well as nausea and/or vomiting4.

Symptoms of extra-esophageal reflux include chronic cough, asthma, sore throat, hoarseness, and sinus or pulmonary problems4.

Alarm symptoms include dysphagia, odynophagia, epigastric mass, unexplained weight loss, as well as hematemesis, anemia, or other signs of upper gastrointestinal bleeding4.

Alarm symptoms, extra-esophageal reflux symptoms, or atypical symptoms raise the possibility of other diseases such as oesophagitis, peptic stricture or ulcer, or cancer and warrant further investigations11.


Back to our case


Impression: 22 year old male with a 6 week history of constant epigastric pain exacerbated post-prandially and associated with pyrosis, nausea, and vomiting. No alarm symptoms are present.  Physical exam and investigations were normal. Patient reported recent stressors exacerbating his GAD.


Biological factors:

  • Anxiety and bipolar illness since early teens
  • Substance abuse

Social factors:

  • Relationship conflicts
  • Stressful home environment
  • Responsibility of caring for his son

Psychological factors:

  • Worsening anxiety due to loss of counselling services and relationship conflits.
  • Anxiety/stress due to the Covid 19 pandemic


Abdominal pain

Abdominal pain represents 5-10% of emergency department visits13. About 25% of patients discharged from the emergency department receive a diagnosis of unspecified abdominal pain while 35- 41% of patients admitted to hospital receive this diagnosis13. Abdominal pain can be challenging to diagnose because it has a broad differential13.  Patients with recurrent abdominal pain are not exempt from a medical emergency so that must always be ruled out; however, repeating interventions or ‘giving a diagnosis’ of medically unexplained symptoms may perpetuate ongoing distress that ‘something” is being missed12. Addressing any psychological and social factors that may be contributing or exacerbating the pain could help relieve symptoms or increase the efficacy of ongoing treatment13.

Concluding management:

  • Compassionately acknowledged that the pain he is experiencing is distressing
  • Reassured him that there is no evidence of a medical emergency
  • Explained GERD and factors that are likely exacerbating his symptoms
  • Lifestyle modifications as in Figure 4
  • Other avenues for counselling services
  • Pantoprazole twice daily
  • Return to the ER if experiencing alarm symptoms
  • Follow up with GP



  1. Farre, A., & Rapley, T. (2017). The new old (and old new) medical model: Four decades navigating the biomedical and psychosocial understandings of health and iIllness. Healthcare (Basel, Switzerland)5(4), 88. https://doi.org/3390/healthcare5040088


  1. Verril-Schurmanj., & Friesen, Craig, A. (2013, November 6). Inflammation and the Biopsychosocial Model in Pediatric Dyspepsia, Dyspepsia. Advances in Understanding and Management, Eldon Shaffer and Michael Curley, IntechOpen. https://doi.org/ 10.5772/56635. Retrieved July 2, 2021, from https://www.intechopen.com/books/dyspepsia-advances-in-understanding-and-management/inflammation-and-the-biopsychosocial-model-in-pediatric-dyspepsia


  1. Wright, C. D., Tiani, A. G., Billingsley, A. L., Steinman, S. A., Larkin, K. T., & McNeil, D. W. (2019). A framework for understanding the role of psychological processes in disease development, maintenance, and treatment: The 3P-Disease Model. Frontiers in Psychology,10, 2498. https://doi.org/10.3389/fpsyg.2019.02498


  1. Vakil, N., van Zanten S., V., Kahrilas, P., Dent,J., Jones, R., Vakil,N.,… Zapata, C. (2006). The Montreal definition and classification of gastroesophageal reflux disease: A global evidence-based consensus. American Journal of Gastroenteroly, 101(8),1900-1920. https://doi.org/10.1111/j.1572-0241.2006.00630.x


  1. Mikami, D., J, & Murayama K., M. (2015). Physiology and pathogenesis of gastroesophageal reflux disease. Surgical Clinics of North America, 95(3), 515-525. https://doi.org/10.1016/j.suc.2015.02.006


  1. Tack, J., & Pandolfino, J. E. (2018). Pathophysiology of Gastroesophageal Reflux Disease. Gastroenterology, 154(2), 277-288. https://doi.org/10.1053/j.gastro.2017.09.047


  1. Martin C., R., Osadchiy, V., Kalani, A., & Mayer, E., A. (2018). The Brain-Gut-Microbiome Axis. Cell Mol Gastroenterol Hepatol, 6(2):133-148. Doi: 10.1016/j.jcmgh.2018.04.003.


  1. Bajic, J., E., Johnston, I., N., Howarth, G., S., & Hutchinson, M., R. (2018) From the bottom-up: Chemotherapy and gut-brain axis dysregulation. Front. Behav. Neurosci. 12:104. doi: 10.3389/fnbeh.2018.00104


  1. Smith, L. (2005). Updated ACG guidelines for diagnosis and treatment of GERD. American Family Physician, 71(12), 2376-2382. Retrieved July 2, 2021, from https//www.aafp.org/afp/2005/0615/p.2376.html


  1. Zeid,, Y., & Confer, J. ( 2016). Standards of care for GERD.  S. Pharmacists, 41(12), 24-29. Retrieved July 2, 2021, from https:/www.uspharmacist.com/article/standards-of-care-for-gerd


  1. Alberta Health Services. GERD primary care pathway. April 2020. Retrieved July 2, 2021, from https://www.albertahealthservices.ca/assets/about/scn/ahs-scn-dh-pathway-gerd.pdf


  1. Kendall, J., L., & Moreira, M. (2020). Evaluation of the adult with abdominal pain in the emergency department. Retrieved July 2, 2021, from https://uptodate.com/contents/evaluation-of-the-adult-with-abdominal-pain-in-the-emergency-department_


  1. Daniels, J., Griffiths, M., & Fisher, E. (2020) Assessment and management of recurrent abdominal pain in the emergency department. Emergency Medicine Journal, 37, 515-521. https://doi.org/1136/emermed-2019-209113
Continue Reading

Cannabis Hyperemesis Syndrome – a hot topic!

Cannabis Hyperemesis Syndrome – A Medical Student Clinical Pearl

Alyssa Dickinson, Med II
Dalhousie Medicine New Brunswick, Class of 2023

Reviewed by Dr. Erin Slaunwhite

Copedited by Dr. Mandy Peach

Case presentation:

A 24yo male, Mr. X, presents to the emergency department with a 12-hour history of sudden onset vomiting. The vomiting came on without warning and was associated with epigastric abdominal pain and sweating. Mr. X took one Gravol at home but was unable to keep it down. He explains that taking a hot shower will briefly relieve his symptoms, and he has already taken four showers today. He is otherwise well, and denies recent fever/chills, chest pain, shortness of breath, or changes in bowel/bladder patterns.

Mr. X has no relevant past medical history and is not currently taking any medications. He denies drinking alcohol but states that he smokes three joints of cannabis daily, and has done so for the past 3 years. He does not use any other recreational drugs.

On physical exam, Mr. X appeared pale and was actively vomiting. All vitals were within normal limits. Cardio, resp, abdo, and neuro exams were all normal.

Cannabis Hyperemesis Syndrome:

Cannabis is the most commonly used recreational drug in the world, with the highest prevalence among those ages 18-25 years old.1,2 Although sometimes used as an anti-emetic, chronic cannabis use has been associated with paradoxical hyperemesis, which has been described as cannabis hyperemesis syndrome (CHS).3 CHS is a chronic functional gastrointestinal disorder that presents with episodic hyperemesis following prolonged cannabis use.4 Most cases of CHS present within 1-5 years of regular weekly cannabis use, although the pathophysiology remains unclear.1 Unfortunately, CHS is underrecognized and underreported, and as a result many patients experience a delay in diagnosis up to 9 years.1,2,5

The clinical course of CHS can be divided into three phases:

  • prodromal,
  • hyperemetic, and
  • recovery phase.2,5

Although similar in presentation, CHS is different then cyclic vomiting syndrome (CVS), as categorized by the Rome IV classification for functional disorders.4

Features that may help distinguish CHS from CVS include the following:
– All patients with CHS will have a history of regular weekly cannabis use, while those with CVS may or may not use cannabis products.

  • CVS may be a manifestation of migraine diathesis, and therefore is associated with a high prevalence of migraines or family history of migraines. CHS is not associated with headaches and will not respond to migraine-abortive medications.6

  • CVS patients are more likely to have psychological comorbidities including depression and anxiety.2

  • Gastric emptying rates in CVS are often accelerated, while in CHS they are more likely to be delayed.2

  • Relief with hot showers is present in 91% of patients with CHS, and only 50% of patients with CVS.1,4

With increasing prevalence of cannabis use, the incidence of CHS is likely to rise.7 It is therefore important to ask all patients with otherwise unexplained cyclic vomiting about cannabis use and compulsive bathing.5

Initial Assessment:

The differential diagnosis for CHS is broad, so it is therefore important to collect a comprehensive history and perform screening tests to rule out other potential causes.


Screening tests include routine blood work with a pregnancy test, if applicable. Further investigations vary based on each individual presentation.

Red flag symptoms that warrant further investigations to rule out alternate diagnoses include hematemesis, neurologic findings on exam, and abdominal tenderness.2



In most cases of CHS, all laboratory, radiographic, and endoscopic results will be negative.1 Diagnosis therefore is based on the following clinical criteria, retrieved from Simonetto et al (2012):

Note: CHS is a diagnosis of exclusion – all other pathologies must be ruled out.



The mainstay of treatment for CHS includes supportive therapy, with or without hospitalization. If volume depletion is present, immediate IV fluid resuscitation is warranted.2 The patient’s condition is expected to resolve within 12-24 hours of fluid replacement therapy.3


The following is the Emergency Medicine Saint John algorithm for CHS:

Notes on Symptom Management:

  • The most effective treatment for CHS symptoms is a warm bath or shower.2 This has been shown to quickly settle nausea, vomiting, and abdominal pain, although these effects do not persist. Symptom relief is temperature dependent, with hotter water producing a greater effect.3
  • Ruberto et al (2020) demonstrated superiority of IV haloperidol (one time dose of 0.05mg/kg) over ondansetron in improving symptoms of nausea, vomiting, and abdominal pain. Patients who received haloperidol also had a shorter discharge time from the ED and had fewer return visits to the ED for ongoing symptoms.
  • Traditional anti-emetic therapy such as 5-HT3 receptor antagonists or H1 receptor antagonists may used in addition to haloperidol, although most patients will have little to no response.2


Prevention of Recurrence:

  • Cannabis cessation is the only proven treatment for CHS.
  • Patients should be counselled on cannabis cessation, ideally from a specialized addiction team member.9 They may also benefit from outpatient treatment options including cognitive behavioural therapy and/or motivational enhancement therapy.2


Case Conclusion:

Mr. X was started on IV fluids to restore volume. He was also given capsaicin 0.075% topical cream and haloperidol (0.05mg/kg) for symptom management. His symptoms resolved within 4 hours and he was discharged home with a plan for outpatient follow-up to support cannabis cessation.


Want a deeper dive into CHS? Visit this medical student clinical pearl


  1. Simonetto, D. A., Oxentenko, A. S., Herman, M. L., & Szostek, J. H. (2012, February). Cannabinoid hyperemesis: a case series of 98 patients. In Mayo Clinic Proceedings(Vol. 87, No. 2, pp. 114-119). Elsevier.
  2. Galli JA, Sawaya RA, Friedenberg FK. Cannabinoid hyperemesis syndrome. Curr Drug Abuse Rev. 2011;4(4):241-249. doi:10.2174/1874473711104040241
  3. Allen JH, de Moore GM, Heddle R, Twartz JC. Cannabinoid hyperemesis: cyclical hyperemesis in association with chronic cannabis abuse. Gut. 2004;53(11):1566-1570. doi:10.1136/gut.2003.036350
  4. Venkatesan T, Levinthal DJ, Li BUK, et al. Role of chronic cannabis use: Cyclic vomiting syndrome vs cannabinoid hyperemesis syndrome. Neurogastroenterology & Motility. 2019;31(S2):e13606. doi:https://doi.org/10.1111/nmo.13606
  5. Soriano-Co M, Batke M, Cappell MS. The cannabis hyperemesis syndrome characterized by persistent nausea and vomiting, abdominal pain, and compulsive bathing associated with chronic marijuana use: a report of eight cases in the United States. Dig Dis Sci. 2010;55:3113–9.
  6. Batke, M., & Cappell, M. S. (2010). The cannabis hyperemesis syndrome characterized by persistent nausea and vomiting, abdominal pain, and compulsive bathing associated with chronic marijuana use: a report of eight cases in the United States. Digestive diseases and sciences55(11), 3113-3119.
  7. Ruberto, A. J., Sivilotti, M. L., Forrester, S., Hall, A. K., Crawford, F. M., & Day, A. G. (2020). Intravenous Haloperidol Versus Ondansetron for Cannabis Hyperemesis Syndrome (HaVOC): A Randomized, Controlled Trial. Annals of Emergency Medicine.
  8. Dezieck L, Hafez Z, Conicella A, et al. Resolution of cannabis hyperemesis syndrome with topical capsaicin in the emergency department: a case series. Clinical Toxicology. 2017;55(8):908-913. doi:10.1080/15563650.2017.1324166
  9. Pélissier F, Claudet I, Gandia-Mailly P, Benyamina A, Franchitto N. Cannabis Hyperemesis Syndrome in the Emergency Department: How Can a Specialized Addiction Team Be Useful? A Pilot Study. The Journal of Emergency Medicine. 2016;51(5):544-551. doi:10.1016/j.jemermed.2016.06.009
Continue Reading

A Case of Herpes Simplex Virus Keratitis in The Emergency Department

A Case of Herpes Simplex Virus Keratitis in The Emergency Department – A Medical Student Clinical Pearl

Patrick Gallagher, MED III

MUN Class of 2022

Reviewed by Dr. Robin Clouston

Copyedited by Dr. Mandy Peach


A 53-year-old female presents to the emergency department with a two-day history of left-eye pain, which she describes as “something being stuck in her eye.” The patient endorses left eye tearing, pruritis, and photophobia. She notes that her eye has been “blurry” since she awoke this morning. The patient denies any infectious symptoms at present but states that a cold sore erupted on her upper lip seven days ago. She does not use contact lenses.

Past medical history: T2DM and hypothyroidism.

Past surgical history: None.

Medications: Metformin 500 mg OD and Synthroid 125 mcg OD.

Physical exam:

Upon inspection, the patient has conjunctival injection and tearing in the left eye. Mild periorbital edema and erythema is noted. The patient’s pupils are equal and reactive to light, and visual acuity is 20/20 in the left eye and 20/40 on the left eye. Extraocular eye movements and visual fields are normal. The patient has decreased corneal sensation.

On slit lamp examination using fluorescein-based dye, a small branching dendritic ulcer was seen (Figure 1).

Figure 1: Dendritic ulcer noted on slit-lamp exam with fluorescein-based dye.


What is the differential diagnosis of dendrites?

• Herpes simplex keratitis
• Acanthamoeba keratitis
• Other keratitis caused by Varicella zoster virus (VZV), cytomegalovirus (CMV), Epstein–Barr virus (EBV), or adenovirus.
• Dendritiform keratopathy
• Ramous epithelial changes
• Limbal stem cell deficiency
• Drug induced corneal changes (epinephrine, antivirals, beta-blockers) 1,2

Herpes simplex virus keratitis :

Herpes simplex is a DNA virus that can cause a wide variety of infections, most commonly involving the mouth, genitalia, and eyes3. While HSV-1 and HSV-2 can involve the eye, HSV-1 is the most common cause of keratitis1. Herpes simplex keratitis (HSK) is characterized by recurrent infections of the corneal epithelium and stroma2. HSK can be classified as primary or recurrent and further divided into three subtypes: epithelial, stromal, and endothelial3. Epithelial keratitis is the most commons subtype of ocular herpes (50% to 80%)2.

Herpes simplex virus (HSV) infections are the leading cause of infectious corneal blindness in developed countries3. It is estimated that 1.5 million people worldwide experience HSV keratitis every year2.


Primary HSV eye infections occur when the virus enters mucous membranes by direct contact. This initial infection is usually subclinical, but it can cause unilateral blepharitis, follicular conjunctivitis, and occasional epithelial keratitis (Figure 2)4. The initial infection is typically asymptomatic, and it occurs in children less than five years old5.

Figure 2: Pictorial representation of blepharitis (inflammation of the eyelid), keratitis (inflammation of cornea), conjunctivitis (inflammation of conjunctiva), and ocular anatomy. Diagram retrieved from 7

After the initial infection, the virus can remain latent in the ophthalmic division of the trigeminal ganglion for the lifetime of the host. HSV reactivation in the latently infected ganglia can lead to corneal scarring, thinning, stromal opacity, and neovascularization5. The cumulative effect of numerous infections results in vision loss and eventually blindness if left untreated.

History and physical:

Diagnosis of HSK is primarily diagnosed by clinical presentation on slit lamp exam using fluorescein and either rose bengal or lissamine green3. However, it is crucial to complete a thorough history and physical exam to narrow the differential diagnosis (Table 1).

Table 1: Key points on history and physical

Figure 3: Slit-lamp corneal findings for patient’s diagnosed with HSV epithelial keratitis. A: Classic dendritic lesion with terminal bulbs. B: More advanced dendritic lesion presenting as geographic ulcer. Figure modified from 6.


The diagnosis of HSVK is based off of clinical findings and does not require additional investigations; however, for atypical lesions, polymerase chain reaction has been used to confirm HSVK. Enzyme-linked immunosorbent assay and viral cultures are also effective in the diagnosis of the HSVK subgroups3.

Treatment/management of HSVK in the emergency department:

In the emergency department, typical findings on the slit lamp exam is diagnostic for epithelial HSVK.

Care providers should initiate treatment immediately to reduce the risk of complications; however, the patient must be referred to ophthalmology within the next few days for follow-up.

Topical and oral antiviral treatments effectively treat epithelial HSVK, although no topical ophthalmic antivirals are currently available in Canada7. It is crucial to adjust the dose of oral antivirals according to the patient’s renal function. See Table 2 for available oral antiviral treatments. For symptomatic management, artificial tears or eye lubricants can ease eye discomfort and over-the-counter analgesics can help relieve pain7.

Table 2: Oral antiviral treatment for epithelial HSVK in adults. Modified from 7

Back to the case:

Given our patient’s classic symptoms of epithelial HSVK (conjunctival injection, tearing, vision changes, foreign body sensation, photophobia, hx of HSV infection) and finding of dendritic ulcers on slit lamp examination, we treated this case as epithelial HSVK until proven otherwise. Therefore, we prescribed the patient valacyclovir 1000mg PO TID and arranged an urgent ophthalmology consult for the following day.


  1. Roozbahani, M., & Hammersmith, K. M. (2018). Management of herpes simplex virus epithelial keratitis. Current opinion in ophthalmology, 29(4): 360-364.

  2. Wilhelmus, K. R. (2015). Antiviral treatment and other therapeutic interventions for herpes simplex virus epithelial keratitis. Cochrane Database of Systematic Reviews, 1.

  3. Azher, T. N., Yin, X. T., Tajfirouz, D., Huang, A. J., & Stuart, P. M. (2017). Herpes simplex keratitis: challenges in diagnosis and clinical management. Clinical Ophthalmology, 11:185–191.

  4. Sibley, D., & Larkin, D. F. (2020). Update on Herpes simplex keratitis management. Eye, 34: 2219–2226.

  5. Toma, H. S., Murina, A.T., Areaux, R.G., Neumann, D.M., & Bhattacharjee, P.S. (2008). Ocular HSV-1 Latency, Reactivation and Recurrent Disease. Seminars in Ophthalmology, 23(4), 249–273.
  6. Leon, S., & Pizzimenti, J. (2017). Be a Hero to Your HSVK Patients. Review of Optometry-Leadership in clinical care. Retrieved from https://www.reviewofoptometry.com/article/ro0717-be-a-hero-to-your-hsvk-patients2
  7. Institut national d’excellence en santé et en services sociaux. (2018). Herpes Simplex Eye Disease. INESSS Guides. Retrieved from https://www.inesss.qc.ca/fileadmin/doc/INESSS/Outils/GUO/Herpes/Guide_HerpesSimplex_web_EN_VF.pdf


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


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”
  • Pantoprazole
  • None known
Past Medical History:
  • Irritable bowel syndrome diagnosed after many presentations to numerous providers and several referrals
  • 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.

  • 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.
  • 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


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


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



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


  • 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.



  • 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 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


Download (PDF, 702KB)



  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

Lateral Canthotomy

Lateral  Canthotomy – A Medical Student Clinical Pearl

Scott Clarke

Med III, Class of 2022

Dalhousie Medical School New Brunswick (DMNB)

Reviewed by Dr. Fraser MacKay

Copyedited by Dr. Mandy Peach



You are a clinical clerk working your first shift in a busy emergency department when you hear overhead those heart stopping, adrenaline pumping words: “Trauma team activation, room 24”. You arrive to find an unconscious 45 year old male. Report from the paramedics tells you there was a workplace accident whereby a tree had fallen and struck the patient in the face. The team works swiftly and efficiently to secure an airway and stabilize his vitals. From the team leader, your role is to perform a brief neurological exam.

Despite heavy sedation and swelling in the face, you are able to identify significant proptosis of his left eye. His right pupil is reactive to light but you notice his left responds significantly less and there is a positive relative afferent pupillary defect (RAPD). You relay your findings to the team lead and suggest an urgent CT scan of the head.


Before departing for CT your attending asks you – what diagnosis are you concerned for? What clinical findings support this diagnosis?

Orbital Compartment Syndrome1

Vision threatening condition where intraocular pressure (IOP) exceeds 40 mmHg.

Clues on exam:

  • Impaired extraocular movements (from a retrobulbar hematoma)
  • Decreased visual acuity
  • RAPD
  • Blown Pupil

Your attending agrees there is concern for orbital compartment syndrome and ophthalmology should be urgently paged – do you wait for CT to confirm retrobulbar hematoma?

No – You quickly grab a tono-pen and measure the intraocular pressure to be 50mmHg. In order to save this patient’s vision, a lateral canthotomy is immediately performed in an attempt to temporarily release pressure before definitive hematoma evacuation can occur.

Procedural Overview:


  1. Tono-pen
  2. Hemostat
  3. Local anesthesia
  4. Curved iris scissors (or scalpel)

Anatomy review:

The globe of the eye is held firmly in place by the strong tarsal plates and the medial and lateral canthal ligaments (Figure 2). By dividing the lateral canthus (inferior limb or both inferior and superior limbs), the globe has room to expand which can greatly reduce pressure3.

Figure 2: Anatomy of the components holding the globe of the eye4.


  1. Clean the lateral portion of the eye using chlorhexidine or a similar solution.
  2. Inject 2-3cc of 1% lidocaine with 1:100,000 epinephrine into the site of the lateral canthus primarily for hemostasis
  3. Insert the hemostat into the lateral portion of the eye and crush the lateral canthus. Hold this for 30-45 seconds. This will devascularize the tissue resulting in further reduction in bleeding.
  4. Using the curved iris scissors (or scalpel), cut the lateral canthus to the rim of the globe, ~1-2cm at a slight downward angle.
  5. The inferior limb of the lateral canthal ligament will be able to be palpated and resembles a guitar string. This should be divided as well.
  6. If significant intraocular pressure remains, divide the superior limb of the lateral canthal ligament as well.
  7. Reassess ocular pressure.


Once the procedure is completed you wait 5 minutes and reassess the intraocular pressure. You notice that it has gone from 50mmHg to 38mmHg. The patient is sent for CT head which confirms a retrobulbar hematoma.

You follow up with the patient during his hospital stay and discover his vision eventually returns to his normal pre-injury.


Keys to remember6:

Indications include trauma patients with:
– Proptosis
– Impaired ocular movements
– Elevated Intraocular pressure, usually >40mmHg
– Decreased visual acuity

Ideally performed within 60-120 min of features of ischemia to the optic nerve1.

Absolute contraindication:
– Globe rupture

Medical treatment can also be initiated with the goal to help decrease intraocular pressure 1:

  • mannitol
  • acetazolamide
  • pilocarpine
  • timolol

See below for video of a lateral canthotomy on an actual patient (viewer discretion advised):


  1. Helman, A. Swaminathan, A. Austin, E. Strayer, R. Long, B, McLaren, J. Brindley, P. EM Quick Hits 24 – Lateral Canthotomy, Cannabis Poisoning, Hyperthermia, Malignant Otitis Externa, BBB in Occlusion MI, Prone CPR. Emergency Medicine Cases. December, 2020. https://emergencymedicinecases.com/em-quick-hits-december-2020/. Accessed [May 5, 2021].
  2. Retrobulbar Hematoma from Warfarin Toxicity and the Limitations of Bedside Ocular Sonography – The Western Journal of Emergency Medicine. https://westjem.com/videos/retrobulbar-hematoma-from-warfarin-toxicity-and-the-limitations-of-bedside-ocular-sonography.html. Accessed March 29, 2021.
  3. Amer E, El-Rahman Abbas A. Ocular Compartment Syndrome and Lateral Canthotomy Procedure. J Emerg Med. 2019;56(3):294-297. doi:10.1016/j.jemermed.2018.12.019
  4. Chan D, Sokoya M, Ducic Y. Repair of the Malpositioned Lower Lid. 2017. doi:10.1055/s-0037-1608711
  5. How to do Lateral Canthotomy – Eye Disorders – Merck Manuals Professional Edition. https://www.merckmanuals.com/en-ca/professional/eye-disorders/how-to-do-eye-procedures/how-to-do-lateral-canthotomy. Accessed March 29, 2021.
  6. Lateral Canthotomy – YouTube. https://www.youtube.com/watch?v=Qs5Smx-cxbo. Accessed March 29, 2021.
Continue Reading