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

ANATOMY REVIEW:

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).

 

IMPORTANT FEATURES ON HISTORY AND PHSYICAL EXAM:

History:

  • 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

 

Exam:

  • 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

https://www.reviewofoptometry.com/article/the-neurologic-exam-stepbystep

Figure 8: Cranial nerve function and testing

DIFFERENTIAL DIAGNOSIS:

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.

 

https://www.statpearls.com/ArticleLibrary/viewarticle/49275

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, TREATMENT:

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

 

Investigations:

  • 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:

  • 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)

 

Treatment:

  • 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).

References:
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

 

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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

Case

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.

Investigations:

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
MRCP
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.

References:

 

  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

 

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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

References

  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

 

 

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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

Case

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.

Investigations

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

 

References

  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
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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.

Investigations:

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

 

Diagnosis:

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.

 

Management:

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

References:

  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
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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

Case

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.

Pathophysiology:

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.

Investigations:

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.

References:

  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

 

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Recognizing and Treating Cannabinoid Hyperemesis Syndrome

Cannabinoid Hyperemesis Syndrome – Med Student Pearl

Eric Plant, Med II, Class 2024

Dalhousie Medicine New Brunswick, Saint John

Reviewed and copyedited by Dr. David Lewis @e_med_doc


Quick Summary: The Pearls You Came Here For

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

Useful Links


Case

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

Initial Presentation Summary:

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

 


 

Introduction to CVS vs CHS

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

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


 

Overview of CVS

Definition and Diagnosis

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

 

Rome IV Criteria for CVS

Pediatric Criteria (all conditions must be met)

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

 

Adult Criteria (all conditions must be met)

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

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

Natural History:

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

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

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

Adapted from UpToDate2, 6, 20

Epidemiology

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

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

Overview of CHS

Definition and Diagnosis

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

 

Rome IV Criteria for CHS

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

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

·     Presentation after prolonged, excessive cannabis use

·     Relief of vomiting by a sustained cessation of cannabis use

 

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

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

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

Natural History

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

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

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

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

Epidemiology

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

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

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

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


 

Physiology of Nausea and Vomiting

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


 

Pathophysiology of CVS and CHS

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

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


 

Assessment

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

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

 

Emergent Complications of CHS15

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

History

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

 

Physical Exam

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

 

Investigations

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

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

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

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

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


 

Treatment

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

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

Treatment in the ED

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

 

Summary of Recommendations for Treatment in the ED

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

 

Definitive Treatment and Counselling

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

 

Case Conclusion

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

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

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

Download (PDF, 702KB)


 

References

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

 

Case:

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:

Equipment:

  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.

Procedure5:

  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
– RAPD

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):

References

  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.
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Carbon Monoxide Poisoning

Carbon Monoxide Poisoning – A Medical Student Clinical Pearl

Mitchell McDonough

DMNB, Class of 2022

Reviewed by Dr. Rachel Goss

Copyedited by Dr. Mandy Peach

Case

A 75 y/o male presented to the Emergency Department one afternoon via EMS with mild confusion and a headache. He recalled a sudden feeling of light-headedness while making breakfast in the morning, lowered himself to the floor, and then has very limited memory of events after this. He did not recall losing consciousness. Given his confusion, he was unable to provide an accurate recount of the events that had initially brought him to the ED and collateral history was required. EMS indicated that he was found by his upstairs neighbour after hearing him yelling. The patient noted that the power went out at his house early during the night, so he turned on his propane stovetop to provide some heat. He admitted to alcohol consumption the night prior but indicated he drinks frequently and that was unlikely to be the culprit of his current state. He had no other complaints at this time and a review of systems was unremarkable apart from a mild headache.

On general assessment the patient appeared well, vital signs were within normal limits. On physical exam he had normal strength in all four extremities. Neurologic, respiratory, cardiac and abdominal exams were unremarkable. The patient was slightly confused but it was difficult to ascertain if this was new or his normal baseline.

Differential for Confusion

Metabolic disorders
• Electrolyte abnormalities
• Endocrine disease
• Hypoglycemia
• Hypoxia

Stroke/CNS structural lesion/Head Injury

Infectious
• Systemic infection
• CNS infection (meningitis, encephalitis)

Intoxication/withdrawal
• Alcohol
• Drugs
• Carbon Monoxide

Investigations

Initial investigations included an ECG, which was normal with no evidence of an ischemic event, a toxicology panel which showed minimal blood alcohol remaining, and a blood gas sample with carboxyhemoglobin. While carbon monoxide poisoning was initially low on our differential, the carboxyhemoglobin level came back severely elevated, at 31%. Interestingly, PO2 from the ABG was within normal limits as the concentration of CO required to cause poisoning is sufficiently low that it does not significantly alter the quantity of oxygen dissolved in the plasma.

Pertinent Arterial Blood Gas Values for our patient:

pH 7.37 [7.35-7.45]
pCO2 36.2mmHg [35-45]
pO2 81.4 mmHg [75-105]
K+ 4.2mmol/L [3.7-4.7]
Na+ 139 mmol/L [136-146]
Ca2+ 1.27 mmol/L [1.15-1.30]
FCOHb 31.4% [0.3-1.8]
ctHb 132g/L [120-150]

 

Carbon Monoxide Poisoning Overview

Carbon monoxide is a gas formed by combustion of hydrocarbons. It is colourless, tasteless and odorless. Carbon monoxide binds to hemoglobin with approximately 200 times greater affinity than oxygen, forming carboxyhemoglobin which results in impaired utilization of oxygen by cells. The mechanism of impaired oxygen usage relates to CO binding cytochrome oxidase in peripheral tissues which prevents cells from using the reduced O2 received.

Potential sources of carbon monoxide include fires, heating systems, stoves, charcoal grills, generators and motor vehicles (1-3).

Figure 1: Oxygen dissociation curve demonstrating the left shift of carbon monoxide (13).

Clinical Presentation

The clinical presentations of carbon monoxide poisoning vary depending on the severity of intoxication and most findings are usually nonspecific (4,5). Patients may describe a general malaise, nausea, dizziness and headaches (6). Depending on the level of intoxication, patients may present with symptoms ranging from confusion to coma, seizures and myocardial ischemia.

Table 2: Symptoms at varying levels of carbon monoxide dissolved in blood. It should be noted that symptoms can vary substantially from individual to individual and that levels of CO do not correlate well with symptoms. For example, a typical cigarette smoker will have up to a 10% level of CO in their blood at baseline. (14).

 

Severe is classified as >30% and the following clinical signs:

  • New neurologic findings
  • Ischaemic ecg
  • Clinically significant metabolic acidosis
  • Requirement for ventilation.

Diagnosis

Diagnosis of carbon monoxide poisoning is based on history, physical exam and elevated carboxyhemoglobin on cooximetry of an arterial or venous blood gas. Due to their similar light absorbancy, standard pulse oximetry is not able to differentiate between carboxyhemoglobin and oxyhemoglobin, and therefore cannot screen for exposure to carbon monoxide (7,8). Because of the similar light absorbancy, SpO2 can also be falsely elevated. It is important to note that even with a normal SpO2 level that the patient is hypoxic.

A non-smoker may have up to 3% carboxyhemoglobin at baseline while a smoker may have 10-15%. Anything above these levels represents carbon monoxide poisoning.

Treatment

Treatment of patients with suspected carbon monoxide poisoning include:

  • removal of the potential source
  • administration of high-flow oxygen by face mask.
  • IV mannitol for any potential cerebral edema.

Indications for treatment with hyperbaric oxygen vary from institution to institution and depend on factors such as symptoms, patient factors, length of exposure to carbon monoxide, as well as COHB levels.

In general, patients that should be considered for hyperbaric oxygen therapy include (4,9-12):

  • carbon monoxide level >25% (>15% in pregnant women)
  • neurosequelae
  • loss of consciousness
  • metabolic acidosis (pH < 7.1)
  • evidence of end-organ ischemia

Case Conclusion

Given their severely elevated carboxyhemoglobin level and prolonged exposure, the patient was given 100% oxygen via a non-rebreather face mask until being transported to a hyperbaric oxygen chamber for further treatment.

This case highlights the importance of carbon monoxide poisoning as a potential diagnosis when a patient presents with a reduced level of consciousness or confusion, especially during the winter months when the risk of exposure is higher.

References

  1. Thomassen Ø, Brattebø G, Rostrup M. Carbon monoxide poisoning while using a small cooking stove in a tent. Am J Emerg Med 2004; 22:204.
  2. Centers for Disease Control and Prevention (CDC). Carbon monoxide poisoning from hurricane-associated use of portable generators–Florida, 2004. MMWR Morb Mortal Wkly Rep 2005; 54:697.
  3. Hampson NB, Dunn SL. Carbon Monoxide Poisoning from Portable Electrical Generators. J Emerg Med 2015; 49:125.
  4. Harper A, Croft-Baker J. Carbon monoxide poisoning: undetected by both patients and their doctors. Age Ageing 2004; 33:105
  5. Kao LW, Nañagas KA. Carbon monoxide poisoning. Emerg Med Clin North Am 2004; 22:985.
  6. Tomaszewski C. Carbon monoxide poisoning. Early awareness and intervention can save lives. Postgrad Med 1999; 105:39.
  7. Bozeman WP, Myers RA, Barish RA. Confirmation of the pulse oximetry gap in carbon monoxide poisoning. Ann Emerg Med 1997; 30:608.
  8. Tremper KK, Barker SJ. Pulse oximetry. Anesthesiology 1989; 70:98.
  9. Ernst A, Zibrak JD. Carbon monoxide poisoning. N Engl J Med 1998; 339:1603.
  10. Weaver LK. Carbon monoxide poisoning. Crit Care Clin 1999; 15:297.
  11. Hampson NB, Dunford RG, Kramer CC, Norkool DM. Selection criteria utilized for hyperbaric oxygen treatment of carbon monoxide poisoning. J Emerg Med 1995; 13:227.
  12. Huang CC, Ho CH, Chen YC, et al. Hyperbaric Oxygen Therapy Is Associated With Lower Short- and Long-Term Mortality in Patients With Carbon Monoxide Poisoning. Chest 2017; 152:943.
  13. https://www.pulmonologyadvisor.com/home/decision-support-in-medicine/pulmonary-medicine/thermal-injury-and-smoke-inhalation/
  14. https://www.cfinotebook.net/notebook/aeromedical-and-human-factors/carbon-monoxide-poisoning

 

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A Case of Posterior Vitreous Detachment

A Case of Posterior Vitreous Detachment – Medical Student Clinical Pearl

Ben McMullin, Clinical Clerk III

Dalhousie Medicine New Brunswick, Saint John

Reviewed by Dr. David Lewis

Copyedited by Dr. Mandy Peach

Case Presentation

A 61 year old female presented to the emergency department complaining of a floater in her right eye, which appeared 3 days prior to presentation. The floater moved with her eye movements. The patient claimed that her vision in the right eye was slightly blurry over the past 3 days but denied any significant decline in visual acuity. She denied any trauma, eye pain, discharge, or redness, but was particularly concerned since she was blind in her left eye since childhood.

On examination, the patients right eye appeared normal, with no discharge or conjunctival injection. Her pupil was roughly 3 mm and reactive to light. Her visual acuity was 20/30 in the right eye, and extraocular eye movements as well as visual field testing were normal. The intraocular pressure in her right eye was 9 mmHg.

Anatomy of the Eye

Figure 1: Normal eye anatomy as seen with ultrasound imaging.1

 

The cornea is the most superficial convex membrane, and immediately posterior to this is the anterior chamber, which is seen as anechoic on sonography. Posterior to the anterior chamber is the iris. Immediately posterior to the lens is the posterior chamber, which is also anechoic on sonography. The outer membrane of the eye from the inner most layer to the outer consists of the retina, choroid, and sclera.2

 

Differential Diagnosis for Non-Traumatic Visual Disturbance
• Posterior vitreous detachment
• Retinal tear
• Vitreous hemorrhage
• Vitreous inflammation
• Ocular lymphoma
• Intraocular foreign body
• Uveitis3

POCUS Ocular Exam

Advantages of POCUS

Ultrasound is a useful tool in the evaluation of some ocular complaints in the ED. Dilated fundoscopic examination is not always easily performed in the ED, but bedside ultrasound is becoming more readily available to physicians.4,5 Ultrasound can be useful in diagnosis of a wide range of ocular complaints, such as retinal detachment, posterior vitreous detachment (PVD), vitreous hemorrhage, and intraocular foreign body.4

Technique

Depending on the clinical history, a bedside ultrasound examination of the eye may be performed with the patient either supine or sitting in a chair.4 A high frequency probe should be used for this exam.1

Liberal amounts of gel should be used when performing a POCUS ocular exam, so as to minimize the amount of pressure placed on the eye.4 The gel does not need to be sterile, however for patient comfort, some physicians place tegaderm over the eye being examined. In order to orient the probe properly, ensure that the indicator on the probe is pointing towards the patients head when performing a longitudinal scan, and to the patients right when performing a transverse scan.1

To ensure that the entire eye is assessed, the eye should be examined in both the longitudinal and transverse planes, and it is important to sweep through in both directions. If the patient is able, it is also helpful to ask them to look to the right and left, as well as up and down with the probe on the eye.1 It is imperative to maximize brightness – if the field is too dark pathology like vitreous detachment can be easily missed.

PVD vs Retinal Detachment on POCUS

Complete retinal detachment will often appear as a V shape on ultrasound, with the apex seen at the optic nerve.5 Partial detachments can be more subtle and can appear differently from case to case.6

PVD is less echogenic than retinal detachment. PVD can often be seen moving with eye movements, more so than with retinal detachment.5 There is often a lag seen between movement of the globe, and movement of the vitreous appendage. In PVD, the detached vitreous is not connected to the optic disc, which contrasts with retinal detatchment.6 PVD can vary widely in size and can be seen with or without vitreous hemorrhage.2

Figure 2: Retinal detachment visualized on point of care ultrasound.6

Figure 3: Retinal detachment on ultrasound. (PoCUS Atlas)

 

Figure 4: Posterior vitreous detachment visualized on point of care ultrasound.2

Figure 5: Vitreous detachment on ultrasound (PoCUS Atlas).

 

Management

In the ED, retinal detachment requires urgent referral to ophthalmology. Retinal detachment can progress to total vision loss and should be seen and treated within 24 hours.3 In contrast, isolated PVD has a much better prognosis. Typically, floaters resolve within 3 to 12 months, but patients should still be referred for follow-up within 3 months to ensure no retinal tear is detected.3

Case Conclusion

Bedside ocular ultrasound showed PVD in the patient’s right eye, with no evidence of vitreous hemorrhage or retinal detachment. The patient was reassured of the prognosis but given that she was completely dependent on her right eye for vision, ophthalmology agreed to assess her the following week.

References

  1. Roque PJ, Hatch N, Barr L, Wu TS. Bedside Ocular Ultrasound. Crit Care Clin 2014; 30(2): 227-241.
  2. Southern, Simon. Ultrasound of the Eye. Australas J Ultrasound Med 2009; 12(1): 32-37.
  3. Arroyo, Jorge G. “Retinal detachment” last modified March 19, 2020, https://www.uptodate.com/contents/retinal-detachment?search=vitreous%20detachment&sectionRank=1&usage_type=default&anchor=H3491968696&source=machineLearning&selectedTitle=1~11&display_rank=1#H1505785278.
  4. Lahham S, Qumber A, Bea MP, Lee C, Fox JC. Role of point of care ultrasound in the diagnosis of retinal detachment in the emergency department. Open Access Emergency Medicine 2019; 11: 265-270. Retrieved from https://search-proquest-com.ezproxy.library.dal.ca/docview/2314891088?accountid=%24%24CLIENTID&pq-origsite=primo.
  5. Botwin A, Engel A, Wasyliw C. The use of ocular ultrasound to diagnose retinal detachment: a case demonstrating sonographic findings. Emerg Radiol 2018; 25: 445-447.
  6. Gandhi K, Shyy W, Knight S, Teismann N. Point of care ultrasound for the evaluation of non traumatic visual disturbances in the emergency department: the VIGMO protocol. Am J Emerg Med 2019; 37 (8): 1547-1553.
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An interesting derm case in the ED: Mycosis Fungoides

Mycosis Fungoides: A Medical Student Clinical Pearl

 

Nicholas Relja, B.Sc.(Hon), M.Sc.
Dalhousie Medicine New Brunswick
M.D. Candidate, Class of 2022

All case histories are illustrative and not based on any individual

Reviewed by Dr. Devon Webster

Copyedited by Dr. Mandy Peach

Case

A 55-year-old male presented to the ED after concerned family brought him in due to ongoing generalized weakness lasting approximately one month. On inspection he had erythematous, scaly, ulcerative lesions covering his entire body with only facial sparing. He mentioned burning-like pain originating from his ulcerative lesions. He had been previously diagnosed with T-cell lymphoma 30 years ago and had gone through multiple rounds of chemo and radiation therapy since that time.

Picture from: Denis D, Beneton N, Laribi K, Maillard H (2019). Management of mycosis fungoides-type cutaneous T-cell lymphoma (MF-CTCL): focus on chlormethine gel. Cancer Management and Research. Vol 11: 2241-2251

Differential for itchy, erythematous rash:

Condition
Atopic dermatitis
Contact dermatitis
Drug eruptions
Erythrodermic psoriasis
Psoriasis
Sezary syndrome
Various lymphomas

 

When reviewing the patient’s past medical history you see they were previously diagnosed with Mycosis Fungoides – a rare cutaneous form of T-cell lymphoma.

Epidemiology

Mycosis fungoides has an incidence of approximately 6 cases per million per year in the United States. It is more common in adults over 50 years of age, with a male to female ratio of 2:1. The disease is also more common amongst the Black population than in Caucasians or Asians.8,9

Etiology

The exact cause of mycosis fungoides is not known; however, there a variety of mechanisms that have been postulated:2

• Genetic and epigenetic abnormalities.3,4
• Environmental and occupational exposure to noxious substances and chemicals.5
• Human T-lymphotropic virus Type 1 – a suspected infection-type etiology.6
• Cytokines such as IL-2 and IL-4 due to their increased presence in patients with mycosis fungoides and Sezary syndrome.7

 

There are three stages of mycosis fungoides and therefore clinical presentation will vary depending on the stage of disease:

Patch stage: Erythematous, or brownish scaly patch, which may show some atrophy. It is possible to have one or multiple lesions develop in areas such as the gluteal region or on the proximal thighs. The likeness of this stage has been compared to “small-plaque” or “large plaque” parapsoriasis; however, the plaques are actually not plaques but patches instead.10

Plaque stage: This is the second stage – lesions will be larger, more numerous and will show infiltration. The lesions appear annular, are raised and have well-defined edges as well as asymmetry in terms of their distribution. Face and scalp involvement can also be seen starting at this stage.11

Tumor stage: The final stage – erythematous-purplish papules or nodules of larger diameter.12

There are other clinical variants of mycosis fungoides, but they are not as common, and some are quite rare.

Sezary syndrome:
In advanced form of the mycosis fungoides, Sezary syndrome may be present. This syndrome involves erythroderma with pruritus, lymphadenopathy and atypical circulating lymphocytes (referred to as Sezary or Lutzner cells).13

Evaluation in the ED

A detailed history and physical exam including checking for lymphadenopathy (most commonly cervical nodes) and organomegaly14,15 in addition to documenting the rash characteristics.

Labs: CBC, liver function tests, LDH

Radiological tests: depends on extent of lymphadenopathy and organomegaly. Can do a CXR in the ED for lung involvement, but otherwise advanced imaging can be decided upon by specialist consultant and may include CT, US, PET or MRI.

Biopsy: lymph nodes and rash – by consultants

Treatment and Management – refer to your friendly neighborhood dermatologist.

Early stage:

Treatment options include topical therapies such as corticosteroids and other agents, UV therapy, local radiation and systemic immunosuppressants 15,16,17.

Advanced Stage:

Treatment for the advanced stages of mycosis fungoides are directed at disease control and symptom relief. Localized radiation, targeted immunotherapy or chemotherapy. 15, 18

Prognosis

The prognosis of mycosis fungoides is variable but in general as the stage gets more advanced and with patients over the age of 60, the prognosis becomes poorer. Other poor prognostic factors include increased LDH, tumor distribution and organ involvement.2

Case Conclusion

The patient seen in hospital by the dermatologist on call and was deemed to be in the plaque stage. He was admitted due to the advancing course and and inability to manage his symptoms from home. Further care will involve palliation and a focus on quality of life.

 

References:

  1. Olisova, O. Y. et al. [Current possibilities of the differential diagnosis of plaque parapsoriasis and the early stages of mycosis fungoides]. Arkh. Patol. 81, 9–17 (2019).
  2. Lim, H. L. J. et al. Epidemiology and prognostic factors for mycosis fungoides and Sézary syndrome in a multi-ethnic Asian cohort: a 12-year review. J. Eur. Acad. Dermatol. Venereol. JEADV 33, 1513–1521 (2019).
  3. Bergallo, M. et al. DNA from Human Polyomaviruses, MWPyV, HPyV6, HPyV7, HPyV9 and HPyV12 in Cutaneous T-cell Lymphomas. Anticancer Res. 38, 4111–4114 (2018).
  4. Väisänen, E. et al. Cutavirus DNA in Malignant and Nonmalignant Skin of Cutaneous T-Cell Lymphoma and Organ Transplant Patients but Not of Healthy Adults. Clin. Infect. Dis. Off. Publ. Infect. Dis. Soc. Am. 68, 1904–1910 (2019).
  5. Slodownik, D., Moshe, S., Sprecher, E. & Goldberg, I. Occupational mycosis fungoides – a case series. Int. J. Dermatol. 56, 733–737 (2017).
  6. Blaizot, R., Ouattara, E., Fauconneau, A., Beylot-Barry, M. & Pham-Ledard, A. Infectious events and associated risk factors in mycosis fungoides/Sézary syndrome: a retrospective cohort study. Br. J. Dermatol. 179, 1322–1328 (2018).
  7. Fujii, K. New Therapies and Immunological Findings in Cutaneous T-Cell Lymphoma. Front. Oncol. 8, 198 (2018).
  8. Amorim, G. M., Niemeyer-Corbellini, J. P., Quintella, D. C., Cuzzi, T. & Ramos-E-Silva, M. Clinical and epidemiological profile of patients with early stage mycosis fungoides. An. Bras. Dermatol. 93, 546–552 (2018).
  9. Amorim, G. M., Niemeyer-Corbellini, J. P., Quintella, D. C., Cuzzi, T. & Ramos-E-Silva, M. Hypopigmented mycosis fungoides: a 20-case retrospective series. Int. J. Dermatol. 57, 306–312 (2018).
  10. Pimpinelli, N. et al. Defining early mycosis fungoides. J. Am. Acad. Dermatol. 53, 1053–1063 (2005).
  11. Burg, G., Dummer, R., Nestle, F. O., Doebbeling, U. & Haeffner, A. Cutaneous lymphomas consist of a spectrum of nosologically different entities including mycosis fungoides and small plaque parapsoriasis. Arch. Dermatol. 132, 567–572 (1996).
  12. Keehn, C. A., Belongie, I. P., Shistik, G., Fenske, N. A. & Glass, L. F. The diagnosis, staging, and treatment options for mycosis fungoides. Cancer Control J. Moffitt Cancer Cent. 14, 102–111 (2007).
  13. Lopez, A. T., Bates, S. & Geskin, L. Current Status of HDAC Inhibitors in Cutaneous T-cell Lymphoma. Am. J. Clin. Dermatol. 19, 805–819 (2018).
  14. Prince, H. M. & Querfeld, C. Integrating novel systemic therapies for the treatment of mycosis fungoides and Sézary syndrome. Best Pract. Res. Clin. Haematol. 31, 322–335 (2018).
  15. Wain, T., Venning, V. L., Consuegra, G., Fernandez-Peñas, P. & Wells, J. Management of cutaneous T-cell lymphomas: Established and emergent therapies. Australas. J. Dermatol. 60, 200–208 (2019).
  16. Dairi, M., Dadban, A., Arnault, J.-P., Lok, C. & Chaby, G. Localized mycosis fungoides treated with laser-assisted photodynamic therapy: a case series. Clin. Exp. Dermatol. 44, 930–932 (2019).
  17. Photiou, L., van der Weyden, C., McCormack, C. & Miles Prince, H. Systemic Treatment Options for Advanced-Stage Mycosis Fungoides and Sézary Syndrome. Curr. Oncol. Rep. 20, 32 (2018).
  18. Alpdogan, O., Kartan, S., Johnson, W., Sokol, K. & Porcu, P. Systemic therapy of cutaneous T-cell lymphoma (CTCL). Chin. Clin. Oncol. 8, 10 (2019).

 

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Well, that’s a pain – in the lower back: A case of back pain in the ED

Lower Back Pain: Medical Student Clinical Pearl

Grace Dao, CC4

MD Candidate

Class of 2021

Case Presentation

Mr. Payne Bach is a 54 yo male who presents to the emergency department via EMS with lower back pain.
He reports that he hurt his back this afternoon when he was picking up a heavy, antique chair. Immediately, he felt something “give out” in his back and reports a sharp 10/10 central lower back pain that radiates unilaterally to the left side. It did not radiate down his legs. He was unable to ambulate due to the pain and called EMS.

He received 975 mg Acetaminophen in the ambulance which did not alleviate his pain. Mr. Bach reports that before picking up the chair he was feeling well. He denies any history of back pain or activities of back overuse. He denies any history of trauma or injury to his back recently or in the past. In the emergency department he reports his pain remains at 10/10 and cannot sit up or move in bed due to the pain.

He denies any change in sensation or pain to his legs. He denies any change in sensation to his perineum or any bowel incontinence. He has not urinated since the incident. Incidentally when reviewing a past medical history he reports an unintentional weight loss of 15 lbs in the last 2 months. He denies any history of a prior cancer diagnosis. On review of systems he denies history of cough, fevers, night sweats, hematochezia or gross hematuria. Mr. Bach has a 20 pack year smoking history.

Mr. Bach had difficulty with the physical exam due to pain. He appeared very distressed. All vital signs were within normal limits. An order for IV opiods was ordered and he was reassessed 30 minutes later.

Physical exam

Inspection: there were no obvious deformities of the back, no scarring or bruising or abrasions. Mr. Bach continued to look uncomfortable but was no longer in any acute distress.
Palpation: Mr. Bach was tender to palpation over L4-5. There was tenderness to palpation of the paraspinal muscles at the same level.
ROM: Mr. Bach was very hesitant to move, thus, it was difficult to assess his range of motion.
Neuro: Reflexes at the knee and ankle were normal. Babinski was negative. Normal sensation throughout all dermatomes. 5/5 strength on flexion/extension at the hip, knee and ankle.
Special tests: Straight leg raise and Lasegue’s test were negative.

Back Pain

Back pain is an extremely common condition. It is estimated that 70-85% of people will experience back pain at some point in their life1. A recent study out of an emergency department in Halifax, found that 3.17% of patients presented with to the emergency department with a complaint of lower back pain2. Back pain is within the top 5 reasons for primary care visits3. The differential diagnosis for lower back pain ranges from mechanical lower back pain to critical conditions that need to be recognized 4. Due to its prevalence and potentially sinister causes it is important to have an evidence-based approach to lower back pain.

 

To Image or Not to Image-That is the Question

Choosing Wisely Canada has put out recommendations for both Family and Emergency physicians with regards to low back pain. For family medicine the recommendation is “don’t do imaging for lower-back pain unless red flags are present” 5. It has been found that imagining those without red flags before 6 weeks does not improve outcomes.5

Similarly, for emergency medicine the recommendation is “don’t order lumbosacral (low back) spinal imaging in patients with non-traumatic low back pain who have no red flags/pathologic indicators.”6

Red flags 6:

Cauda Equina Syndrome
Severe worsening pain, especially at night
Significant trauma
Weight loss
History of Cancer
Fever
Night sweats
Steroid use
IV drug use
First episode of back pain in age > 50, especially concerning if age > 65
Widespread neurological signs (loss of sensation, loss of motor function, loss of reflexes in the legs)

 

It is also important to remember that not all red flags are created equal and to include clinical judgement in the decision making process.8 A systematic review examining the predictive value of commonly assessed red flags found that for fracture older age, prolonged steroid use, severe trauma, and contusion/abrasion increased the probability of fracture to 10-33%, and if multiple red flags are present fracture risk increases to 42-90%.

When considering red flags that increase risk of malignancy, previous history of malignancy increased risk 7-33%; while older age, unexplained weight loss, and failure to improve after one month all were found to have post-test probabilities of less than 3% when predicting malignancy risk8.

Back to our case

Mr. Bach has red flags for both fracture and malignancy:

Severe, worsening pain
Age > 50
Weight loss

XRs of the lumbar spine were ordered and indicated several compression fractures, with one area suspicious for a metastatic lesion. Follow CT spine was ordered and confirmed metastatic disease. Mr. Bach was admitted to hospital for pain control, physiotherapy and a malignancy work up.

 

References
1. Andersson, G. B. (1999). Epidemiological features of chronic low-back pain. Lancet 354(9178):581-585. doi:10.1016/S0140-6736(99)01312-4
2. Edwards, J., Hayden, J., Asbridge, M., & Magee, K. (2018). The prevalence of low back pain in the emergency department: A descriptive study set in the Charles V. Keating Emergency and Trauma Centre, Halifax, Nova Scotia, Canada. BMC Musculoskeletal Disorders, 19(1), 306. https://doi.org/10.1186/s12891-018-2237-x
3. Finley, C. R., Chan, D. S., Garrison, S., Korownyk, C., Kolber, M. R., Campbell, S., Eurich, D. T., Lindblad, A. J., Vandermeer, B., & Allan, G. M. (2018). What are the most common conditions in primary care? Systematic review. Canadian family physician Medecin de famille canadien, 64(11), 832–840.
4. Patel, A.T., & Ogle, A.A. (2000). Diagnosis and management of acute low back pain. Am Fam Physician 61(6):1779-1790.
5. College of Family Physicians of Canada. Choosing Wisely Canada. Thirteen Things Physicians and Patients should question. July, 2019. Retrieved from: https://choosingwiselycanada.org/family-medicine/
6. Canadian Association of Emergency Physicians. Choosing Wisely Canada. Ten things Physicians and Patients Should Question. July, 2019. Retreived from: https://choosingwiselycanada.org/emergency-medicine/
7. Toward Optimized Practice (TOP). (2011). Guideline for the evidence-informed primary care Management of Low Back Pain. Retrieved from: https://portal.cfpc.ca/resourcesdocs/uploadedFiles/Directories/Committees_List/Low_Back_Pain_Guidelines_Oct19.pdf
8. Downie, A., Williams, C. M., Henschke, N., Hancock, M. J., Ostelo, R. W. J. G., de Vet, H. C. W., Macaskill, P., Irwig, L., van Tulder, M. W., Koes, B. W., & Maher, C. G. (2013). Red flags to screen for malignancy and fracture in patients with low back pain: Systematic review. BMJ, 347.

Copyedited by Dr. Mandy Peach

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