Delirium vs. Dementia: Different side on the same coin

Delirium vs. Dementia: Different side on the same coin: A Medical Student Pearl

Khoi Dao, Med III

Dalhousie Medicine New Brunswick

Reviewed by Dr. Todd Way

Copyedited by Dr. Mandy Peach

Case:

Mr. D is an 83yo M today presents to Emergency Department through ambulance after a fall. Paramedics report stated that his wife found him pale and heard his complaints of shortness of breath (SoB), chest pain, and feeling weak. She later heard him called for help on the floor and called ambulance. Furthermore, the report also mentioned that he had a fall a week ago. When having a conversation with Mr. D, he stated that everything is fine, that he had no trouble breathing, or chest pain. The only pain that he felt was from his left arm and leg from the fall. He seems to be confused. He stated that he is from Nova Scotia, currently at an airport, and waiting for his friend to pick him up to go to their cabins at New Brunswick.

His initial vitals taken by paramedics was normal except for O2 Sat in 80’s. At the Emergency Department, he received O2 4L in air cannula and his SatO2 quickly brought up to 95%. He was afebrile, blood pressure at normal range, and heart rate was irregularly irregular. There were bruises at his left facial, left upper flank at axillary region, and left arm. There were no signs of basal skull fractures, nor any lacerations on his head. Cranial nerves exam was normal. Upper extremity motor, sensory, and reflex exams were within normal limits. Lower extremity motor found his dorsal flexion and extension on the left side was weaker compared to right side. Patella reflex exam was within normal limits. Respiratory exam was within normal limit. Cardiac exam reveals irregularly irregular pulse, but normal heart sound, no murmur, no extra heartbeat. Abdomen exam was within normal limits.

Past Medical History: hypertension, dyslipidemia, nephrolithiasis, chronic subdural hematoma, infection secondary to left ankle replacement, and Guillain-Barre syndrome (acute inflammatory demyelinating polyneuropathy)

Past Surgical History: bilateral ankle replacements

Initial Investigations:

With his initial presentation, blood work and imaging were ordered. Mr. D’s CBC showed elevated WBC, CRP, with stable Hgb. His ECG showed a new A-Fib.  Chest X-ray found he has consolidation of his left lower lobe, suggestive of pneumonia. Initial CT scan confirmed of left lower lobe consolidation, with multiple new and old rib fractures.

First, establish between Mild Cognitive Impairment (MCI) and Delirium

Dementia, Mild Cognitive Impairment, and delirium are grouped under the umbrella term of neurocognitive disorders, according to DSM-V. However, each of them has their own definitions, underlying pathology, and maybe etiology.

Dementia, or newly named major neurocognitive disorder in DSM-V, is characterized as cognitive decline involving one or more of neurocognitive domains (learning, memory, attention, executive function, perceptual-motor, and social cognition) that is severe enough to interfere with daily function and independence. These daily functioning includes instrumental ADL (iADL) and ADL (Table 1).

To meet the criteria of diagnosing dementia, one must have an evident decline of one or more cognitive domains, either through a collateral history of someone who is close to the patient, or through standardized neuropsychological testing (MMSE, MOCA, …). The decline of cognitive domains should not occur in the context of delirium and are not better explained by another mental disorder.

 Mild cognitive impairment can be considered somewhere between normal cognition and dementia. While it is considered to have deficit of one or more cognitive domains, it does not interfere with daily function activities. Like dementia, the diagnostic criteria require exclusively not in the context of delirium, and that it is not better explained by another mental disorder.

Delirium, on the other hand, is defined of any disturbance of attention and awareness along with cognition (e.g. memory deficit, disorientation, language, visuospatial ability, or perception) over a short period of time (hours to days). It can persist from days to month. Delirium is typically caused by medical conditions, substance intoxications, or medication side effect. Thus, for the diagnostic criteria for delirium to be met, there needs to have evidence from history presentation, physical examination, or laboratory findings of physiological changes that consequently may explain the cognitive disturbances.

Cognition decline as a clinical sign can be challenging for a physician since it is overlapped by neurocognitive disorders. However, there are characteristics that are different between them, which can be shown in Table 2.

Mainly, dementia has a gradual onset, whereas delirium has a more abrupt and acute onset. Attention and orientation are usually impaired in delirium, but generally preserved in dementia in earlier stage.

Collateral History:

Initial history taking could be proven to be challenging when patient presents with difficulties with memory or attention. Thus, obtaining a collateral history is pertinent as it is an indicator and a key component to differentiate between dementia and delirium4. Although collateral history is a core clinical skill, it is sometimes overlooked 5. In taking a collateral history, one would need to establish patient’s cognition at their baseline. For instance, questions relate about  a person’s daily activities and whether if they have any difficulties should be explored. Clarification of the onset and progressions of the cognitive changes need to be documented. Furthermore,  other cognitive domains should be also screened, as questions can be seen in Table 2 below 6.

After taking initial history, you thought that Mr. D is confused and could not give a good history of presenting illness, so you decide to call his substitute decision maker (SDM), who happens to be his wife. His wife recalled that he looked pale at lunch, complained of SoB, and when he walked she thought he looked weaker than usual. Then, she heard a called for help and found him on the floor, conscious. He couldn’t get up by himself and so she decided to call an ambulance. His wife mentioned that Mr. D has had some memory loss over half a year, where there were multiple episodes of Mr. D forgetting things. However, a week ago he had a fall walking outside, and she reported that his memory has been progressively worse since the fall. There were several nights when he woke up and asked her what the dates or where he is at. He also appeared to be weak, and, the day before his emergency admission, he complained of chest pain. When asked whether he has any difficulty of performing activity of daily living (ADL), his wife mentioned he had hard time getting dressed. His wife reported he had not seen a specialist for memory decline. She was concerned, however, that his memory was acutely declining over a week compared to the last few months. When asked about EtOH use, he had history of excessively drinking in the past, but currently only one serving per day.

As Mr. D was suspected of delirious that is overlapping of MCI, more investigations were added to investigate the cause of his delirium.

Risk and Precipitating factors of delirium:

Most identified risk factors are involving with underlying brain pathologies (e.g dementia, stroke, or Parkinson)7. With respect to precipitating factors, common examples include, but not limited to, polypharmacy, infection, dehydration, immobility, malnutrition, and the use of bladder catheters (predisposes patient to urinary tract infections)

Differential Diagnoses:

Besides major neurocognitive disorders (e.g. dementia) and mild cognitive impairment that were discussed above, other differential diagnoses should also be considered such as2:

Sundowning – behaviour deterioration seen in evening hours that might be due to impaired circadian regulation or nocturnal factors in the environment

Focal syndromes – includes temporal-parietal, occipital, and frontal dysfunctions

Nonconvulsive status epilepticus – patients often showed non-classical ictal features, but with the following features such as: prominent bilateral facial twitching, unexplained nystagmoid eye movements during obtunded periods, spontaneous hippus, prolonged “postictal state”, automatism, and acute aphasia without structural lesion

Psychiatric illnesses – includes bipolar and depressive disorders with psychotic features

Acute stress disorder – associated with fear, anxiety, and dissociative symptoms, such as depersonalization

Approach to the source of delirium:

As Mr. D was suspected to be delirious, the potential causes can be reflected through laboratory results as well as imaging studies. Sources of cognitive decline can be from systemic illness, isolated organ system dysfunction, drug adverse reactions, intoxications or withdrawal, psychiatric illness, trauma, or neurologic disease2,3. A concise and comprehensive acronym that could be used to establish the source of change in delirium can be used like DIMES8:

Drugs – anticholinergic, anti-emetics, anti-parkinsonian, beta-blockers

Infections – pneumonia, urinary, skin/soft tissue, CNS-related

Metabolics – altered pH, hypo/hyper Na+ or Ca+, acute organ failure, hypoglycemia

Enviromentals – heavy metals,

Structurals – brain injury, CNS pathology, malignancy

Treatment for delirium usually is to manage the underlying cause of the delirium.

Case continues:

                Although Mr. D’s initial imaging investigations found lower lobe consolidation that suggestive of pneumonia, he has a past medical history of chronic subdural hematoma in 2010. A CT head scan was ordered to rule out if there any new bleeding. When the CT head was negative it was most likely his newfound delirium and A-fib were secondary to pneumonia . Blood culture was done, and 2g IV Ceftriaxone was given empirically for his pneumonia. He was transferred to Hospitalist Unit for monitoring for improvement and referred to Geriatric Unit at St. Joseph’s Hospital for further investigation to his MCI.

Key points:

  1. Delirium is characterized as disturbance in attention and in cognition domain over a short period of time that could not be explained by other neurocognitive disorder.
  2. Delirium shared many cognitive declines feature with dementia and MCI. However, features such as acute onset, inattention, and evidence of physiological changes can be used to differentiate
  3. Collateral history is an important clinical tool to identify between delirium and other neurocognitive disorders.
  4. Mnemonics in approaching for delirium can be remembered as DIMES

References:

  1. American Psychiatric Association. (2013). Neurocognitive Disorders. In American Psychiatric Association, Diagnostic and Statistical Manual of Mental Disorders. https://doi-org.ezproxy.library.dal.ca/10.1176/appi.books.9780890425596.dsm17
  2. Francis J., Young, G.B. (2021). Diagnosis of delirium and confusional states. Retrieved from https://www.uptodate.com/contents/diagnosis-of-delirium-and-confusional-states?search=delirium&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1
  3. Larson, E.B. (2021). Evaluation of cognitive impairment and dementia. UpToDate. Retrieved from https://www.uptodate.com/contents/evaluation-of-cognitive-impairment-and-dementia?search=delirium%20and%20dementia&source=search_result&selectedTitle=4~150&usage_type=default&display_rank=4
  4. Dyer, A. H., Foley, T., O’Shea, B., & Kennelly, S. P. (2018). Cognitive assessment of older adults in general practice: the collateral history. Irish Journal of Medical Science (1971-), 187(3), 683-687
  5. Fitzpatrick, D., Doyle, K., Finn, G., & Gallagher, P. (2020). The collateral history: an overlooked core clinical skill. European Geriatric Medicine, 11(6), 1003-1007.
  6. Mahdy, R., Amer, M. S., Adly, N. N., & Rasheedy, D. (2021). The Value of Collateral History in Screening for Mild Cognitive Impairment in Elderly with Diabetes Mellitus in Outpatient Clinics. The Egyptian Journal of Geriatrics and Gerontology, 8(1), 21-28.
  7. Fick, D. M., Agostini, J. V., & Inouye, S. K. (2002). Delirium superimposed on dementia: a systematic review. Journal of the American Geriatrics Society, 50(10), 1723-1732.
  8. Melady, D. (2013). Cause of delirium. In Geri-EM. Retrieved from https://geri-em.com/cognitive-impairment/causes-of-delirium/
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A Case of Pyelonephritis

A Case of Pyelonephritis: A Medical Student Clinical Pearl

Natasha Glover

MUN Medicine, CC4

Class of 2022

Reviewed by Dr. Paul VanHoutte

Copyedited by Dr. Mandy Peach

Case

Ms. X, a 23 year old mother of 2 presents to the Emergency Department with a 3 day history of left flank pain and vomiting. She describes the pain as sharp, constant, and worse with touch. Her boyfriend observed her sweating and shivering the night before. She has also experienced a loss of appetite, having been unable to keep any food or liquids “down”. In the ED waiting room, she vomits and describes bright red “streaks” mixed with the vomitus.

2 weeks prior to her visit, she describes having dysuria and suprapubic pressure. She has a history of frequent UTIs, so she took an old bottle of unfinished amoxicillin from a previous diagnosis of cystitis and took the remaining 3 pills over the course of the 3 days. Reports that dysuria and pressure subsided afterwards.

 

PMHx:
Frequent UTIs

 

Medications:
No prescription medications

 

Social:

Smokes marijuana daily

No EtOH consumption

No other recreational drug use

1 month ago became sexually active with a new partner, reports that partner was tested prior to beginning their sexual relationship

 

Physical Exam:

HR 112 BP 132/88 T 37.8 RR 18 SpO2 97%

Appears in mild discomfort. No respiratory distress. Oriented to person, place, and time. Dry oral mucosa. Skin tenting. No facial edema.

Mild tachycardia, otherwise normal cardiac exam. Equal breath sounds to the bases, no adventitious sounds. Abdomen was non-distended, soft, moderate tenderness in the LUQ and LLQ, no rebound tenderness, no masses, no evidence of hepatosplenomegaly. Tenderness at the left flank.

Peripheral pulses present, equal, capillary refill <2s . No peripheral edema.

 

Differential Diagnosis:

  1. Pyelonephritis
  2. Renal colic
  3. Ectopic pregnancy
  4. Gonorrhea/chlamydia infection
  5. Nephrotic syndrome
  6. Splenic flexure syndrome

 

Urinalysis:

Leukocyte esterase 25

Blood casts 50

Protein 20

HCG negative

Culture: E.coli positive (reported after 24 hours in lab)

 

Labs:

Sodium 140

Potassium 4.2

Chloride 108

Creatinine 274

Hgb 135

HCT 0.450
LKC 23.7

PLT 281

CRP 506.3

Lipase 8

Bedside renal U/S unable to detect any hydronephrosis.

A CT is ordered to rule out infected renal stone.

Left kidney is markedly larger than the right kidney. Stranding around the left kidney. No evidence of obstruction, hydronephrosis or hydroureter.

Assessment:

This patient is mildly hypovolemic. She also has a new AKI, likely pre-renal as the result of NSAID use and volume depletion. She has a left sided pyelonephritis given her recent history of cystitis (likely suboptimally treated by the use of old remaining antibiotics for a previous UTI), left flank pain with costovertebral tenderness and various abnormal lab findings

Imaging rules out obstructive causes and other complicating factors. As a result, she requires fluid resuscitation, pain management, nausea/vomiting management, IV antibiotics, and admission to the hospitalist unit.

 

Let’s Break it Down; Assessment of Acute Kidney Injury:

Pathogenesis of Pyelonephritis:

 

The majority of pyelonephritis cases are the result of lower genitourinary infections that travel up through the ureters and into the kidneys. Other sources of infection occur through hematogenous spread, which is most often seen in chronically ill and immunocompromised patients. Additionally, metastatic manifestations of fungal and staphylococcus may spread distantly from the skin. Escherichia coli is the most common pathogen observed in cases of pyelonephritis.

 

Treatment of pyelonephritis is highly dependent on whether or not it is classified as a complicated UTI or an uncomplicated UTI.

 

Complications:

 

-Higher mortality among elderly, immunocompromised patients, and those who develop septic shock

-A small number of individuals, particularly those with structural abnormalities, complex renal obstructions, congenital anomalies, develop chronic pyelonephritis. Chronic pyelonephritis is characterized by nonspecific symptoms as well as histologic findings of lymphoplasmacytic infiltrates, thyroidization, tubulointerstitial scarring, glomerulosclerosis, and fibrosis.  It accounts for approximately 20% of end-stage kidney disease.

Figure 2: Chronic pyelonephritis with focal and segmental glomerulosclerosis with periglomerular fibrosis (Jones silver stain) from the National Kidney Foundation

Management for Ms. X:

Ceftriaxone 1mg IV q24h because she was systemically unwell
Fluid resuscitation with normal saline
Pain management with acetaminophen 975 PO QID and morphine 5mg SC q3h PRN
Nausea and vomiting management with ondansetron (Zofran) 8mg IV q8h PRN
Admit to hospitalist for further monitoring and management

 

References:
1. Hooton, T., Gupta K. Acute complicated urinary tract infection (including pyelonephritis) in
adults. UpToDate. https://www.uptodate.com/contents/acute-complicated-urinary
-tract-infection-including-pyelonephritis-in-adults. Published 2021. Accessed July 14,
2021.
2. Buonaiuto VA, Marquez I, De Toro I, et al. Clinical and epidemiological features and
prognosis of complicated pyelonephritis: a prospective observational single
hospital-based study. BMC Infect Dis. 2014;14(1):639. doi:10.1186/s12879-014-0639-4
3. Fogo AB, Lusco MA, Najafian B, Alpers CE. AJKD Atlas of Renal Pathology: Chronic
Pyelonephritis. Am J Kidney Dis. 2016;68(4):e23-e25. doi:10.1053/j.ajkd.2016.08.001
4. Khanna R. Clinical presentation &amp; management of glomerular diseases: hematuria,
nephritic &amp; nephrotic syndrome. Mo Med. 2011;108(1):33-36.
http://www.ncbi.nlm.nih.gov/pubmed/21462608. Accessed July 14, 2021.
6. NB Provincial Health Authorities Anti-Infective Stewardship Committee. Treatment of adult
urinary tract infections. 2021. doi:10.1002/14651858.CD003237.pub2
7. Rahman M, Shad F, Smith MC. Acute kidney injury: A guide to diagnosis and management.
Am Fam Physician. 1970;86(7):631-639. https://www.aafp.org/afp/2012/1001/
p631.html. Accessed July 14, 2021.
8. Scheid DC. Diagnosis and Management of Acute Pyelonephritis in Adults. Vol 71.
American Academy of Family Physicians; 1970. https://www.aafp.org/afp/
2005/0301/p933.html. Accessed July 12, 2021.

 

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Murmurs for the Learners: An approach to pediatric heart murmurs

Murmurs for the Learners: An approach to pediatric heart murmurs – A Medical Student Clinical Pearl

Luke MacLeod, Med IV

DMNB Class of 2022

Reviewed by Dr. Tushar Pishe

Copyedited by Dr. Mandy Peach

Case:

You are a senior medical student working in the emergency department and are asked to see Charlie, a 3-year-old boy who had a fall.  He is accompanied by his uncle Kevin, who gives you the history.  About one hour ago, Charlie was climbing onto a chair when he fell off and hit his head.  The chair was only a few feet off the ground and the floor was covered with a rug.  Charlie cried for several minutes after the fall, but there was no loss of consciousness or vomiting following the event.

Kevin tells you that Charlie is a healthy boy with no known medical issues or surgical history. There have been no concerns with his growth or development thus far.  He has no allergies, does not take any medications, and is up to date on his immunizations.  Kevin is unable to tell you much about Charlie’s family history.  He recently adopted Charlie, whose biological parents are no longer involved.

On exam, you observe an active and responsive 3-year-old.  He is afebrile with stable vital signs.  He has normal colour and shows no signs of respiratory distress.  There is a small bump on the top of his head, but no other injuries are noted.  His neurological exam reveals no focal neurological deficits.  To complete the exam, you feel his abdomen, which is soft and non-tender with no organomegaly, and auscultate his heart and lungs.  His lungs are clear with no crackles or wheeze. On auscultation of the heart, you detect a soft, non-radiating systolic murmur that seems to go away with inspiration.

You are reassured from the history and exam that Charlie’s head injury was very minor and that no further investigations or interventions are necessary, but you wonder about the significance of his heart murmur.

 

What is a heart murmur?

 

A heart murmur is an additional sound, often described as whooshing or blowing noise, heard between heart beats that is generated by turbulent blood flow in or near the heart.1,2  Heart murmurs are very common, with up to 90% of children having one either during infancy or later in childhood.  However, less than 1% of these murmurs are due to congenital heart disease.3  If the heart murmur is related to a serious underlying condition, the child may have signs or symptoms such as cyanosis, cough, shortness of breath, or light-headedness.1  Most murmurs are asymptomatic, but the absence of symptoms does not always mean that the murmur is benign.3 In some cases a murmur may be the only sign of an underlying heart condition.4

 

How to describe a murmur

 

Before picking up your stethoscope, you’ll want to make sure you have clean ear canals so you can pick up subtle murmurs.  The characteristics use to describe a murmur can be remembered with the pneumonic Q-TIP ROLS (note: this is not a recommendation to clean your ears with cotton swabs).

 

Quality

The quality of a murmur can be described as harsh, blowing, musical, rumbling, or vibrating.3

 

Timing

Timing describes when the murmur occurs in the cardiac cycle.  A systolic murmur occurs between S1 and S2.  These can be further categorized into four sub-types:

  • Early systolic: heard with or immediately after S1 and ends about halfway through systole.
  • Mid-systolic/systolic ejection murmur: heard midway between S1 and S2. Increases then decreases in volume (crescendo-decrescendo).
  • Mid-to-late systolic: heard about halfway through systole and ends before S2
  • Holosystolic/pansystolic: heard throughout systole.

Click here to listen to a holosystolic murmur: https://www.youtube.com/watch?v=MzORJbyHTT0

 

A diastolic murmur occurs between S2 and S1.  These can be further categorized into three sub-types:

  • Early diastolic: a high-pitched murmur heard with or immediately after S2.
  • Mid-diastolic: heard soon after S2 and ends before S1.
  • Late diastolic/presystolic: heard just before S1.

 

A continuous murmur is heard throughout the cardiac cycle.3

 

Intensity

A grading system from 1-6 is used to describe a murmur’s intensity, with higher values representing greater volumes.3  The following table details what each grade indicates:5

Pitch

A murmur can have low, medium, or high pitch.  High pitch murmurs are best detected using the diaphragm of the stethoscope, while low pitch murmurs are easier to hear using the bell.3

 

Radiation

This is the furthest point from the location (see below) where the murmur can still be detected.3

 

Other sounds

S3: heard in early diastole (shortly after S2).  S3 can be present in hyperdynamic states or with a large VSD.  This sound is best heard with the bell over the apex (for blood flow to the left ventricle) or the lower left sternal border (for blood flow to the right ventricle). When an S3 is present, the heart beat cadence is often described using the word “Kentucky” where “Ken” is S1, “tuc” is S2, and “ky” is S3.5

 

S4: heard late in diastole (just before S1) when there is turbulent blood flow into a stiff ventricle, such as in hypertrophic cardiomyopathy, myocardial dysfunction, semilunar valve stenosis, or tachycardia-induced cardiomyopathy.  S4 is best heard with the bell and is a pathologic exam finding.  When an S4 is present, the heart beat cadence is often described using the word “Tennessee,” where “Ten” is S4, “nes” is S1, and “see” is S2.5

 

Click below to listen to S3 and S4 heart sounds

https://www.youtube.com/watch?v=o8eqYHCy7dw

 

Ejection clicks

These are high pitch sounds that are often generated by abnormal heart valves.  The affected valve is determined based on the location, timing, and nature of the click as shown in the table below:5

Pericardial friction rub

A coarse grinding sound heard with pericarditis. This is best heard along the left sternal border.5

 

Location

This is the point where the murmur is most easily heard.3

 

Shape

Shape describes a murmur’s volume pattern. A few examples are shown below:6

What are the characteristics of benign and pathological murmurs?

 

Some red flag characteristics of pathologic murmurs are listed below.4,7

  • Holosystolic
  • Diastolic
  • Grade 3 or higher
  • Harsh quality
  • Systolic click
  • Max intensity at upper left sternal border
  • Abnormal S2
  • Greater intensity with standing

 

Characteristics of benign murmurs can be remembered using The Seven S’s.4,8

  • Systolic
  • Soft
  • Short (not holosystolic)
  • Small (non-radiating)
  • Sweet (not harsh)
  • Single (no clicks or gallops)
  • Sensitive (changes with position or respiration)

 

Click below to listen to an innocent heart murmur

https://www.youtube.com/watch?v=uFyWHPfrRak

 

Here are some examples to practice differentiating innocent from pathological murmurs:

https://teachingheartauscultation.com/pediatric-murmur-recognition-program-intro

 

What are some of the more common pediatric heart murmurs?

 

Innocent9

  • Classic vibratory parasternal-precordial stills murmur
  • Pulmonary ejection murmur
  • Systolic murmur of pulmonary flow in neonates
  • Venous hum
  • Carotid bruit

 

Pathologic4

  • Ventricular septal defect
  • Atrial septal defect (example: https://www.youtube.com/watch?v=W8gg2S-mvSQ)
  • Patent ductus arteriosus
  • Teratology of Fallot
  • Pulmonary stenosis
  • Coarctation of the aorta
  • Aortic stenosis
  • Transposition of the great arteries

 

Next steps

 

In patients with a heart murmur and an abnormal chest X-ray or ECG, an echocardiogram is indicated.  The echocardiogram is the gold standard test to diagnose congenital heart defects.  While the chest X-ray and ECG are low cost tests and can help rule out other diagnoses, they are not particularly useful in identifying the cause of a heart murmur. 3

An innocent heart murmur in an asymptomatic patient with an otherwise normal exam does not require referral to cardiology.  However, the patient should be followed by their family physician to monitor the murmur.

Patients who are symptomatic, have a pathologic murmur, and/or have other concerning exam findings should be referred to a pediatric cardiologist.10

 

Case Conclusion

 

Charlie’s heart murmur lacked any of the red flag characteristics.  It was soft (grade 2) systolic murmur that did not radiate and changed with inspiration, which are all reassuring signs.  He was also asymptomatic and had an otherwise normal exam.

You explain to Kevin that Charlie looks well and that there are no signs of serious head trauma.  You mention that you did notice a heart murmur that is likely benign.  Charlie does not need to see a specialist, but you recommend that he have a follow up appointment with his family doctor in the next few weeks to monitor the heart murmur.

 

 

References:

  1. Heart Pulse Sound Wave Icon Stock Vector – Illustration of blood, healthcare: 91331428. Accessed November 19, 2021. https://www.dreamstime.com/stock-illustration-heart-pulse-sound-wave-icon-background-image91331428
  2. Heart Murmur | NHLBI, NIH. Accessed November 18, 2021. https://www.nhlbi.nih.gov/health-topics/heart-murmur
  3. Heart murmurs: MedlinePlus Medical Encyclopedia. Accessed November 18, 2021. https://medlineplus.gov/ency/article/003266.htm
  4. Pediatric Heart Murmurs: Evaluation and management in primary care. Accessed November 18, 2021. https://oce-ovid-com.ezproxy.library.dal.ca/article/00006205-201103000-00006/HTML
  5. Frank JE, Jacobe KM. Evaluation and Management of Heart Murmurs in Children. Am Fam Physician. 2011;84(7):793-800.
  6. Approach to the infant or child with a cardiac murmur – UpToDate. Accessed November 18, 2021. https://www.uptodate.com/contents/approach-to-the-infant-or-child-with-a-cardiac-murmur?search=heart%20murmurs&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1
  7. Physical Examination – Textbook of Cardiology. Accessed November 18, 2021. https://www.textbookofcardiology.org/wiki/Physical_Examination
  8. Pediatric Heart Murmur Recognition Program intro. Teaching Heart Auscultation to Health Professionals. Accessed November 19, 2021. https://teachingheartauscultation.com/pediatric-murmur-recognition-program-intro
  9. Bronzetti G, Corzani A. The Seven “S” Murmurs: an alliteration about innocent murmurs in cardiac auscultation. Clin Pediatr (Phila). 2010;49(7):713. doi:10.1177/0009922810365101
  10. Begic E, Begic Z. Accidental Heart Murmurs. Med Arch. 2017;71(4):284-287. doi:10.5455/medarh.2017.71.284-287
  11. McConnell ME, Adkins SB, Hannon DW. Heart murmurs in pediatric patients: When do you refer? Am Fam Physician. 1999;60(2):558-565.

 

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A Case of Smoke Inhalation Injury

A Case of Smoke Inhalation Injury – A Medical Student Clinical Pearl

Emmanuel Hebert

MD Candidate, Class of 2022

Dalhousie Medicine New Brunswick

Reviewed by Dr. Matthew Greer

Copyedited by Dr. Mandy Peach

Case

 A 54-year-old Male presents to the emergency room via EMS. He woke up at nighttime to his house on fire. He says he woke up coughing due to the smoke and was able to crawl out of the house while ablaze and called EMS. He was then transported to the hospital. He also reports that his voice is more rough than usual and that he has pain on his back.

Past Medical History: Unremarkable

Medications: No prescriptions medications.

Physical Examination: Patient is seen wearing a non-rebreather mask with an oxygen rate of 12L/min. He appears well and is in no acute distress. He has singed scalp hair and appears flushed. The patient’s vitals are HR-110, BP-125/80, Temp-36.5, O2 sat- 99%. Patient weighs 130 kg. His back appears very red but there are no open lacerations or blisters. There is good air entry bilaterally with no adventitious sounds or wheeze.  There is soot in the mouth as far back as can be visualized. The oropharynx is dry and mucous contains soot.

Figure 1: First degree burns on the back.

 

Initial bloodwork:

  • WBC: 10×10^9/L
  • Hgb: 135
  • Plt: 300×10^9/L
  • Na: 135
  • K: 4
  • Glu: 6
  • Carboxyhemoglobin: 5%
  • EtOH: Neg

 

What is the differential diagnosis of dysphonia?

-Acute laryngitis

-Functional dysphonia

-Tracheal Injury

-Injury to recurrent laryngeal nerve

-Caustic ingestion, smoke inhalation injury, blister chemical agents

-Neck masses (benign and malignant) [5,7]

 

Smoke Inhalation Upper Respiratory Tract Injury

 

Definition: Inhalation injury refers to damage to the respiratory tract or lung tissue from heat, smoke, or chemical irritants carried into the airway during inspiration [1].

Damage to the airway can be broken into three different affected zones with their own clinical consequences:

 

Upper Airway

  • The leading injury in the upper airway (above the vocal cords) is thermal injury due to heat exchange in the oro- and nasopharynx.
  • Injuries occurring early include erythema, ulcerations, and edema.
  • It is for this reason that aggressive fluid resuscitation should be avoided as the edema resulting from the heat transfer, can be compounded with fluid resuscitation, resulting in a further compromised airway. [2]

 

Tracheobronchial

  • Injuries to the tracheobronchial system occurs due to the chemical makeup of the smoke. When smoke stimulates the vasomotor and sensory nerve endings, neuropeptides get released which cause bronchoconstriction and vasodilation. Due to this inflammatory response, a loss of plasma proteins and fluid from the intravascular space into the alveoli and bronchioles ensues. This causes alveolar collapse and causes a VQ mismatch resulting in hypoxia. [3]

 

Parenchymal Injury

  • Injuries to the parenchyma occur because of the above mechanism resulting in alveolar collapse, which then cause increased transvascular fluid flux, a decrease in surfactant, and a loss of hypoxic vasoconstriction and therefore impaired oxygenation. [3]

Figure 2. Mechanisms of smoke inhalation injury in tracheobronchial area [4]

 

Management

Patients with smoke inhalation injuries are also at risk for carbon monoxide poisoning. It is for this reason that carboxyhemoglobin is used to assess degree of carbon monoxide toxicity. The treatment for this is 100% oxygen via non-rebreather. Another treatment that can be used is hyperbaric therapy. Choice of hyperbaric therapy should be made in consultation with a hyperbaric specialist and patient must be stable prior to transport. [3]

One of the earliest decisions to make in the management of patients with suspected smoke inhalation injuries is whether to secure the airway. In patient whom the airway is non-patent or there is an obstruction, the decision is easy to either attempt intubation via endotracheal tube or secure a surgical airway. The decision is less straight forward when the patient does not seem to be having any difficulties with ventilation and oxygenation. In the case of smoke inhalation injury, early intubation can be lifesaving. [6] This is due to the delayed fashion of bronchoconstriction in addition to the thermal changes that result from heat/smoke inhalation. Clinical judgement must be used however, to avoid intubating everyone prematurely. There are several red flag symptoms that physicians can use to assess whether a patient with smoke inhalation injury requires prophylactic intubation. [5]

 

Indications for early intubation:

  • Signs of airway obstruction: hoarseness, stridor, accessory respiratory muscle use, sternal retraction
  • Extent of the burn (TBSA burn > 40-50%)
  • Extensive and deep facial burns
  • Burns inside the mouth
  • Significant edema or risk for edema
  • Difficulty swallowing
  • Signs of respiratory compromise: inability to clear secretions, respiratory fatigue, poor oxygenation or ventilation
  • Decreased level of consciousness where airway protective reflexes are impaired
  • Anticipated patient transfer of large burn with airway issue without qualified personnel to intubate en route

 

Back to the case:

Due to our patient having progressive hoarseness, as well as soot throughout his oropharynx, the decision was made to secure his airway before it became too difficult to do so. A discussion was had with the patient about the risks and benefits to intubation and sedation while the inflammatory response could take its course and he consented to the procedure. Using rapid sequence intubation, rocuronium, a paralytic was used at a dose of 1mg/kg=130mg and propofol was used as a sedative at 1mg/kg=130mg. Fentanyl was used for analgesia at a dose of 1mcg/kg= 130mcg.

Due to the complexity of intubating a patient with possible impending upper airway collapse, it is important to have the best person available for intubation with one pass and ENT should be consulted so that a surgical airway can be obtained. One should also consider awake intubation due to high risk of upper airway occlusion. With this patient, a video laryngoscope was used to place the endotracheal tube.

Figure 3: Video laryngoscopy of an airway with smoke inhalation injury

 

During the intubation, it was seen that the tissue surrounding the airway was quite edematous with black soot present as well. This was an impending airway collapse! The endotracheal tube was placed, and the patient was monitored in the ICU overnight. As expected, edema ensued and oropharynx, tongue became edematous. The patient was stabilized on propofol drip over the next 2 days and was extubated on the third day post intubation.

 

Key Takeaways

  • Early identification of smoke inhalation injury is critical to survival.
  • The longer delay of intubation is, the harder it becomes. Consider awake intubation.
  • Red flag symptoms: Respiratory distress, respiratory depression, or altered mental status, Progressive hoarseness, Supraglottic or laryngeal edema/inflammation on bronchoscopy or NPL, Full thickness burns to face or perioral region, Circumferential neck burns, Major burns over 40-60% of body surface
  • Early intubation=lower mortality

 

References:

 

  1. Woodson CL. Diagnosis and treatment of inhalation injury. In: Total Burn

Care, 4 ed, Herndon DN (Ed), 2009.

  1. Sheridan RL. Fire-Related Inhalation Injury. N Engl J Med 2016; 375:1905.
  2. Rehberg S, Maybauer MO, Enkhbaatar P, et al. Pathophysiology, management and treatment of smoke inhalation injury. Expert Rev Respir Med 2009; 3:283.
  3. Herndon, D. N. (2018). 16. In Total burn care (pp. 174–183). essay, Elsevier.
  4. ABLS Provider Manual. (2019). Ameriburn.org
  5. Cioffi WG, Mason AD Jr, et al. The risk of pneumonia in thermally injured patients requiring ventilatory support. J Burn Care Rehabil 1995; 16:262.
  6. Reiter R, Hoffmann TK, Pickhard A, Brosch S. Hoarseness-causes and treatments. Dtsch Arztebl Int. 2015;112(19):329-337. doi:10.3238/arztebl.2015.0329

 

 

 

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Approach to Medical Abortion Complications in the ED

Approach to Medical Abortion Complications in the ED – A Medical Student Clinical Pearl

Victoria Mercer

MD Candidate | Class of 2023
Dalhousie Medicine New Brunswick

Case:

A 28 year old female presents to the ED with cramping abdominal pain and heavy vaginal bleeding ongoing for 4 days. She has soaked through 4 regular pads in the last 2 hours, an increase from her ongoing bleeding. She also describes an increase in lower abdominal pain and some lightheadedness. Taking her medical history you discover she was 9 weeks pregnant and had a medical abortion approximately 4 days ago.

Vitals: HR 101, BP 101/65, RR 19, SpO2 98%, T 37.5°C

Brief Review of Medical Abortion

Medical abortions account for approximately 40% of abortions and is both an effective and safe method of terminating pregnancies that are <11 weeks(1). Serious complications are rare but must be recognized by the emergency physician to prevent morbidity and mortality.

Standard regimen of medical abortions includes administration of 200mg oral Mifepristone, a progesterone receptor antagonist, followed by 800mg of Misoprostol, a synthetic prostaglandin, 24-48 hours later (1). Mifepristone disrupts pregnancy growth and misoprostol induces uterine contractions to aid in the expulsion of the pregnancy contents (2).

Expectations vs complications

Bleeding

Bleeding and cramping generally begin 1-4 hours after ingestion of misoprostol however the heaviest bleeding generally occurs 3-8 hours post ingestion as the pregnancy tissue is expelled from the uterus (2). Duration of bleeding is generally 11 to 17 days (1,2). Heavy bleeding is defined as soaking through 2 pads per hour for at least 2 hours, upon which patients should be counselled to seek medical assistance (1,2).

Differential diagnosis of post medical abortion hemorrhage: Uterine atony (40-50%), retained products of conception (POC), placenta previa or accreta, coagulopathies

Cramping & Pain

Over 90% of patients following mifepristone-misoprostol will experience cramping (3). This may be moderate pain that responds to oral analgesics such as acetaminophen, ibuprofen or in some cases, an opioid (3). When pain is not improving or controlled by oral medication, this could be concerning (2,3).

Differential of refractory pain: incomplete abortion, ectopic pregnancy, infection

Fever

Temperatures above 38.0 °C for several hours despite antipyretics is abnormal and should warrant investigation for infection. Most cases of postabortion infections are due to endogenous flora or pre-existing infections. If retained POC is identified via ultrasound, broad spectrum antibiotics should be administered and obstetric and gynecology should be consulted for surgical management (2).

Pearl:

Post-abortion triad includes pain, low-grade fever and bleeding. Most often caused by RPOC(4).

Approach to Patient in ED After a Medical Abortion

 

 

Case Continued:

Pelvic examination findings include a soft and enlarged uterus. No cervical lacerations are identified. On ultrasound you notice increase heterogenicity within the endometrial cavity and a thickened endometrial wall. You suspect the cause for her post-abortion hemorrhage is due to RPOC.

You begin a bimanual uterine massage and initiate methylergonovine administration. After 3 repeat doses, the bleeding begins to subside. Vital signs remain stable and OB/GYN is consulted for further management.

 

References

  1. First-trimester pregnancy termination: Medication abortion – UpToDate [Internet]. [cited 2021 Nov 8]. Available from: https://www.uptodate.com/contents/first-trimester-pregnancy-termination-medication-abortion?search=medical%20abortion&source=search_result&selectedTitle=1~72&usage_type=default&display_rank=1#H2018734958
  2. Orlowski MH, Soares WE, Kerrigan KL, Zerden ML. Management of Postabortion Complications for the Emergency Medicine Clinician. Annals of Emergency Medicine. 2021. 77(2):221-232. doi.org/10.1016/j.annemergmed.2020.09.008
  3. Kruse B, Poppema S, Creinin MD, Paul M. Management of side effects and complications in medical abortion. American Journal of Obstetrics and Gynecology. 2001. 183(2):S65–75.
  4. Abortion Complications Clinical Presentation: History, Physical, Causes [Internet]. [cited 2021 Nov 9]. Available from: https://emedicine.medscape.com/article/795001-clinical#b4
  5. Yahya B. Retained products of conception [Internet]. [cited 2021 Nov 9]. Available from: https://radiopaedia.org/articles/retained-products-of-conception
  6. Kerns J, Steinauer, J. Management of postabortion hemorrhage. Contraception (Stoneham). 2013. 87(3): 331-342. 10.1016/j.contraception.2012.10.024

 

 

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Allergic Acute Coronary Syndrome (Kounis Syndrome)

Allergic Acute Coronary Syndrome (Kounis Syndrome) – A Medical Student Clinical Pearl

Amar Bhardwaj CC3

Dalhousie Medicine New Brunswick

Class of 2022

Reviewed and edited by Dr. Kavish Chandra

Copyedited by Dr. Mandy Peach

 

Case presentation

A 52-year-old female presents to the ED with sudden onset left sided chest with radiation to her left arm shortly after eating.  The patient is diaphoretic and has been experiencing exertional dyspnea since her meal.  Patient also noted they developed an itchy red rash on their face and torso. There was no evidence of angioedema or other classical clinical signs or symptoms of anaphylaxis.

The patient is otherwise healthy and has a family ischemic heart disease.

Her vitals are BP 160/90, temperature 36.4, HR: 152, RR: 20, Sats:98% O2 on room air. The cardiovascular and respiratory exam are otherwise normal. The ECG shows sinus tachycardia without evidence of other abnormalities.

 

Image source: Burns, Ed. “Sinus Tachycardia • LITFL • ECG Library Diagnosis.” Life in the Fast Lane • LITFL, 7 Feb. 2021, litfl.com/sinus-tachycardia-ecg-library/.

Her hsTnT is 8 and the repeat marker is unchanged and the diagnosis of Kounis syndrome is considered.

 

Kounis syndrome

Kounis syndrome is defined as a concurrent acute coronary syndrome (ACS) in the setting of mast cell activation, which can be spontaneous or secondary to an allergic reaction (Lerner et al. 2017).  Kounis syndrome can be triggered by food, insect stings, drugs, environmental exposure and underlying medical conditions (Rodrigues et al. 2013). Allergen induced mast cell activation and release of inflammatory mediators leads to vasospasms, intimal thickening, and upregulation of proinflammatory cytokines that affect the coronary arteries and potential for occlusion progressing to an acute MI. The epidemiology remains scarce, and thus the prevalence is not entirely known as it is often missed or under diagnosed (Kounis, 2013; Kounis 2016).

Patients with Kounis syndrome can present with dyspnea, angioedema, pruritis, urticaria, gastrointestinal distress and hemodynamic instability. Airway compromise is of high importance in severe anaphylactic reactions with the potential to progress to anaphylactic shock. Along with an anaphylactic response, the coronary arterial effect can accelerate plaque rupture and cause symptoms indistinguishable from ACS.

Kounis Syndrome can be classified into three types (Kounis 2013)

Type I:

Acute coronary syndrome with normal or near-normal coronary arteries.

Type II:

Pre-existing atherosclerotic disease with syndrome causing coronary artery spasm, plaque rupture or erosion leading to acute MI.

Type III:

Coronary artery stent thrombosis with evidence of aspirated thrombus specimens containing eosinophils and mast cells respectively.

 

Presentation

Patients with this Kounis syndrome typically present with anaphylactic signs and symptoms accompanied with chest pain and associated signs and symptoms of acute coronary syndrome.  Table 1 depicts pertinent signs and symptoms that may point you in the right direction.

Table 1. Clinical and laboratory findings in Kounis syndrome (Adapted from Kounis 2016)

 

Kounis syndrome is a clinical diagnosis.

Management

There are no guidelines addressing the management of Kounis syndrome. However, treatment needs to address any hemodynamic instability as well as the cardiac and allergic concerns. Involvement of cardiology and allergy specialists can be helpful.

Concurrent management of anaphylaxis does not generally interfere with management of ACS however careful analysis of the risks and benefits of epinephrine administration to treat anaphylaxis without exacerbating cardiac ischemia. Case reports describe the successful treatment of Kounis syndrome patients with intramuscular epinephrine (Lerner et al. 2017). Other agents that have shown to aid symptomatically in allergic responses are H1 and H2 blockers as well as systemic corticosteroids for prevention of potential delayed phase reactions.

ACS management may be guided by cardiology and does not differ from traditional management with the exception that aspirin may be omitted due to its potential role propagating anaphylaxis (Lerner et. 2017). Other anti-platelets can be administered however beta-blockers are avoided as analgesics like morphine (further histamine release; Lerner et al. 2017). The timing and role of cardiac catheterization will be guided by cardiology and may involve intracoronary vasodilator infusion or thrombus evacuation (Carr and Helman, 2016).

Summary

In a patient presenting with ACS and severe allergic reaction/anaphylaxis, consider Kounis syndrome. There are no guidelines to assist in the management but the key aspects of managing ACS and anaphylaxis are critical in treating Kounis syndrome as well early consultation with cardiology and allergy.

References:
Carr, D. Helman A. Anaphylaxis and Anaphylactic Shock. Emergency Medicine Cases. February, 2016. https://emergencymedicinecases.com/anaphylaxis-anaphylactic-shock.

Kounis, N. G. (2016). Kounis syndrome: an update on epidemiology, pathogenesis, diagnosis and therapeutic management. Clinical Chemistry and Laboratory Medicine (CCLM), 54(10), 1545-1559
Kounis, N. G. (2013). Coronary hypersensitivity disorder: the Kounis syndrome. Clinical therapeutics, 35(5), 563-571.

Lerner M, Pal RS, Borici-Mazi R. Kounis syndrome and systemic mastocytosis in a 52-year-old man having surgery. CMAJ. 2017 Feb 6;189(5):E208-E211. doi: 10.1503/cmaj.151314. Epub 2016 Aug 2. PMID: 27486207; PMCID: PMC5289872.

Mattu, A. Demeester, S. Cardiology Corner: Kounis Syndrome. EMRAP. June, 2021. https://www.emrap.org/episode/emrap2021june1/cardiology

Rodrigues MC, Coelho D, Granja C. Drugs that may provoke Kounis syndrome. Braz J Anesthesiol. 2013 Sep-Oct;63(5):426-8. doi: 10.1016/j.bjan.2013.04.006. PMID: 24263049.

 

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Paediatric Supracondylar Fractures

Paediatric Supracondylar Fractures – A Medical Student Clinical Pearl

 

Reviewed by Dr. Joanna Middleton

Copyedited by Dr. Mandy Peach

Christine Crain (She/Her), CC3
Dalhousie Medicine MD Candidate, Class of 2022

Relevant Case:

On a Saturday, a three-year-old presented to the emergency department with his mother. He’d been playing in the backyard with his older sister who was on their swing. Unfortunately, the boy walked in front of the swing and was hit by his sister. He fell onto an outstretched hand and immediately began to cry and hold his elbow.

Problem:

There are two kinds of Supracondylar fracture; extension, which accounts for up to 95% of these fractures; and the far less common flexion fracture which occurs almost exclusively in older adults.

When a paediatric patient falls into an outstretched hand, the olecranon engages with the fossa, then acts as a fulcrum hyperextending the elbow, punching the olecranon through the relatively thin and weak supracondylar region of the humerus.

Figure 1: Case courtesy of Dr Samir Benoudina, Radiopaedia.org, rID: 39938

The Gartland classification (Fig.1) of supracondylar humeral fractures are based on the degree and direction of any displacement where Type 1 fractures imply little (1b) to no displacement (1a). Type 2 fractures displace the anterior humeral line (Fig.2) but leaves the posterior cortex intact; while type 3 fractures are completely displaced.

Figure 2: The anterior humeral line should pass through the middle third of the humeral capitulum. Case courtesy of Dr Samir Benoudina, Radiopaedia.org, rID: 41167.

Since these fractures commonly occur in children, learners especially need to be aware of the ossification centers within the elbow to be certain that they’re recognized as normal anatomy and not additional fractures. The age of the child should help you to estimate, with the help of a handy mnemonic, which ossifications centers should be visible on radiograph:

Figure 3: Case courtesy of Leonardo Lustosa, Radiopaedia.org, rID: 80555

In our case, with a three-year-old male, we would expect to see the Capitellum and Radial Head, but no other centers. We know any “fragments” in these areas are not additional fractures.

Most commonly in supracondylar fractures, there are other signs we look for that may indicate injury to the cartilage and forming bone:

  • Sail Sign shows a joint effusion under the Anterior fat pad (Fig. 4)
  • Posterior Fat Pad sign is the same, only on the posterior aspect of the elbow (Fig. 4)
  • And, as noted above, the Anterior Humeral Line should intersect the middle third of the Capitellum (Fig. 2)

Figure 4: Showing both Anterior and Posterior fat pad sign. Case courtesy of Assoc Prof Frank Gaillard, Radiopaedia.org, rID: 13527

Finally, given the number of vascular/neural structures that pass through the elbow, what complications are there to be aware of? As with all fractures, there is a risk of non/malunion, this is a relatively low risk however and is beyond the scope of this pearl.

Vascular complications include Volkmann’s contracture which can occur with injury to the brachial artery. This can result in a volar compartment syndrome leading to fibrosis and contracture of flexor muscles.

Finally, injury to any of the nerves that travel to innervate the hand/forearm can occur. Innervation through the Radial, Median (as well as the Anterior Interosseous nerve), and Ulnar nerves can be verified by a few quick and easy maneuvers as seen in Figure 5.

Figure 5: Innervation of the hand for the purposes of nerve injury screening.

Case Resolutions:

Inspection prior to radiographs showed intact sensation, brisk capillary refill with strong distal pulses, and ongoing ability to move joints below the injury. He was sent for radiographs which reported a supracondylar fracture. We casted his elbow and sent him for follow up to the Ortho fracture clinic the following week.

Conclusion

While learners may initially think ossification centers of the elbow are fracture fragments, using CRITOE they will be able to rule out joint involvement. This will allow you to move more quickly onto other radiographic signs of fracture.

References

  1. https://radiopaedia.org/articles/supracondylar-humeral-fracture-2
  2. https://radiopaedia.org/articles/gartland-classification-of-supracondylar-humeral-fractures
  3. https://radiopaedia.org/articles/anterior-humeral-line
  4. https://radiopaedia.org/articles/elbow-ossification-mnemonic
  5. https://radiopaedia.org/articles/sail-sign-elbow-1
  6. https://www.orthobullets.com/pediatrics/4007/supracondylar-fracture–pediatric

 

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Polymyalgia Rheumatica

Polymyalgia Rheumatica – A Medical Student Clinical Pearl

Alexis Lamontagne

MD Candidate, Class of 2022

DMNB, Dalhousie University

Case:

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

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

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

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

 

Polymyalgia Rheumatica:

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

Differential:

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

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

 

Investigations:

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

 

Treatment:

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

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

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

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

 

Pathophysiology:

The cause of polymyalgia rheumatica (PMR) is unknown.

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

 

Relationship to Giant Cell Arteritis:

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

 

Conclusion:

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

 

References:

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

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

 

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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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