A Case of Herpes Simplex Virus Keratitis in The Emergency Department

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

Patrick Gallagher, MED III

MUN Class of 2022

Reviewed by Dr. Robin Clouston

Copyedited by Dr. Mandy Peach

Case

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

Past medical history: T2DM and hypothyroidism.

Past surgical history: None.

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

Physical exam:

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

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

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

 

What is the differential diagnosis of dendrites?

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

Herpes simplex virus keratitis :

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

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

Pathophysiology:

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

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

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

History and physical:

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

Table 1: Key points on history and physical

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

Investigations:

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

Treatment/management of HSVK in the emergency department:

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

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

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

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

Back to the case:

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

References:

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

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

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

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

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

 

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Recognizing and Treating Cannabinoid Hyperemesis Syndrome

Cannabinoid Hyperemesis Syndrome – Med Student Pearl

Eric Plant, Med II, Class 2024

Dalhousie Medicine New Brunswick, Saint John

Reviewed and copyedited by Dr. David Lewis @e_med_doc


Quick Summary: The Pearls You Came Here For

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

Useful Links


Case

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

Initial Presentation Summary:

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

 


 

Introduction to CVS vs CHS

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

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


 

Overview of CVS

Definition and Diagnosis

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

 

Rome IV Criteria for CVS

Pediatric Criteria (all conditions must be met)

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

 

Adult Criteria (all conditions must be met)

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

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

Natural History:

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

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

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

Adapted from UpToDate2, 6, 20

Epidemiology

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

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

Overview of CHS

Definition and Diagnosis

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

 

Rome IV Criteria for CHS

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

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

·     Presentation after prolonged, excessive cannabis use

·     Relief of vomiting by a sustained cessation of cannabis use

 

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

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

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

Natural History

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

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

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

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

Epidemiology

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

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

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

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


 

Physiology of Nausea and Vomiting

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


 

Pathophysiology of CVS and CHS

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

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


 

Assessment

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

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

 

Emergent Complications of CHS15

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

History

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

 

Physical Exam

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

 

Investigations

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

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

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

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

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


 

Treatment

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

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

Treatment in the ED

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

 

Summary of Recommendations for Treatment in the ED

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

 

Definitive Treatment and Counselling

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

 

Case Conclusion

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

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

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

Download (PDF, 702KB)


 

References

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

Lateral  Canthotomy – A Medical Student Clinical Pearl

Scott Clarke

Med III, Class of 2022

Dalhousie Medical School New Brunswick (DMNB)

Reviewed by Dr. Fraser MacKay

Copyedited by Dr. Mandy Peach

 

Case:

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

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

 

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

Orbital Compartment Syndrome1

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

Clues on exam:

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

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

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

Procedural Overview:

Equipment:

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

Anatomy review:

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

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

Procedure5:

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

 

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

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

 

Keys to remember6:

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

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

Absolute contraindication:
– Globe rupture

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

  • mannitol
  • acetazolamide
  • pilocarpine
  • timolol

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

References

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

Carbon Monoxide Poisoning – A Medical Student Clinical Pearl

Mitchell McDonough

DMNB, Class of 2022

Reviewed by Dr. Rachel Goss

Copyedited by Dr. Mandy Peach

Case

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

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

Differential for Confusion

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

Stroke/CNS structural lesion/Head Injury

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

Intoxication/withdrawal
• Alcohol
• Drugs
• Carbon Monoxide

Investigations

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

Pertinent Arterial Blood Gas Values for our patient:

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

 

Carbon Monoxide Poisoning Overview

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

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

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

Clinical Presentation

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

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

 

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

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

Diagnosis

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

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

Treatment

Treatment of patients with suspected carbon monoxide poisoning include:

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

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

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

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

Case Conclusion

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

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

References

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

 

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A Case of Posterior Vitreous Detachment

A Case of Posterior Vitreous Detachment – Medical Student Clinical Pearl

Ben McMullin, Clinical Clerk III

Dalhousie Medicine New Brunswick, Saint John

Reviewed by Dr. David Lewis

Copyedited by Dr. Mandy Peach

Case Presentation

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

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

Anatomy of the Eye

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

 

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

 

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

POCUS Ocular Exam

Advantages of POCUS

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

Technique

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

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

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

PVD vs Retinal Detachment on POCUS

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

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

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

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

 

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

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

 

Management

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

Case Conclusion

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

References

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

Mycosis Fungoides: A Medical Student Clinical Pearl

 

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

All case histories are illustrative and not based on any individual

Reviewed by Dr. Devon Webster

Copyedited by Dr. Mandy Peach

Case

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

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

Differential for itchy, erythematous rash:

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

 

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

Epidemiology

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

Etiology

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

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

 

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

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

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

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

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

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

Evaluation in the ED

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

Labs: CBC, liver function tests, LDH

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

Biopsy: lymph nodes and rash – by consultants

Treatment and Management – refer to your friendly neighborhood dermatologist.

Early stage:

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

Advanced Stage:

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

Prognosis

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

Case Conclusion

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

 

References:

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

 

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

Lower Back Pain: Medical Student Clinical Pearl

Grace Dao, CC4

MD Candidate

Class of 2021

Case Presentation

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

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

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

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

Physical exam

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

Back Pain

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

 

To Image or Not to Image-That is the Question

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

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

Red flags 6:

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

 

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

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

Back to our case

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

Severe, worsening pain
Age > 50
Weight loss

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

 

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

Copyedited by Dr. Mandy Peach

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Detection of Foreign Bodies in Soft Tissue – A PoCUS-Guided Approach

 

Medical Student Clinical Pearl

Sophia Miao, CC4

MD Candidate, Class of 2021

Dalhousie University

 

Reviewed & Edited by Dr David Lewis (@e_med_doc)

All case histories are illustrative and not based on any individual.


 

Case Report

A 33-year-old woman presents to the ED with pain and swelling over the third digit of her right hand.  One week prior to this, she had shattered a jar and a small glass splinter lodged into her finger.  This was promptly removed at home, and the puncture wound healed without intervention.

She presented to the emergency room 7 days later with new pain and swelling surrounding the initial puncture wound.  There is no significant past medical history and most recent Td booster was given 2 years ago.  On examination, there was some mild erythema, swelling, and tenderness on palpation of the lateral aspect of the middle phalanx of the right hand.  She is otherwise well.  You wonder about the possibility of a retained foreign body.


 

PoCUS-Guided Approach to the Detection of Foreign Bodies in Soft Tissue

Foreign bodies in soft tissue are a common complaint in the emergency department, with open wounds comprising 5.7 million (or 4.5% of total) visits to the ED in 2010.[1]  Foreign bodies were found in up to 15% of wounds.[2]  If retained, complications of these include allergic reaction, inflammation, delayed wound healing, damage to adjacent tissue structures, neurovascular damage, tetanus, and infectious complications including cellulitis, necrotizing fasciitis, synovitis, and abscess formation.[3],[4]  Proper detection, and subsequent removal, of retained foreign bodies is therefore essential to evaluate the wound and prevent associated complications.

Diagnosis of a retained FB requires a high index of suspicion.  Clinical suspicion should be raised when there is a compelling history and physical exam.  The latter may include signs of inflammation and/or infection, including warmth, swelling, erythema, tenderness, abscess formation, and discharging wound).[5],[6]

Conventional radiography is known to commonly miss radiolucent materials such as wood and plastic.  It has been shown that plain radiographs have only a 7.4% sensitivity in the detection of wood foreign bodies.5  Remarkably, even glass – a radiopaque material – has been demonstrated to have been missed in up to 35% of x-ray film studies.[7]  There is increasingly compelling evidence for the clinical usefulness and accuracy of bedside ultrasonography in the detection of soft-tissue foreign bodies.  It has been shown to have a specificity of 92% (95% CI = 88%-95%) and sensitivity ranging from 83.3% to 100%.[8],[9]


PoCUS Technique

Probe selection: the use of a high-frequency ultrasound probe is recommended.  This allows for greater axial resolution at the expense of less penetration, which is suitable for the detection of small foreign bodies, as they typically lodge in superficial tissues.[10]

If the wound is open, a transparent covering such as a Tegaderm or probe cover can be used to cover either the wound or probe before scanning.[11]

Medium: standard technique for assessment of soft-tissue structures by ultrasound involves the use of a standoff pad or gel mound.  However, this is not always possible due to the irregular curvature of extremities such as fingers and feet, which may result in poor contact between the probe and skin, decreased field of view, and patient discomfort.  A water-bath technique can circumvent this and has been shown to be superior in such cases.[12]

Method: the area of interest should be scanned in both longitudinal and transverse planes.  Foreign bodies are best detected when the transducer aligns with the longitudinal axis of the foreign body, and therefore revealing the span of the object.[13]  As foreign bodies tend to embed less than 2 cm below the surface of the skin, the depth of field should remain superficial in order to avoid false positives.

US Probe: Ultrasound Water Bath for Distal Extremity Evaluation

 


Findings

Ultrasonography and plain film findings of foreign bodies in soft tissue are summarized in the table below.

Table 1. Ultrasound and x-ray findings of foreign bodies.6,[14],[15],[16]

Material Ultrasound findings X-ray findings
Wood Hyperechoic; may become isoechoic with surrounding tissue as it denatures over time

Posterior acoustic shadowing

Radiolucent, often undetectable
Glass Hyperechoic, bright

Posterior acoustic shadowing

± Posterior comet tail reverberation, diffuse beam scattering

Radiopaque
Plastic Hyperechoic

Posterior acoustic shadowing

Radiolucent, often undetectable
Metal Hyperechoic, bright

Posterior acoustic shadowing

± Posterior comet tail reverberation

Radiopaque

 

Foreign bodies may also display a straight or regular contour.6

 

Image 1 – Wood splinter in volar aspect digit, mildly hyperechoic, surrounding hypoechoic halo, irregular acoustic shadowing

Image 2 – Plastic FB, within tendon sheath, volar aspect digit, brightly hyperechoic, long axis

Image 3 – Plastic FB, within tendon sheath, volar aspect digit, brightly hyperechoic, short axis

 

Image 4 – Glass FB – brightly echogenic, posterior reverberation, FB long axis

 

Image 5 – Metal FB – brightly echogenic, posterior reverberation, FB long axis

 

 

It is important to note that the acoustic shadowing may be complete or partial, as this is dependent on the angle of sonography and foreign body material.[17]  It is also possible to see a hypoechoic halo around the FB, which may be suggest edema, abscess formation, granulation tissue, or other inflammatory process.[18]  As the inflammatory reaction develops, the halo effect becomes more apparent; therefore the foreign body is therefore best visualized by PoCUS several days after the initial injury.6


PoCUS-Guided Foreign Body Removal

There are several options for removal of a foreign body with PoCUS:[19]

  1. Needle localization. Once the foreign body has been identified on PoCUS, a hollow injection needle can be inserted under ultrasound guidance and local anesthetic is delivered through this.  This can be done in either the transverse or longitudinal plane.  The ultrasound probe is then removed, and an incision is made along the needle.  Through the incision site, tweezers or forceps can be used to remove the foreign body.
  2. Real-time ultrasound-guided extraction. This technique is similar to the needle localization method. However, rather than removing the transducer following the needle insertion, the entire procedure is done under direct ultrasound visualization.  The probe is held in the longitudinal plane to visualize both the forceps and the foreign body during the extraction process.

 

There is a risk of obscuring the view of the foreign body on ultrasound with air as a result of the incision itself or through anesthetic delivery.  Saline may be used to irrigate and therefore mitigate the issue.19

The patient’s tetanus status should be verified and updated, if required.  Antibiotic therapy may also be provided, should the risk of infection justify it.


Limitations

There is the possibility of false positives.  Foreign bodies must be differentiated from other hyperechoic body structures, including ossified cartilage, sesamoid bones, scar tissue, gas bubbles, and intermuscular fascia.14  Visualization is therefore important in both longitudinal and transverse planes, as well as comparison with the opposite side.  Acoustic shadowing, hypoechoic halo, and posterior comet tails, if present, can also be indicative of a FB rather than organic body tissue.

Traumatic air injection as a result of penetrating injury can create a scatter artifact on ultrasound, which can be misinterpreted as an acoustic shadow associated with a foreign body.  To differentiate this from a true acoustic shadow, pressure may be applied through the transducer to displace the scatter artifact.6

As is commonplace with all emergency ultrasonography, limitations also include the technical skill of the operator.[20]  A foreign body may also be too small to be detectable by ultrasound.  It is therefore important to remember that a negative scan does not necessarily rule out the possibility of a retained foreign body, and the history and physical examination must be considered in conjunction with the ultrasound findings.

 


 

References

[1] National Center for Health Statistics. Emergency Department Visits. Available from: http://www.cdc.gov/nchs/fastats/emergency-department.htm.

[2] Steele MT, Tran LV, Watson WA, Muelleman RL. Retained glass foreign bodies in wounds: predictive value of wound characteristics, patient perception, and wound exploration. Am J Emerg Med. 1998 Nov;16(7):627-30. DOI: 10.1016/s0735-6757(98)90161-9. PMID: 9827733.

[3] Skinner EJ, Morrison CA. Wound Foreign Body Removal. In:StatPearls. Treasure Island (FL): StatPearls Publishing; 2020. Available from: https://www.ncbi.nlm.nih.gov/books/NBK554447/.

[4] Ebrahimi A, Radmanesh M, Rabiei S, Kavoussi H. Surgical removal of neglected soft tissue foreign bodies by needle-guided technique. Iran J Otorhinolaryngol. 2013 Winter;25(70):29-36. PMID: 24303416; PMCID: PMC3846242.

[5] Levine MR, Gorman SM, Young CF, Courtney DM. Clinical characteristics and management of wound foreign bodies in the ED. Am J Emerg Med. 2008 Oct;26(8):918-22. DOI: 10.1016/j.ajem.2007.11.026. PMID: 18926353.

[6] Atkinson P, Bowra J, Harris T, Jarman B, Lewis D. Point of Care Ultrasound for Emergency Medicine and Resuscitation. Oxford, United Kingdom: Oxford University Press; 2019. DOI: 10.1093/med/9780198777540.001.0001.

[7] Kaiser, C. William MD; Slowick, Timothy MBA; Spurling, Kathleen Pfeifer RN, JD; Friedman, Sissie MA. Retained Foreign Bodies, The Journal of Trauma: Injury, Infection, and Critical Care: July 1997 – Volume 43 – Issue 1 – p 107-111.

[8] Davis J, Czerniski B, Au A, Adhikari S, Farrell I, Fields JM. Diagnostic Accuracy of Ultrasonography in Retained Soft Tissue Foreign Bodies: A Systematic Review and Meta-analysis. Acad Emerg Med. 2015 Jul;22(7):777-87. DOI: 10.1111/acem.12714. Epub 2015 Jun 25. PMID: 26111545.

[9] Atkinson P, Madan R, Kendall R, Fraser J, Lewis D. Detection of soft tissue foreign bodies by nurse practitioner-performed ultrasound. Crit Ultrasound J. 2014 Jan 29;6(1):2. DOI: 10.1186/2036-7902-6-2. PMID: 24476553; PMCID: PMC3922659.

[10] Dean AJ, Gronczewski CA, Costantino TG. Technique for emergency medicine bedside ultrasound identification of a radiolucent foreign body. The Journal of Emergency Medicine. 2003;24(3):303–8. DOI: 10.1016/S0736-4679(02)00765-5.

[11] Chen KC, Lin AC, Chong CF, Wang TL. An overview of point-of-care ultrasound for soft tissue and musculoskeletal applications in the emergency department. J Intensive Care. 2016 Aug 15;4:55. DOI: 10.1186/s40560-016-0173-0. PMID: 27529031; PMCID: PMC4983782.

[12] Krishnamurthy R, Yoo JH, Thapa M, Callahan MJ. Water-bath method for sonographic evaluation of superficial structures of the extremities in children. Pediatr Radiol. 2013 Mar;43 Suppl 1:S41-7. DOI: 10.1007/s00247-012-2592-y. Epub 2013 Mar 12. PMID: 23478918.

[13] Rooks VJ, Shiels WE 3rd, Murakami JW. Soft tissue foreign bodies: A training manual for sonographic diagnosis and guided removal. J Clin Ultrasound. 2020 Jul;48(6):330-336. DOI: 10.1002/jcu.22856. Epub 2020 May 8. PMID: 32385865.

[14] Mohammadi A, Ghasemi-Rad M, Khodabakhsh M. Non-opaque soft tissue foreign body: sonographic findings. BMC Med Imaging. 2011 Apr 10;11:9. DOI: 10.1186/1471-2342-11-9. PMID: 21477360; PMCID: PMC3079678.

[15] Lewis D, Jivraj A, Atkinson P, Jarman R. My patient is injured: identifying foreign bodies with ultrasound. Ultrasound. 2015 Aug;23(3):174-80. DOI: 10.1177/1742271X15579950. Epub 2015 Mar 26. PMID: 27433254; PMCID: PMC4760591.

[16] Campbell EA, Wilbert CD. Foreign Body Imaging. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020. Available from: https://www.ncbi.nlm.nih.gov/books/NBK470294/.

[17] Anderson MA, Newmeyer WL 3rd, Kilgore ES Jr. Diagnosis and treatment of retained foreign bodies in the hand. Am J Surg. 1982 Jul;144(1):63-7. DOI: 10.1016/0002-9610(82)90603-1. PMID: 7091533.

[18] Little CM, Parker MG, Callowich MC, Sartori JC. The ultrasonic detection of soft tissue foreign bodies. Invest Radiol. 1986 Mar;21(3):275-7. DOI: 10.1097/00004424-198603000-00014. PMID: 3514541.

[19] Paziana K, Fields JM, Rotte M, Au A, Ku B. Soft tissue foreign body removal technique using portable ultrasonography. Wilderness Environ Med. 2012 Dec;23(4):343-8. DOI: 10.1016/j.wem.2012.04.006. Epub 2012 Jul 25. PMID: 22835803.

[20] Pinto A, Pinto F, Faggian A, Rubini G, Caranci F, Macarini L, Genovese EA, Brunese L. Sources of error in emergency ultrasonography. Crit Ultrasound J. 2013 Jul 15;5 Suppl 1(Suppl 1):S1. DOI: 10.1186/2036-7902-5-S1-S1. Epub 2013 Jul 15. PMID: 23902656; PMCID: PMC3711733.

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Periorbital Inflammation – Red Eye – Red Flags

 

Medical Student Clinical Pearl

Alysha Roberts

MD Candidate, Class of 2021

Dalhousie University

@aeroberts_21

Reviewed & Edited by Dr David Lewis (@e_med_doc)

All case histories are illustrative and not based on any individual.


Case

A 40 year old male presents to the emergency department with a red, swollen eye. Without a known trigger, he had a one day history of progressive pain, erythema, and edema surrounding his left eye. He denied any fever or chills or visual changes, or headache. A thorough review of systems was negative, except for a complaint of worsening pain with extraocular movement.

On exam, he was afebrile and his vital signs were within normal limits. His visual acuity was normal, and pupils were equal and reactive to light. Extraocular movements were intact but associated with worsening pain. The periorbital tissue was erythematous, edematous, and hot to touch. Examination is limited by the severity of the patient’s swelling. Figure 1 illustrates an example of a patient with severe, unilateral eyelid swelling and erythema.

You suspect periorbital cellulitis.

Figure 1. Unilateral eyelid edema. Retrieved from https://www.merckmanuals.com/professional/eye-disorders/orbital-diseases/preseptal-and-orbital-cellulitis


 

Periorbital Versus Orbital Cellulitis

Periorbital cellulitis, commonly referred to as pre-septal cellulitis, is an infection of the skin and soft tissue surrounding the orbit. Most commonly, it is the result of an infection spreading from the sinuses or from local trauma.1,2 It presents as a unilateral swelling of the eye-lid. Both periorbital and orbital cellulitis are most commonly caused by Staphylococcus Aureus and Streptococcus Pneumoniae. It is important to distinguish periorbital from orbital cellulitis, which is an infection of the orbit itself extending beyond the orbital septum. Orbital cellulitis is a sight-threatening emergency, and urgent imaging should be acquired in addition to consultation with ophthalmology or otolaryngology.3 Other complications of orbital cellulitis include orbital or subperiosteal abscess, and cavernous sinus thrombosis. Figure 2 illustrates the difference between periorbital (preseptal) and orbital cellulitis, as well as its complications.

Figure 2. Orbital anatomy and potential complications from orbital cellulitis. Retrieved from https://www.merckmanuals.com/professional/eye-disorders/orbital-diseases/preseptal-and-orbital-cellulitis

Any patient with unilateral eyelid edema should be evaluated for red flags of orbital cellulitis, given its potential seriousness. Red flag signs and symptoms include:3,4

  • Painful or restricted extraocular movements
  • Reduced visual acuity
  • Relevant afferent pupillary defect
  • Diplopia
  • Proptosis
  • Chemosis
  • Severe headache

 

Differential Diagnosis

Other considerations for the differential diagnosis in a unilateral, swollen red eye include:5

  • Periorbital ecchymosis due to blunt trauma
  • Contact dermatitis secondary to local irritant
  • Atopic dermatitis due to allergic sensitivity
  • Orbital tumors

 

Risk Factors

Risk factors for periorbital and orbital cellulitis include:6

  • Sinusitis
  • Dental infection
  • Insect bite
  • Trauma

 

Periorbital cellulitis is most commonly caused by an insect bite in children, and trauma in adults. Comparatively, orbital cellulitis is most often the result of trauma in children, and sinusitis in adults.


 

Diagnostic Investigations

Patients who are febrile or appear unwell should have early initiation of IV antibiotics following blood cultures. Though periorbital cellulitis is a clinical diagnosis, if there is suspicion for orbital cellulitis a CT scan of the orbits and sinuses is the gold standard. Positive findings include inflammation of extraocular muscles, anterior globe displacement, and fat stranding. Inflammation of the sinuses should not be used to differentiate periorbital from orbital cellulitis, as up to 41% of cases of periorbital cellulitis may have CT evidence of sinusitis. Figure 3 displays a labelled CT image with common findings in orbital cellulitis.7

 

Figure 3. Orbital CT image with labels. Retrieved from https://ctscanmachines.blogspot.com/2018/07/ct-scan-of-periorbital-cellulitis.html

In addition to CT imaging, there may be a role for point of care ultrasound (PoCUS) in the diagnosis and management of periorbital and orbital cellulitis. However, research is currently lacking on whether its use may avoid the need for further diagnostic imaging.8 Findings from pediatric emergency medicine suggest that orbital ultrasound may be preferred in evaluating young patients who are unable to cooperate with a thorough physical examination.9 One important application of orbital PoCUS is in the assessment of orbital abscesses. Subperiosteal abscesses may complicate more than 50% of cases of orbital cellulitis, and are not reliably detected by CT.10 Additionally, orbital ultrasound may be an appropriate alternative in settings where advanced imaging is not available, in order to guide early initiation of antibiotics.

Orbital Abscess from – The PoCUS Atlas


 


 

Treatment Best Practices  

Antibiotic choice should be guided by local susceptibility guidelines. An appropriate choice would cover S. aureus, S. pyogenes, and anaerobes.11,12 In this case, we initiated intravenous ceftriaxone and metronidazole while awaiting CT results.

The following therapeutic guidelines are from Bugs and Drugs – It is recommended that that guidelines for therapy are accessed directly from their website or from other reputable sources.

Periorbital Cellulitis

 

Orbital Cellulitis

From Bug and Drugs

 


Case Conclusion

Given this patient’s complaint of increased pain with extraocular movement, a CT orbit was performed. Fortunately, there were no signs of orbital cellulitis. The patient was treated with IV ceftriaxone and metronidazole and scheduled to return to the emergency department the next day for re-evaluation and consideration of step-down to oral antibiotics.


Summary

Orbital cellulitis is a serious condition that should be carefully distinguished from periorbital cellulitis. On history, clinicians should ensure they inquire about recent sinus or dental infections, trauma to the orbit, or possible insect bites. Physical exam should carefully assess for signs of orbital cellulitis, including proptosis, chemosis, and limited extraocular movements. Any positive red flag or clinical suspicion warrants a CT scan of the orbits and sinuses to exclude orbital cellulitis.


Further Reading

Great photo article in Canadian Family Physician

Management algorithm

Patient Information Leaflet

 

 


 

References

  1. Preseptal and Orbital Cellulitis – Eye Disorders – Merck Manuals Professional Edition. (n.d.).Retrieved January 12, 2021, from https://www.merckmanuals.com/professional/eye-disorders/orbital-diseases/preseptal-and-orbital-cellulitis
  2. Lightning Learning: Orbital Cellulitis — #EM3: East Midlands Emergency Medicine Educational Media. (n.d.). Retrieved January 12, 2021, from https://em3.org.uk/foamed/7/5/2019/lightning-learning-orbital-cellulitis
  3. Periorbital cellulitis — entsho.com. (n.d.). Retrieved January 12, 2021, from https://entsho.com/periorbital-cellulitis
  4. Distinguishing Periorbital from Orbital Cellulitis. (2003). American Family Physician, 67(6), 1349.
  5. Differential Diagnosis of the Swollen Red Eyelid – American Family Physician. (n.d.). Retrieved January 12, 2021, from https://www.aafp.org/afp/2015/0715/p106.html
  6. Risk factors of preseptal and orbital cellulitis – PubMed. (n.d.). Retrieved January 12, 2021, from https://pubmed.ncbi.nlm.nih.gov/19149979/
  7. Ct Scan Of Periorbital Cellulitis – ct scan machine. (n.d.). Retrieved January 12, 2021, from https://ctscanmachines.blogspot.com/2018/07/ct-scan-of-periorbital-cellulitis.html
  8. Kang, T. L., Seif, D., Chilstrom, M., & Mailhot, T. (2014). Ocular ultrasound identifies early orbital cellulitis. Western Journal of Emergency Medicine, 15(4), 394. https://doi.org/10.5811/westjem.2014.4.22007
  9. Seguin, J., Le, C.-K., Fischer, J. W., Tessaro, M. O., & Berant, R. (2019). Ocular Point-of-Care Ultrasound in the Pediatric Emergency Department. Pediatric Emergency Care, 35(3), E53–E58. https://doi.org/10.1097/PEC.0000000000001762
  10. Derr, C., & Shah, A. (2012). Bedside ultrasound in the diagnosis of orbital cellulitis and orbital abscess. Emergency Radiology, 19(3), 265–267. https://doi.org/10.1007/s10140-011-0993-0
  11. Orbital Cellulitis – StatPearls – NCBI Bookshelf. (n.d.). Retrieved January 12, 2021, from https://www.ncbi.nlm.nih.gov/books/NBK507901/
  12. Periorbital Cellulitis – StatPearls – NCBI Bookshelf. (n.d.). Retrieved January 12, 2021, from https://www.ncbi.nlm.nih.gov/books/NBK470408/
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A case of cholecystitis

Medical Student Clinical Pearl

Alana Jewell

M.D. Candidate, Class of 2022

Memorial University Faculty of Medicine

Reviewed & Edited by Dr. Mandy Peach

All case histories are illustrative and not based on any individual.

 

Case Presentation

A 70-year-old gentleman presented with four days of right upper abdominal pain radiating to the LUQ with nausea + vomiting, anorexia, flatulence, and bloating. Patient has PMHx of Crohn’s disease with a history of small bowel obstruction (SBO) and multiple surgeries. He felt these symptoms were like his SBO but he continued to have normal bowel movements. He had a similar episode a few months ago after eating fast food, but did not seek care for.

You suspect cholecystitis.

 

Differential Diagnosis

Can’t miss diagnoses for atraumatic abdominal pain 4:

ruptured AAA
pancreatitis
cholangitis
mesenteric ischemia
obstruction
perforated viscus
complicated diverticulitis
ruptured ectopic pregnancy

Differential for RUQ pain :

hepatitis
biliary colic
cholecystitis
cholangitis
pancreatitis
pneumonia
pleural effusion
pulmonary embolism

 

There is no single exam finding or laboratory test that has the ability to rule out acute cholecystitis5.

 

A combination of clinical evaluation, laboratory values, and diagnostic imaging are key to differentiate abdominal pain and make a diagnosis.

 

Cholecystitis

Cholecystitis is defined as inflammation of the gallbladder, typically caused by persistent stone obstruction in the cystic duct.

Acute cholecystitis (AC): Stone obstruction leads to bile trapping, increased intraluminal pressure, and an acute inflammatory process, typically presenting with RUQ pain, leukocytosis, and fever1.

Chronic cholecystitis: defined as recurrence of these events and is associated with fibrosis and mucosal atrophy2.

Acalculous cholecystitis: consider in chronically debilitated patients, classically elderly patients in ICU on total parental nutrition after sustained trauma or significant burn injury11.

Ascending (or acute) cholangitis: an important complication of cholecystitis – a serious bacterial infection of the common bile duct. It presents with Charcot’s triad of fever, jaundice, and abdominal pain2.

 

Acute cholecystitis is diagnosed and graded on severity by using the Tokyo Guidelines3.

 

 

 

Gallstones (which cause 95% of acute cholecystitis) are common in Western society, with about 10% of people affected, and 80% of those affected being asymptomatic1,3. The risk of pain or complications is 1-4% per year2.

 

Risk factors for cholesterol gallstones (the most common type) 2:

increased age
female gender
pregnancy
parity
race
high calorie
low fibre diet
low activity
obesity

 

 

 Clinical Presentation and findings

Clinical presentation varies with severity.

On history, a patient may have anorexia, emesis, fever, nausea, and RUQ pain.  On examination, guarding, Murphy’s sign (pain upon deep inspiration while palpating RUQ), rebound tenderness, abdominal rigidity, and RUQ tenderness may be seen2. Patients may describe a history of biliary colic, but with the presenting episode being more severe and longer in duration.

Mild-moderate cases have RUQ pain, fever, leukocytosis, and may have a palpable mass in the RUQ2. The most severe patients may have jaundice and, if have a secondary bacterial infection, could have signs of sepsis.

 

Case Continued

 

Physical Exam

Patient was tender to light palpation over RUQ and epigastric region. No rigidity, rebound tenderness, or guarding was noted.

Bloodwork

  • Elevated WBC with neutrophilic shift
  • C reactive protein > 250
  • Normal lipase, liver enzymes and renal function.

The most common laboratory findings in acute cholecystitis are an increased CRP and leukocytosis2.

 

This patient requires imaging to confirm the suspected diagnosis.

 

Diagnostic Imaging

Ultrasound

Ultrasound is the first-choice modality for imaging of AC. It is easily available in any emergency department, cost-effective, and minimally invasive3. Ultrasound findings can include5,6,9, as seen below 6.

 GB wall thickening > 3.5 mm
pericholecystic fluid
biliary sludge
gallstones
sonographic Murphy sign

 

If an ultrasound is positive, there is no need for further testing.

If negative, a CT should be ordered to exclude other diagnoses2,7.

 

CT findings for AC may include 3,6 as seen below 2:

thickening of GB wall
enlargement of GB
gallstones in GB neck or cystic duct
fluid accumulation around GB
pericholecystic fat stranding

 

Many gallstones are not radiopaque and may be missed on CT7

 

Management

Assessment with Tokyo Guideline diagnostic criteria can be used every 6-12 hours until a diagnosis is clear if initially uncertain, and to check severity until surgical management8.

In the Emergency Department, a patient is best managed with supportive care.

IV fluids,
NPO
Analgesia (NSAIDs are first-line treatment for AC. If ineffective, opioids are second line2. )

 

Secondary infection can result from bile stasis. Empiric antibiotics may be started against E. coli, Klebsiella, and Enterococcus5.

Definitive treatment for AC is cholecystectomy, with the gold standard being done laparoscopically (lap-C)2,7. Having a lap-C within 24-72 hours of symptom onset is recommended to decrease complication rates. If left unoperated for more than 72 hours chronic inflammation may occur, potentially complicating the surgery1. If a patient is ineligible for surgery, percutaneous cholecystostomy (gallbladder drainage) may be performed7.

 

Case Conclusion

Formal ultrasound found a hydropic gallbladder with pericholecystic fluid, thickened wall, and stranding. Cholecystitis was diagnosed. The patient was given analgesia and covered with ceftriaxone and metronidazole10. He went on to have an uncomplicated lap cholecystectomy.

 

References

  1. Indar, Adrian A, and Beckingham, Ian J. “Acute Cholecystitis.” BMJ, vol. 325, no. 7365, 2002, pp. 639–643.
  2. Wilkins, Thad, MD, MBA, et al. “Gallbladder Dysfunction: Cholecystitis, Choledocholithiasis, Cholangitis, and Biliary Dyskinesia.” Primary Care, vol. 44, no. 4, 2017, pp. 575–597.
  3. Yokoe, Masamichi, et al. “Tokyo Guidelines 2018: Diagnostic Criteria and Severity Grading of Acute Cholecystitis (with Videos).” Journal of Hepato-Biliary-Pancreatic Sciences, vol. 25, no. 1, 2018, pp. 41–54.
  4. Anjum, Omar, et al. “Ottawa’s Clerkship Guide to Emergency Medicine.” Department of Emergency Medicine, University of Ottawa, Mar. 2018.
  5. Jain, Ashika, et al. “History, Physical Examination, Laboratory Testing, and Emergency Department Ultrasonography for the Diagnosis of Acute Cholecystitis.” Academic Emergency Medicine, vol. 24, no. 3, 2017, pp. 281–297.
  6. Chawla, Ashish, et al. “Imaging of Acute Cholecystitis and Cholecystitis-Associated Complications in the Emergency Setting.” Singapore Medical Journal, vol. 56, no. 8, 2015, pp. 438–444.
  7. Bagla, Prabhava, et al. “Management of Acute Cholecystitis.” Current Opinion in Infectious Diseases, vol. 29, no. 5, 2016, pp. 508–513.
  8. Mayumi, Toshihiko, et al. “Tokyo Guidelines 2018: Management Bundles for Acute Cholangitis and Cholecystitis.” Journal of Hepato-Biliary-Pancreatic Sciences, vol. 25, no. 1, 2018, pp. 96–100.
  9. Flemming, Lewis & Henneberry (2017). PoCUS – Measurements and Quick Reference http://sjrhem.ca/pocus-measurements-quick-reference/
  10. Bugs & Drugs Medical App
  11. Forsythe (2016). Cholecystitis. First Aid for the Emergency Medicine Boards, Third Edition: Abdominal and Gastrointestinal Emergencies. McGraw-Hill Education. China.

 

 

 

 

 

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A Case of Ectopic Pregnancy

 

Medical Student Clinical Pearl – December 2020

Marisa O’Brien

@mbob58

MD Candidate, Class of 2021

Memorial University of Newfoundland

Reviewed and Edited by Dr. David Lewis

All case histories are illustrative and not based on any individual

 


Case Report

A 36-year-old G2P1 female presented to the Emergency Department following a pre-syncopal episode at work. The patient noted a sudden onset of significant abdominal cramping, nausea, and vaginal bleeding with clots that morning followed by an episode of lightheadedness while sitting at her desk. The patient denied any loss of consciousness, no dyspnea, no chest pain, no palpitations, and no fevers/chills. She had no known allergies and no current medications. She was a non-smoker and denied any alcohol or drug usage.

The patient’s past medical history was significant for recent treatment with methotrexate for an ectopic pregnancy eight days prior. The patient had a history of amenorrhea for 7 weeks and a serum β-hCG of 302 mlU/mL at that time. A transvaginal ultrasound was performed at 8 weeks for abdominal pain and light spotting which revealed an IUD in situ with no evidence of an intrauterine pregnancy. An early ectopic pregnancy was diagnosed and the patient was consented to receive medical management with methotrexate. She was followed up with serial β-hCG’s which gradually, but slowly, trended down to 110 mIU/ml by day 6. The patient noted slight abdominal cramping and PV bleeding following the methotrexate however this had settled after 3 days with no ongoing symptoms until today.

On initial assessment, the patient appeared well, no acute distress, and all vital signs were stable.  The abdominal exam revealed bowel sounds present in all four quadrants and the abdomen was tympanic to percussion. On palpation the abdomen was soft and nondistended with LLQ and suprapubic tenderness however, no guarding or rebound tenderness was appreciated.

Initial investigations included a CBC, β-hCG, PT & PTT, type and screen, urinalysis, EKG, & POCUS.

 


Definition

An ectopic pregnancy occurs when a fertilized egg implants at a site other then the endometrium of the uterus, most commonly the fallopian tubes. They often present as vaginal bleeding and/or abdominal pain in the setting of a positive β-hCG.1

A critical complication is a ruptured ectopic pregnancy which occurs by erosion through the tissue the zygote has implanted in resulting in intraabdominal bleeding from the exposed vessel and possible hypovolemic shock.2 Rupture should be suspected in patients presenting with hemodynamic instability including syncope, hypotension, and tachycardia. However, young healthy females may appear vitally stable initially due to compensatory mechanisms. Additional physical exam findings suggestive of a ruptured ectopic pregnancy include severe abdominal pain with guarding or rebound tenderness and abdominal distention. Pain may radiate to the shoulder due to irritation of the diaphragm from blood in the peritoneal cavity.1,3

 


Risk factors for ectopic pregnancy4

  • Previous ectopic pregnancy
  • Prior fallopian tube surgery
  • Previous pelvic or abdominal surgery
  • Sexually transmitted infections
  • Pelvic inflammatory disease
  • Endometriosis
  • Cigarette smoking
  • Maternal age > 35 years
  • History of infertility
  • Assisted reproductive technology (IVF)

 

 


Differential diagnosis for vaginal bleeding in early pregnancy1:

  • Physiologic
  • Spontaneous abortion
  • Cervical, vaginal, or uterine pathology
  • Subchorionic hematoma
  • Heterotopic pregnancy
  • Gestational trophoblastic disease

 


Sonography

According to the discriminatory zones, an intrauterine pregnancy is expected to be visualized on a transvaginal ultrasound at β-hCG levels of 1500 – 2000 mlU/mL and on a transabdominal ultrasound at levels of 4000 – 6500 mlU/mL.5

Gestational Age Β-hCG range (mlU/mL)
<1 week 5 – 50
1-2 weeks 50 – 500
2-3 weeks 100 – 5000
3-4 weeks 500 – 10,000
4-5 weeks 1000 – 50,000
5-6 weeks 10,000 – 100,000
6-8 weeks 15,000 – 200,000
8-12 weeks 10,000 – 100,000

Table 1: Estimated β-hCG levels in relation to gestational age.3

In the first trimester of a normal pregnancy, the serum β-hCG should increase by ≥ 53% every 48 hrs until 41 days of gestation.1,3 Serum β-hCG will then continue to rise more slowly until approximately 10 weeks after which it will begin to decline until reaching a plateau. Serum β-hCG levels are noted to raise more slowly in an ectopic pregnancy, thus a slower rate of increase, plateau, or decline in serum β-hCG in the first 41 days suggests a possible miscarriage or ectopic pregnancy.1

Note on β-hCG Discriminatory Zones

The value of discriminatory zones in the emergency management of ectopic pregnancy is low, with many considering it unreliable and potentially dangerous. In short, a low β-hCG does not exclude an ectopic. This useful post provides a good summary on ectopic rule-out in the ED:

Rule Out Ectopic in the Emergency Department

 

An intrauterine pregnancy is confirmed by visualization of a gestational sac and a yolk sac within the uterus (juxtaposed to bladder).1 A gestational sac alone is not sufficient for diagnoses of an intrauterine pregnancy as it may be a pseudogestational sac formed by hormonal stimulation from an ectopic pregnancy.5 Additionally, if an intrauterine pregnancy is visualized, a heterotopic pregnancy should also be considered.1 The risk of heterotopic pregnancy when conceived normally is estimated to be 1 in 30,000.

Figure 1: Visualization of an intrauterine pregnancy on a transvaginal ultrasound.3

 

 

Structure Transvaginal Ultrasound Transabdominal Ultrasound
Gestational Sac 4.5-5 weeks 5.5-6 weeks
Yolk Sac 5-5.5 weeks 6-6.5 weeks
Fetal Pole 5.5-6 weeks 7 weeks
Cardiac Activity 6 weeks 7 weeks
Fetal Parts 8 weeks >8 weeks

Table 2: Ultrasound findings based on gestational age.5

 


Diagnosis of Ectopic Pregnancy

An ectopic pregnancy is suspected in all women with a positive pregnancy test when no intrauterine pregnancy is visualized on ultrasonography. A low β-hCG or declining β-hCG does not exclude an ectopic. Ultrasound findings of an ectopic pregnancy may include an extrauterine gestational sac or embryonic cardiac activity outside of the uterus, a complex adnexal mass, or intraperitoneal fluid.3

From emupdates.com

 


Management of Ectopic Pregnancy

Is the patient unstable?

  • If the patient is hemodynamically unstable (tachycardia or hypotension or pale or syncopal) then commence immediate resuscitation (IV Access, CBC, type & crossmatch,  iv fluids, transfusion, etc) and stat consult to ObGyn.

In stable patients

  • Consult ObGyn
  • The gold-standard of treatment for ectopic pregnancy is surgical management however, treatment options include expectant, or medical management.6 Medical management with methotrexate, a folic acid antagonist that inhibits DNA synthesis and cell production, has a higher success rate when initiated at lower β-hCG levels. Methotraxate is initiated if β-hCG is <5000 mlU/mL and is reserved for those with reliable follow up as β-hCG levels are required to be trended until they are undetectable. Individuals with renal disease, hepatic disease, active pulmonary disease, or immunodeficiencies are not candidates for methotrexate.3,7 Individuals who do not meet the criteria for medical management, are hemodynamically unstable, have failed methotrexate, or a ruptured ectopic is suspected, will receive surgical management.6

 


Case Report Continued

The patient was hemodynamically stable on presentation. Her vital signs were normal. As part of the initial assessment, PoCUS was used to further evaluate for the presence of free fluid in the abdomen or pelvis. Free fluid was identified in the RUQ in both Morrison’s pouch and surrounding the caudal tip of the liver. Intraperitoneal fluid was also seen in the LUQ in both the subphrenic and splenorenal spaces. Free fluid was also visualized in Douglas’ pouch in the pelvic view.

RUQ

LUQ

Pelvis

 

Throughout the PoCUS examination the patient remained well appearing, however she had become hypotensive with a blood pressure of 90/53 mmHg. Her initial bloodwork had come back at this time revealing a β-hCG of 32 mlU/mL and a Hgb of 67 g/L. The patient received 1g of TXA, and a 1L bolus of normal saline while PRBC’s were ordered. She was documented to be Rh+ thus, she did not require RhoGAM (anti-D immune globulin). An urgent consultation to Obstetrics and Gynecology was made following the visualization of intraabdominal fluid and the patient underwent an exploratory laparotomy shortly after.

 


Key Points

  • Ectopic pregnancy should be considered in the differential diagnosis of any female patient, of childbearing age, presenting with abdominal pain, syncope or shock
  • An Intrauterine contraceptive device does not exclude an ectopic
  • Unless a previous ultrasound has documented the presence of an intrauterine pregnancy, an empty uterus in a patient with a positive pregnancy test should be considered to be a possible ectopic until ruled out
  • An intrauterine pregnancy on ultrasound requires the following to be confirmed:
    • A gestational sac and a yolk sac, in the uterus which is juxtaposed to the bladder
    • or a gestational sac containing a normal fetal pole, in the uterus which is juxtaposed to the bladder
  • A low β-hCG or declining β-hCG does not exclude an ectopic
  • Medical management of ectopic pregnancy with methotrexate requires close follow-up. Failure can occur. Ruptured ectopic pregnancy can still occur.

 


Further Reading

Ectopic Pregnancy and Ruptured Ectopic: Pitfalls in Diagnosis

ED Rounds – Early Pregnancy

The Pregnant ED Patient – A Compendium of Pearls

 

 


References

  1. Tulandi, T. (2020, November 2). Ectopic pregnancy: Clinical manifestations and diagnosis. Retrieved from: https://www.uptodate.com/contents/ectopic-pregnancy-clinical-manifestations-and-diagnosis?search=ectopic%20pregnancy&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1#H1
  2. Toy, E.C., Simon, B.C., Takenaka, K.Y., Liu, T.H., & Rosh, A.J. (2017). Ectopic Pregnancy. Case Files Emergency Medicine. (4th, pp. 369-376). McGraw-Hill Education.
  3. Hang, B.S. (2016). Obstetrics and Gynecology. Tintinalli’s Emergency Medicine: A Comprehensive Guide. (8th, pp. 629-633). McGraw-Hill Education.
  4. The American College of Obstetricians and Gynecologists. (2018, February). Retrieved from: https://www.acog.org/womens-health/faqs/ectopic-pregnancy
  5. Leonard, N.J. (2019, January 23). The Pregnant Pelvic POCUS. EMRounds. Retrieved from: https://emrounds.org/the-pregnant-pelvic-pocus/
  6. Tulandi, T. (2020, March 31). Ectopic pregnancy: Choosing a treatment. Retrieved from: https://www.uptodate.com/contents/ectopic-pregnancy-choosing-a-treatment?search=ectopic%20pregnancy&topicRef=5407&source=see_link#H2976630177
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Small Bowel Obstruction & PoCUS

Small Bowel Obstruction & PoCUS – Medical Student Pearl

Patrick Rogers, Clinical Clerk (CC3)

Memorial University of Medicine Class of 2021

Reviewed by Dr. Kavish Chandra

Small bowel obstructions (SBO) are a common cause of acute abdominal pain in emergency departments across Canada. Diagnostic imaging plays a key role in the diagnosis and management of SBO as the history, clinical examination and laboratory investigations lack the sensitivity and specificity needed. Furthermore, diagnostic imaging may help differentiate SBO from other causes of abdominal pain (hernias, malignancies, intussusception, etc).

Historically, plain film abdominal radiography (AXR) has been an initial investigation in emergency departments when an SBO is suspected.  However, the current literature suggests that abdominal radiography is a relatively poor test for the diagnosis or exclusion of SBO when compared to other available modalities like US, CT, or MRI. In fact, multiple studies argue for the reduction of abdominal x-rays, especially when patients come in presenting with general abdominal tenderness. 1 Fortunately, there exists a compelling alternative: point of care ultrasound (PoCUS), and is being increasingly used as a first line investigation for SBO. 2

There are several reasons why physicians may start to choose PoCUS over traditional diagnostic modalities:

  • PoCUS avoids the radiation exposure that patients receive from cumulative plain films and abdominal CT’s. 3
  • PoCUS has been shown to reduce time to diagnosis and treatment in comparison to abdominal plain films. 3
  • PoCUS is more sensitive/specific modality when compared to abdominal plain film. 4
  • PoCUS allows for serial examination in the ED. 5
  • PoCUS may be rapidly available to centers with limited access to CT scanner. 6

The current evidence is highly favorable for the diagnostic efficacy of PoCUS in SBO. Here are the findings of peer-reviewed studies on the subject (published between 2013-2020):

  • PoCUS has high diagnostic accuracy and may also decrease time to diagnosis of SBO in comparison to other imaging modalities like CT and plain film.2
  • PoCUS has been found to have superior diagnostic accuracy for SBO in comparison to plain abdominal radiography. 4
  • PoCUS has been shown to be an accurate tool in the diagnosis of SBO with a consistently high sensitivity of 94-100% and specificity of 81-100%. 5
  • Current evidence suggests PoCUS is comparable in sensitivity and specificity to a CT scan when diagnosing SBO. 6
  • Ultrasound was found to be equivalent to CT in terms of diagnostic accuracy with a sensitivity of 92.31% (95% CI, 74.87% to 99.05%) and a specificity of 94.12% (95% CI, 71.31% to 99.85%) in the diagnosis of SBO. 7
  • In a study comparing XR, US, CT, and MRI, the abdominal x-ray was shown to be to be the least accurate imaging modality for the diagnosis of SBO. AXR’s were found to have a positive likelihood ratio of 1.64 (95% CI 1.07 to 2.52). In contrast, CT and MRI were both quite accurate in diagnosing SBO with positive likelihood ratios of 3.6 (95% CI = 2.3 to 5.4) and 6.77 (95% CI = 2.13 to 21.55). The use of ultrasound was found to have a positive likelihood ratio of 9.55 (95% CI = 2.16 to 42.21) and a negative likelihood ratio of 0.04 (95% CI = 0.01 to 0.13) for beside scans. 4

There are two major barriers identified in the literature that may prevent the effective use of PoCUS in the diagnosis of SBO. First, not every emergency physician has been trained on the use of PoCUS. Fortunately, two recent studies show that even minimally trained ED physicians can use it accurately. 8 Secondly, some surgeons have argued that PoCUS does not show the location of the obstruction accurately. This becomes a concern when the care team elects for surgical management of the patient’s SBO. However, recent evidence suggests that PoCUS may lead to quicker time to diagnosis and enteric tube insertion in conservative management. 8

Finally, how can learners use this technology? 5 Here are some specific sonographic findings to look for when evaluating a patient for SBO with US:

 

  • Dilatation of small bowel loops > 25 mm *
  • Altered intestinal peristalsis *
  • Increased thickness of the bowel wall
  • Intraperitoneal fluid accumulation

Figure 1. Dilatation of small bowel loops. Image courtesy Dr. Kavish Chandra

Figure 2. Altered intestinal peristalsis*. Image courtesy Dr. Kavish Chandra

Figure 3. – abnormal peristalsis “to and fro”9

References

  1. Denham G, Smith T, Daphne J, Sharmaine M, Evans T. 2020. Exploring the evidence-practice gap in the use of plain radiography for acute abdominal pain and intestinal obstruction: a systematic review and meta-analysis. International Journal of Evidence Based Healthcare. DOI: 10.1097/XEB.0000000000000218
  2. Guttman J, Stone M, Kimberly H, Rempell J. 2015. Point of care ultrasonography for the diagnosis of small bowel obstruction in the emergency department. CJEM. DOI: 10.2310/8000.2014.141382
  3. Flemming H, Lewis D. 2016. SBO- A New Focus for PoCUS. Saint John Regional Hospital Department of Emergency Medicine
  4. Taylor M, Lalani N. 2013. Adult small bowel obstruction. Academic Emergency Medicine. DOI: 10.1111/acem.12150
  5. Pourman A, Dimbil U, Shokoohi H. 2018. The accuracy of point of care ultrasound in detecting small bowel obstruction in emergency department. Emergency Medicine International. DOI: 10.1155/2018/3684081
  6. Gottlieb M, Peska, G, Pandurangadu A, Nakitende D, Takhar S, Seethala R. 2018. Utilization of ultrasound for the evaluation of small bowel obstruction: A systematic review and meta-analysis. The American Journal of Emergency Medicine. DOI: 10.1016/j.ajem.2017.07.085
  7. Tamburrini S, etal. 2019. Diagnostic accuracy of ultrasound in the diagnosis of small bowel obstruction. Diagnostics. DOI: 10.3390/diagnostics9030088
  8. Carpenter C. 2013. The end of X-Rays for suspected small bowel obstruction? Using evidence-based diagnostics to inform best practices in emergency medicine. Academic Emergency Medicine. https://doi.org/10.1111/acem.12143
  9. The PoCUS Atlas. https://www.thepocusatlas.com/bowel-gi

Copyedited by Dr. Mandy Peach

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