Drop it like it’s Hot – Tetracaine eye drops following corneal abrasion?

Drop it like it’s Hot- A case presentation and critical appraisal on the use of tetracaine eye drops following corneal abrasion: A Medical Student Pearl

Claudia Cullinan

DMNB, Med 3

Reviewed by Dr. Kavish Chandra


Case:

It’s a sunny July afternoon and you are just starting your shift in the ED when a 25-year-old male presents with sudden onset of severe right eye pain. You bring him into the exam room, and he explains he ran into a tree branch. He is reluctant to open his eye due to the pain and his eye is watering uncontrollably. He also keeps his sunglasses on while you talk because his eye is now extremely sensitive to the bright ED lights.

The patient is visibly in a lot of distress, so you do a quick penlight exam and attempt to assess visual acuity to confirm there is no evidence of penetrating trauma.

At this point you suspect a corneal abrasion, so you move onto a slit lamp and fluorescein examination and add a tetracaine 0.5% (topical anesthetic) to the affected eye. The patient appears more comfortable within seconds. You are able to complete the exam with the patient sitting comfortably in the exam chair. There is no evidence of Seidel sign (streaming fluorescein caused by leaking aqueous humor) and no visible foreign body in the eye. You can visualise a linear yellow lesion along the lateral cornea when viewed with fluorescein under cobalt blue light and you are confident this is a simple corneal abrasion.


Figure 1. Corneal abrasion viewed with cobalt blue light after fluorescein staining. Accessed from DFOptometrists.com


You explain to the patient that he has a corneal abrasion, prescribe him erythromycin 0.5% ophthalmic ointment to be inserted into the affected eye QID for 5 days and encourage him to avoid rubbing his eyes. He can also take PRN ibuprofen if needed. He asks “That one eye drop made my eye feel so much better, can I have a bottle of that to bring home?”

You know he is talking about Tetracaine, and you remember learning about the controversy of using topical anesthetics for the outpatient treatment of corneal abrasions….what do you tell him?


Critical Appraisal : Short-term topical tetracaine is highly efficacious for the treatment of pain caused by corneal abrasions: a double-blind, randomized clinical trial. (2020)

Background:

Corneal abrasions are among the most common ophthalmic presentations to the emergency department (ED). They occur when the corneal epithermal becomes disrupted, such as when tiny foreign bodies land in your eye or when your new puppy accidentally scratches the surface of your eye.  Although corneal abrasions typically heal rapidly with minimal risk of complication, they are often VERY painful and can be extremely debilitating. There has been controversy on whether patients should be discharged home with topical anesthetics for short term management of corneal abrasions because of previously described safety concerns regarding toxicity. However, recent literature is beginning to surface suggesting there may be a role for short term topical analgesia following simple corneal abrasion, with appropriate follow up.

Figure 2. Anatomy of the cornea. Accessed form AAFP.org

Clinical Question:

How effective is the home use of topical tetracaine every 30 minutes PRN pain for 24 hours following corneal abrasion?

Reference

Shipman, S., Painter, K., Keuchel, M., & Bogie, C. (2021). Short-Term Topical Tetracaine Is Highly Efficacious for the Treatment of Pain Caused by Corneal Abrasions: A Double-Blind, Randomized Clinical Trial. Annals of Emergency Medicine, 77(3), 338–344.       https://doi.org/10.1016/j.annemergmed.2020.08.036


Study Overview:

Population: Patients 18-80 years old presenting to an urban ED in Oklahoma City with suspected acute corneal abrasion.

Intervention: 2mL bottle of Tetracaine 0.5% one drop applied q30 minutes PRN pain for a maximum of 24 hours + antibiotic ophthalmic solution (polymyxin B sulfate/ trimethoprim sulfate) 2 drops to affected eye q4h.

Control: 4 separate 0.5mL ampules of artificial tears (Systane) one drop applied q30 minutes PRN pain for a maximum of 24 hours + antibiotic ophthalmic solution (polymyxin B sulfate/ trimethoprim sulfate) 2 drops to affected eye q4h.

Outcome: Pain rating at 24-48h follow up.

Methods:

  • Prospective, double blind, randomised control trial of topical tetracaine vs control (artificial tears) in the ED following diagnosis of corneal abrasion in the ED.
  • Took place in an urban Oklahoma ED from 2015 to 2017.
  • One hundred and eleven patients were included and were randomly assigned to the treatment or control group.
  • The patients in both groups had similar baseline characteristics and baseline numeric rating scale (NRS) pain scores (0-10, 10 being the most pain).

Inclusion criteria:

Patients 18 to 80 years old, presenting to the ED with suspected acute corneal abrasion, and gave written informed consent.

Exclusion criteria:

Contact lens wearers, previous corneal surgery or transplant in the affected eye, presented more than 36 hours after their injury, had a grossly contaminated foreign body, had coexisting ocular infection, currently pregnant, retained foreign body, penetrating eye injury, receiving immunosuppression, allergy to study medication, unable to attend follow-up, unable to fluently read and speak English or Spanish, and any injury requiring urgent ophthalmologic evaluation.

Results:

Main outcomes at the 24-48hr follow up appointment:

  • The overall numeric rating scale (NRS) pain score was significantly lower in the tetracaine group compared to the control group (1 versus 8, P<0.001).
  • The number of patients found to have a small residual corneal abrasion on their follow up slit-lamp examination was similar between groups (18% in the tetracaine group and 11% in the control group).
  • There were only two complications in the tetracaine group (versus 6 in the control group), with similar rates of worsening corneal abrasions in both groups. All patients had normal healing after 10 days. No serious adverse outcomes were encountered.

Table 1. Patient baseline demographics and 24-48hr follow up data points.

Group Tetracaine (n=59) Control (n=59)
Age, y 35 (28-43) 38 (27-47)
Male patients, No. (%) 36 (61) 34 (58)
Baseline pain rating 7 (6-7.5) 7 (6-8)
24-48hr pain rating 1 (1-2) 8 (7-8)
No. of hydrocodone tablets recorded 1 7
Adverse Events, No (%) 2 (3.6) 6 (11)

Limitations and suggestions for future studies:

  • Although this was a double-blind study, there are two things that could have made patients aware of their treatment group. First, the control was packaged in 4 ampules and the treatment was packaged in a single bottle. Second, Tetracaine burns when administered to the eye and Systane (control) does not.
  • The study was slightly underpowered for the primary outcome of efficacy and certainly not powered to determine safety for rare adverse events associated with topical anesthetics. That being said, there are more patients in this trial demonstrating short term safety than previous care reports and series demonstrating tetracaine harm.
  • There was an extensive exclusion criterion, including patients who wear contacts (which are a common cause of corneal abrasions). By broadening the inclusion criteria, the results could be applied to a greater number of patients.
  • Patients were required to return for follow up at which time they were required to return their “study drops” so the drops cannot be abused. It would be more feasible to limit the amount of eye drops in the bottle so the patient does not have to return to the ED for bottle disposal.

Our conclusions:

Short term topical tetracaine is an efficacious analgesic for acute corneal abrasions, is associated with less hydrocodone use compared to control, and appears to be safe.

 


Case

Back to our original question…what do we tell our patient?

Provide him with a limited number of tetracaine drops and administer one drop in affected eye q30 minutes PRN pain for a maximum of 24 hours. Advise him to return to ED if his symptoms persist beyond 48 hours or get worse.


References

McGee, H. T., & Fraunfelder, F. (2007). Toxicities of topical ophthalmic anesthetics. Expert Opinion    on Drug Safety, 6(6), 637–640. https://doi.org/10.1517/14740338.6.6.637

Shipman, S., Painter, K., Keuchel, M., & Bogie, C. (2021). Short-Term Topical Tetracaine Is Highly        Efficacious for the Treatment of Pain Caused by Corneal Abrasions: A Double-Blind, Randomized             Clinical Trial. Annals of Emergency Medicine, 77(3), 338–344.       https://doi.org/10.1016/j.annemergmed.2020.08.036

Wipperman, J. L., & Dorsch, J. N. (2013). Evaluation and management of corneal abrasions.    American Family Physician, 87(2), 114–120.

Yu, C. W., Kirubarajan, A., Yau, M., Armstrong, D., & Johnson, D. E. (2021). Topical pain control for     corneal abrasions: A systematic review and meta-analysis. Academic Emergency Medicine, 28(8), 890–908. https://doi.org/10.1111/acem.14222

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A Seal Barking… In the ED?? – Croup Management in the Emergency Department

A Seal Barking… In the ED?? – Croup Management in the Emergency Department: A Medical Student Clinical Pearl

Kalpesh Hathi, CC3
MD Candidate, Class of 2023
Dalhousie Medicine New Brunswick

Reviewed by Dr. Jeremy Gross

Copyedited by Dr. Mandy Peach

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

Case Presentation:

You are the clinical clerk in the ED on a cold Monday, December afternoon. You pick up a chart that describes a 12-month-old baby boy, with a 1-day history of subjective fever of 38.4 C at its highest, respiratory distress, decreased PO intake and mom noting a barking cough.

Vitals: HR: 100 BPM, RR: 45, SpO2: 98% RA, BP: 90/65, Temp: 36.8 C, GCS 15, Wt: 10.2 kg.

You pull out your normal pediatrics vitals chart, and note that aside from a mildly elevated RR, these vitals are within normal limits for this child’s age and the child is afebrile.

 

What would you want to include in your history and physical?

 

History:

On history, mom says that the child began having classic URTI symptoms on Sunday (1 day ago) including a cough, rhinorrhea, and increased work of breathing. He also had a temperature of 38.4 C by ear on Sunday. Today, he began having what mom describes as increased work of breathing and a barking seal like cough.

Mom shows you two videos from this morning of the increased work of breathing and the barking-seal like cough:

Example of increased work of breathing (assume this is at home without the monitors attached):

https://www.youtube.com/watch?v=KQTEu1mpRY8&t=3s

As an astute clerk, you look for signs of increased work of breathing including tracheal tug, chest wall indrawing (inter, supra, or subcostal), abdominal breathing, grunting, head bobbing, cyanosis, nasal flaring, pursed lip breathing, and tachypnea.

Example of barking seal-like cough:

https://www.youtube.com/watch?v=UWOrKzgp3Wc

You agree that this sounds classically like a croup presentation.

The rest of the history including pregnancy, family, social, developmental, medications, allergies, and medical is largely unremarkable. The child’s vaccinations are up to date.

Mom is concerned as she feels the child is feeding and drinking less, but they are still having a normal number of wet (~6/day) and dirty (~1/day) diapers.

 

Physical Exam:

The child appears well in the ED, they are fussy and fighting your exam, they are jumping on the bed and playing with mom, they find comfort in mom, and they are even playing peek-a-boo with the RNs. You currently do not hear the barking seal like cough, nor stridor. They have mild intercostal indrawing, but no other signs of respiratory distress. No cyanosis is present.

Vitals are unchanged from the chart; the RR is still mildly elevated at ~40-45/min.

Resp: Mildly decreased air entry bilaterally, no crackles/wheezes. Mild stridor transmitted from upper respiratory tract upon agitation.

Fluid Status: Moist mucous membranes, fontanelles not bulging or sunken in, skin turgor is normal (no excessive tenting of skin), and when prompted they drink apple juice mixed with water.

You complete a thorough head to toe exam including HEENT, Neuro, Cardio, Abdo, GU, and MSK, aside from some cerumen in the ears and some rhinorrhea, the exam is within normal limits.

Differential Diagnosis [1-3]:

Croup

Bacterial tracheitis

Epiglottitis

COVID-19

Foreign body aspiration

Neoplasm

Hemangioma

Peritonsillar abscess

Retropharyngeal abscess

Acute anaphylaxis reaction

 

Bronchiolitis

  • Bronchiolitis and lower respiratory tract infections would present with wheeze rather than stridor [1-3].
  • Peritonsillar and retropharyngeal abscesses would have a hot potato voice, and potentially a mass on the neck [1-3].
  • In children <6 months old it is important to consider congenital presentations such as choanal atresia and tracheoesophageal fistula [1-3].
  • URTI symptoms would not be present in isolated foreign body aspiration but should be considered [1-3].
  • It is important to differentiate croup from epiglottitis because epiglottitis can lead to rapid deterioration and often requires operating room intubation [1,2]. Drooling suggests epiglottitis whereas cough suggests croup, both have a high sensitivity and specificity for each respective diagnosis [1-3,4].
  • Bacterial tracheitis the child would look much sicker and more toxic, and this would be represented on vital signs as well [1-3].

 

Croup:

Croup is a viral illness most commonly caused by parainfluenza virus, it is formally called laryngotracheobronchitis as it is inflammation of upper airway including the larynx, trachea, and bronchi [1,5].

Croup is a common presentation to Canadian emergency departments, most of which will be mild forms of croup, however occasionally hospitalization will be required, and rarely intubation is needed [1,6]

Classically croup will present in children between 6 months – 3 years old, with a 1-2 day history of URTI symptoms followed by a barking cough and stridor [1,7,8]. As this causes inflammation and obstruction of the upper respiratory tract, stridor will be present and often is more pronounced with agitation and at night [1,2]. A low-grade fever may be present, but is not required for the diagnosis, the child will not typically have drooling or dysphagia (if this is present consider epiglottitis) [1-3]. Parents will often be concerned/alarmed by the barking cough sounds.

As with most viral infections, croup is a self-limiting illness and most management is supportive, improvement should be noted within 2-7 days [1,6,7].

The diagnosis of croup is a clinical one of the child meeting the clinical picture outlined above and ruling out other causes with history and physical [1-3]. A radiograph is not needed to diagnose croup however if obtained due to uncertainty, will often show a narrowing of the glottic and subglottic areas in a classic steeple sign [3]. Whereas epiglottitis will show a thumb sign [9].

Picture taken from: https://www.pinterest.ca/pin/541980136386136007/

Picture taken from: https://kidshealth.org/Nemours/en/parents/az-croup.html

Workup of the Patient…

You remember some clinical decision aids for croup management… So, you employ the Westley Scoring System for Croup Severity [10]. As our child has a normal LOC, no cyanosis, stridor with agitation, mildly decreased air entry, and moderate retractions. They receive a Westley Score of 4 = moderate croup.

 

Mild </= 2

Moderate = 3-7

Severe = >/=8

Picture taken from: https://www.uptodate.com/contents/image/print?imageKey=PEDS%2F100744&topicKey=PEDS%2F6004&rank=1~60&source=see_link&search=croup&utdPopup=true

Based on this you pull out a trusted croup decision aid guide [1,11]:

Taken from: https://cps.ca/documents/position/acute-management-of-croup

In summary:

Mild croup, children will be given oral dexamethasone classically the dose is 0.6 mg/kg of body weight, however literature has shown equal effectiveness with 0.3 mg/kg, therefore some practitioners may opt for this lower in patients with moderate or mild croup [1,11,12]. Parents will be educated, and the child will be discharged home [1,11].

Moderate croup, the child will be given the same dose of dexamethasone and will be observed for 4 hours for improvement and sent home if symptoms have improved [1,11].

Severe croup, the child will be given blow-by O2 if cyanosis present, racemic epinephrine 2.25% (0.5 ml in 2.5 ml of normal saline) OR L-epinephrine 1:1000 5 mL, and the same dose of dexamethasone as above [1,11]. They will be observed for 2 hours and either sent home or admitted based on response [1,11].

Of note… previously aerosolized racemic epinephrine or L-epinephrine was given, however to reduce aerosolized treatments during the COVID-19 pandemic some emergency departments have received special authorization to give a puffer with epinephrine which was previously only approved in the US.

 

Case Conclusion

As our child had moderate croup and weighs 10.2 kg, they were given 0.3 mg/kg of dexamethasone which was 3.6 mg. We also performed a viral swab, which returns negative for COVID-19, but positive for parainfluenza virus, re-enforcing your diagnosis of croup. They were observed in the ED and quickly improved with no more increased work of breathing, and no stridor at rest. As such they were discharged to the care of their parents, and the parents’ received education on supportive management and indications to re-seek medical care. In fact, the SJRH ED has a handy parent information sheet that you give to the mother, which she is very appreciative of.

References:

  1. Ortiz-Alvarez O, Canadian Pediatric Society, Acute Care Committee. Acute management of croup in the emergency department. J Paediatr Child Health. 2017;22(3):166-9. https://cps.ca/documents/position/acute-management-of-croup#ref1
  2. Sizar O, Carr B. Croup. [Updated 2021 Jul 26]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. https://www.ncbi.nlm.nih.gov/books/NBK431070/
  3. Smith DK, McDermott AJ, Sullivan JF. Croup: Diagnosis and Management. Am Fam Physician. 2018;97(9):575-80. https://www.aafp.org/afp/2018/0501/p575.html
  4. Tibballs J, Watson T. Symptoms and signs differentiating croup and epiglottitis. J Paediatr Child Health. 2011;47(3):77-82. https://pubmed.ncbi.nlm.nih.gov/21091577/
  5. Rihkanen H, Rönkkö E, Nieminen T, et al. Respiratory viruses in laryngeal croup of young children. J Pediatr 2008;152(5):661–5. https://pubmed.ncbi.nlm.nih.gov/18410770/
  6. Rosychuk RJ, Klassen TP, Metes D, Voaklander DC, Senthilselvan A, Rowe BH. Croup presentations to emergency departments in Alberta, Canada: A large population-based study. Pediatr Pulmonol 2010;45(1):83–91. https://pubmed.ncbi.nlm.nih.gov/19953656/
  1. Johnson DW. Croup. BMJ Clin Evid. 2014. https://pubmed.ncbi.nlm.nih.gov/25263284/
  2. Bjornson CL, Johnson DW. Croup in children. CMAJ. 2013;185(15):1317-23. https://www.cmaj.ca/content/185/15/1317
  3. Takata, Fujikawa, Goto. Thumb sign: acute epiglottitis. BMJ Case Rep. 2016. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4904439/
  4. Yang WC, Lee J, Chen CY, Chang YJ, Wu HP. Westley score and clinical factors in predicting the outcome of croup in the pediatric emergency department. Pediatr Pulmonol. 2017;52(10):1329-34. https://pubmed.ncbi.nlm.nih.gov/28556543/
  5. Toward Optimized Practice. Diagnosis and Management of Croup. Clinical Practice Guideline, January 2008. www.topalbertadoctors.org/download/252/croup_guideline.pdf.
  6. Geelhoed GC, Macdonald WB. Oral dexamethasone in the treatment of croup: 0.15 mg/kg versus 0.3 mg/kg versus 0.6 mg/kg. Pediatr Pulmonol. 1995;20(6):362-8. https://pubmed.ncbi.nlm.nih.gov/8649915

 

 

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Delirium vs. Dementia: Different side on the same coin

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

Khoi Dao, Med III

Dalhousie Medicine New Brunswick

Reviewed by Dr. Todd Way

Copyedited by Dr. Mandy Peach

Case:

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

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

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

Past Surgical History: bilateral ankle replacements

Initial Investigations:

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

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

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

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

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

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

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

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

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

Collateral History:

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

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

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

Risk and Precipitating factors of delirium:

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

Differential Diagnoses:

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

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

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

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

Psychiatric illnesses – includes bipolar and depressive disorders with psychotic features

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

Approach to the source of delirium:

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

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

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

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

Enviromentals – heavy metals,

Structurals – brain injury, CNS pathology, malignancy

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

Case continues:

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

Key points:

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

References:

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

A Case of Pyelonephritis: A Medical Student Clinical Pearl

Natasha Glover

MUN Medicine, CC4

Class of 2022

Reviewed by Dr. Paul VanHoutte

Copyedited by Dr. Mandy Peach

Case

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

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

 

PMHx:
Frequent UTIs

 

Medications:
No prescription medications

 

Social:

Smokes marijuana daily

No EtOH consumption

No other recreational drug use

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

 

Physical Exam:

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

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

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

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

 

Differential Diagnosis:

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

 

Urinalysis:

Leukocyte esterase 25

Blood casts 50

Protein 20

HCG negative

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

 

Labs:

Sodium 140

Potassium 4.2

Chloride 108

Creatinine 274

Hgb 135

HCT 0.450
LKC 23.7

PLT 281

CRP 506.3

Lipase 8

Bedside renal U/S unable to detect any hydronephrosis.

A CT is ordered to rule out infected renal stone.

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

Assessment:

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

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

 

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

Pathogenesis of Pyelonephritis:

 

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

 

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

 

Complications:

 

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

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

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

Management for Ms. X:

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

 

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

 

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Murmurs for the Learners: An approach to pediatric heart murmurs

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

Luke MacLeod, Med IV

DMNB Class of 2022

Reviewed by Dr. Tushar Pishe

Copyedited by Dr. Mandy Peach

Case:

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

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

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

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

 

What is a heart murmur?

 

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

 

How to describe a murmur

 

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

 

Quality

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

 

Timing

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

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

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

 

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

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

 

A continuous murmur is heard throughout the cardiac cycle.3

 

Intensity

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

Pitch

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

 

Radiation

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

 

Other sounds

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

 

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

 

Click below to listen to S3 and S4 heart sounds

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

 

Ejection clicks

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

Pericardial friction rub

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

 

Location

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

 

Shape

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

What are the characteristics of benign and pathological murmurs?

 

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

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

 

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

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

 

Click below to listen to an innocent heart murmur

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

 

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

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

 

What are some of the more common pediatric heart murmurs?

 

Innocent9

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

 

Pathologic4

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

 

Next steps

 

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

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

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

 

Case Conclusion

 

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

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

 

 

References:

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

 

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Colovesicular fistula

Approach to diagnosing Colovesicular fistula- A Medical Student Clinical Pearl

Emmanuel Hebert

Med 4, Dalhousie Medicine

Reviewed by Dr. Chris Doiron

Copyedited by Dr. Mandy Peach

Case

54 y/o M presents with a bizarre presenting complaint at 10am Monday morning…

You enter the room to see a man in no apparent distress who tells you that for the past two days something that looks like feces is coming out of his penis. The patient went to the bathroom to urinate Sunday night and noted air coming out of his penis that felt as if he were passing flatus. He then noticed brown foul-smelling liquid upon urinating. There was no blood. He reports no suprapubic fullness, pain with urination, or urgency. He denies any abdominal or pelvic pain. He noted chills Sunday evening which resolved and have not returned after a single dose of acetaminophen 500mg.

 

Past Medical History:

Hypertension

Adenocarcinoma of rectum- 2019

Radiation Therapy- 2019

Partial Bowel resection with ileostomy and stoma- 2019

Reversion of ileostomy- 2020

Medications: Coversyl Plus

Allergies: Codeine, penicillin

Physical Examination:

Patient is comfortable and appears well. Vitals: HR 85; Temp 36.5; BP: 125/80; O2Sat99% on RA. Abdominal exam is unremarkable. There is no suprapubic or CVA tenderness on palpation. Pelvic exam reveals a penis with no discharge or tenderness.

 

Initial bloodwork:

  • WBC: 11×10^9/L
  • Hgb: 135
  • Plt: 300×10^9/L
  • Na: 135
  • K: 4.0
  • CRP: 80
  • Lactate: 1.0
  • Creatinine: 100
  • eGFR: N

Urinalysis: Grossly brown with + leukocytes, Nitrite positive and RBCs present

 

What is the differential diagnosis of pneumaturia?

  • Recent urinary tract instrumentation, catheterization.
  • Urinary tract infection with a gas forming organism (emphysematous cystitis).
  • Emphysematous pyelonephritis (rare) [1]
  • Colovesicular  and enterovesicular Fistula as a result of complicated Diverticulitis, Crohn’s Disease or Carcinoma of the Colon or Bladder

Colovesicular Fistula

Colovesicular and enterovesicular fistulas are defined as connections between the enteric lumen and the bladder. [2] There are many ways that tissue can develop a fistula but in the enteric system there are several common etiologies [3]:

  • Diverticulitis: 65–79% of cases
  • Cancer (mostly adenocarcinoma): 10–20%
  • Crohn’s Disease: 5-7%
  • Previous radiation, bowel surgery, perforated peptic ulcer, genitourinary coccidioidomycosis, pelvic actinomycosis, and appendicitis make up the remaining cases.

Symptoms of Colovesicular Fistula

Figure 1: Graphic showing the common symptoms of colovesicular fistula

 

The classic findings of enterovesicular and colovesicular fistulas known as Gouveneur’s Syndrome are suprapubic pain, frequency, dysuria, and tenesmus.

Notwithstanding, pneumaturia, fecaluria and recurrent UTIs are pathognomonic with over 75% of patients presenting with these three findings. [3]

 

Investigations

Urinalysis (U/A) and culture can be useful on initial presentation to help guide diagnosis. In colovesicular fistula, U/A can reveal white blood cells and feces in the urine. Cultures will typically grow bacteria associated with the enteric system with E. coli being the most common pathogen (81% ). [3] (Note: E. coli is a common pathogen in the setting of an uncomplicated UTI thus E. coli growth does not necessarily mean the patient has a fistula)

 

It is important to assess for evidence of sepsis in any patient with suspected colovesicular fistula. If the patient displays signs of fever and/or shock, blood and urine cultures and other labs to guide resuscitation and management are indicated. There are no blood tests that help definitively diagnose a colovesicular fistula.

 

When the clinical suspicion of colovesicular fistula is high, computed tomography (CT) of the abdomen and pelvis with oral/rectal contrast but without IV contrast is indicated. IV contrast is excreted by kidneys and can appear in the bladder confusing the origin of the contrast. Rectal contrast, however, should not appear in the bladder and its presence can help confirm the diagnosis. CT findings indicative of colovesicular fistula include air in the bladder/ureters, visualization of the fistula tract, oral/rectal contrast in the bladder, and bladder thickening adjacent to a thickened loop of bowel. [3]

Point of care ultrasound may identify echogenic material (fecal material), reverberation artifact indicative of gas within the bladder or thickened bowel abutting the bladder though is not generally nor should be considered a modality for the diagnosis of colovesicular fistula.

MRI provides excellent resolution of a fistula tract and potential underlying pathology however, given lack of access and the associated time and financial costs, CT remains the modality of choice for the diagnosis of colovesicular fistula in the emergency department. [3]

Figure 2: CT Abdomen-Pelvis revealing pneumoureter in the left image and the colovesicular tract in the right image.

Management

The definitive management of a colovesicular fistula is surgical repair. Timing is dependent on several factors including hemodynamics at presentation, patient comorbidities, and etiology of the fistula (diverticulitis vs malignancy). In rare cases, conservative management may be considered if the patient is too frail for surgery. Septic patients should be resuscitated as per sepsis guidelines while stable patients should receive broad spectrum antibiotics with ciprofloxacin and metronidazole or amoxicillin-clavulanate being common regimens. Surgical consultation is recommended in all patients after initial resuscitation and imaging. [2]

Back to the case:

CT abdomen-pelvis was performed which showed air in the ureter and bladder as well as a tract connecting the sigmoid colon to the bladder. General Surgery was consulted and Piperacillin/Tazobactam 3.375g IV q6h was started. As the patient was stable, surgery asked that the patient be held in the ED until they could be seen latter in the day.

Two Hours Later

• On reassessment, patient appeared unwell and visibly diaphoretic. He was febrile with a temp of 38.5, a HR of 110 and a BP of 100/70. Repeat labs showed a white count of 14 and a lactate of 2.5.
• Diagnosis of septic shock was made and resuscitation started.
• Surgery was notified who opted to bring the patient to the OR for emergent exploratory laparotomy.

In the OR:

• The bladder was attached to the sigmoid colon via a thick adhesion. The surgeon had difficulty discerning what was bladder and what was intestine.
• Intestine was resected and an ileostomy was placed with stoma.
• Patient tolerated procedure well and was admitted to ICU for monitoring.

Figure 3: Laparoscopic View of bowel adhered to the bladder

 

Key Takeaways

  • Most colovesicular fistulas are the result of complicated diverticulitis.
  • Pneumaturia is highly suggestive for enterovesicular fistula in the absence of recent bladder instrumentation.
  • CT abdomen/pelvis with oral and rectal contrast without IV contrast is the imaging modality of choice.
  • Patients can go from stable to septic shock quickly.
  • The definitive management is surgical [2]

 

References:

 

  1. Youssef S. Tanagho, Jonathan M. Mobley, Brian M. Benway, Alana C. Desai, “Gas-Producing Renal Infection Presenting as Pneumaturia: A Case Report”, Case Reports in Medicine, vol. 2013, Article ID 730549, 3 pages, 2013. https://doi.org/10.1155/2013/730549
  2. Granieri, S., Sessa, F., Bonomi, A., Paleino, S., Bruno, F., Chierici, A., Sciannamea, I. M., Germini, A., Campi, R., Talso, M., Facciorusso, A., Deiana, G., Serni, S., & Cotsoglou, C. (2021). Indications and outcomes of enterovesical and colovesical fistulas: systematic review of the literature and meta-analysis of prevalence. BMC surgery21(1), 265. https://doi.org/10.1186/s12893-021-01272-6
  3. Tomasz Golabek, Anna Szymanska, Tomasz Szopinski, Jakub Bukowczan, Mariusz Furmanek, Jan Powroznik, Piotr Chlosta, “Enterovesical Fistulae: Aetiology, Imaging, and Management”, Gastroenterology Research and Practice, vol. 2013, Article ID 617967, 8 pages, 2013. https://doi.org/10.1155/2013/617967
  4. Kavanagh, P. Neary, J. D. Dodd, K. M. Sheahan, D. O’Donoghue, and J. M. P. Hyland, “Diagnosis and treatment of enterovesical fistulae,” Colorectal Disease, vol. 7, no. 3, pp. 286–291, 2005.

 

 

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QUICK TIPS on STEMI equivalents

QUICK TIPS on STEMI equivalents – A Medical Student Clinical Pearl

Ilya Abelev

MD Candidate, Class of 2022

Dalhousie Medical School New Brunswick

Reviewed by Dr. Jay Mekwan

Copyedited by Dr. Mandy Peach

 

Why recognize STEMI’s?2

STEMI’s indicate an infarction pattern on ECG, and can guide emergency physicians to identify patients who would benefit from emergent catheterization and revascularization.

What is a STEMI?

(S-T Segment Elevation Myocardial Infarction)

A patient presents with clinical symptoms consistent with an acute coronary syndrome together with S-T segment elevation (STE) on ECG or a new LBBB.

What is a STEMI equivalent?

A STEMI equivalent is an ECG pattern suggestive of ischemia that should trigger emergency physicians to consult specialists such as interventional cardiologists for revascularization interventions – similar to a STEMI.

MI Definition1

• ≥ 2.5 mm STE in V2-V3 for males < 40 years*
• ≥ 2 mm STE in V2- V3 for males ≥ 40 years*
• ≥ 1.5 mm STE in V2-V3 for females regardless of age*
• ≥ 1 mm STE all other leads

• New J-point elevation ≥ 1 mm from prior ECG should be considered ischemic
• The J-point is defined as the junction between the QRS termination and the ST-segment onset, and the ST-segment should be measured against the isoelectric TP segment (assuming a stable baseline)3

J point in a) normal; b) c) J point elevation; d) J point depression; e) with J wave (Osborn wave)

Osborn wave: Characteristically seen in hypothermia (typically T < 30C), but they are not pathognomonic (4)

Mnemonic for Stemi Equivalents – PTSD (5)

  1. Posterior MI
  2. T wave Abnormalities
  3. Sgarbossa Criteria
  4. Diffuse ST depression with ST elevation in AVR

Posterior MI (1,6)

“Posterior MIs are easily missed because of the absence of any ST elevation. Posterior involvement is estimated to occur in 15-21% of all acute myocardial infarctions and in isolation ~3% of the time, typically due to occlusion of the left circumflex or right coronary arteries.”

More Information(7)

“As the posterior myocardium is not directly visualised by the standard 12-lead ECG, reciprocal changes of STEMI are sought in the anteroseptal leads V1-3.”

Posterior MI is suggested by the following changes in V1-3:

  1. Horizontal ST depression
  2. Tall, broad R waves (>30ms)
  3. Upright T waves
  4. Dominant R wave (R/S ratio > 1) in V2” (7)

Image illustrating reciprocal changes in V2 and how a ST depression in V2 can appear like a STEMI when flipped (reciprocal)

Where to expect reciprocal changes?

PAILS (8)

Posterior MI – anterior reciprocal changes
Anterior MI – inferior reciprocal changes
Inferior MI – lateral reciprocal changes

Lateral MI <-> inferior or septal reciprocal changes*** exception to mnemonic
Septal MI – posterior reciprocal changes

 

T wave abnormalities

de Winter T-waves (9,10)

Key 12-Lead Features

  1. “J-Point depression with up-sloping ST segments.
  2. Tall, prominent, symmetric T waves in the precordial leads.
  3. Upsloping ST segment depression > 1mm at the J-point in the precordial leads.
  4. Absence of ST elevation in the precordial leads.
  5. ST segment elevation (0.5mm-1mm) in aVR.
  6. “Normal” STEMI morphology may precede or follow the DeWinter pattern.”

 

Wellens Syndrome(11)

Rhinehart et al (2002) describe the following Diagnostic criteria(12) for Wellens syndrome:

• “Deeply inverted or biphasic T waves in V2-3 (may extend to V1-6)
• ECG pattern present in pain-free state
• Isoelectric or minimally-elevated ST segment (< 1mm)
• No precordial Q waves
• Preserved precordial R wave progression
• Recent history of angina
• Normal or slightly elevated serum cardiac markers”

“There are two patterns of T-wave abnormality in Wellens syndrome:

Type A/1 – Biphasic, with initial positivity and terminal negativity (25% of cases)
Type B/2 – Deeply and symmetrically inverted (75% of cases)”

Sgarbossa Criteria(13,14)

In patients with left bundle branch block (LBBB) or ventricular paced rhythm, infarct diagnosis based on the ECG can be difficult
Abnormal depolarisation should be followed by abnormal repolarisation, manifesting as ST-segment and T-wave deviations that do not necessarily indicate acute ischaemia (“appropriate discordance”)

  1. Concordant ST elevation > 1mm in leads with a positive QRS complex (score 5)

  1. Concordant ST depression > 1 mm in V1-V3 (score 3)

  1. Excessively discordant ST elevation > 5 mm in leads with a -ve QRS complex (score 2)

“These criteria are specific, but not sensitive (36%) for myocardial infarction. A total score of ≥ 3 is reported to have a specificity of 90% for diagnosing myocardial infarction.”(13)

Diffuse ST depression with ST elevation in AVR(1)

“STE ≥ 1 mm in aVR or V1 with STD ≥ 1 mm in ≥ 6 leads can suggest left main coronary artery insufficiency, proximal LAD insufficiency, or triple vessel disease, especially if accompanied by pathologic Q-waves, hemodynamic compromise, and/or refractory symptoms.”

• Widespread deep ST depression involving V2-6, I, II, aVL
• ST elevation in aVR > V1

 

Examples of STEMI Equivalents(16): Resource to test knowledge of STEMI equivalents

Conclusion:

  1. Definition of MI varies by age and sex
  2. Use PTSD mnemonic to remember the STEMI equivalents.
    a. Use PAILS to remember appropriate location of reciprocal changes
  3. Initiate appropriate consultation to revascularize/ stent for both STEMI and STEMI equivalents

 

References

  1. Daniel Kreider; Jeremy Berberian. STEMI Equivalents: Can’t-Miss Patterns EMRA [Internet]. [cited 2022 Feb 19]. Available from: https://www.emra.org/emresident/article/stemi-equivalents/
  2. Thygesen K, Alpert JS, Jaffe AS, Chaitman BR, Bax JJ, Morrow DA, et al. Fourth Universal Definition of Myocardial Infarction (2018). Circulation. 2018 Nov 13;138(20):e618–51.
  3. J point ECG Interval • LITFL • ECG Library Basics [Internet]. [cited 2022 Feb 19]. Available from: https://litfl.com/j-point-ecg-library/
  4. Slovis C, Jenkins R. Conditions not primarily affecting the heart. BMJ. 2002;
  5. STEMI Equivalents for ECGs – YouTube [Internet]. [cited 2022 Feb 19]. Available from: https://www.youtube.com/watch?v=lH19cYBdvaQ
  6. van Gorselen EOF, Verheugt FWA, Meursing BTJ, Oude Ophuis AJM. Posterior myocardial infarction: the dark side of the moon. Neth Heart J. 2007;
  7. Posterior Myocardial Infarction • LITFL • ECG Library Diagnosis [Internet]. [cited 2022 Feb 19]. Available from: https://litfl.com/posterior-myocardial-infarction-ecg-library/
  8. Tiny Tips: STEMI? Don’t forget your PAILS! – CanadiEM [Internet]. [cited 2022 Feb 19]. Available from: https://canadiem.org/chest-pain-pails/
  9. de Winter RJ, Verouden NJW, Wellens HJJ, Wilde AAM. A New ECG Sign of Proximal LAD Occlusion. N Engl J Med. 2008;
  10. DeWinter’s T-Waves [Internet]. [cited 2022 Feb 19]. Available from: https://handbook.bcehs.ca/clinical-practice-guidelines/pr-clinical-procedure-guide/pr16-12-lead-ecgs/stemis-equivalents-imposters/stemi-equivalents/dewinters-t-waves/
  11. Wellens Syndrome: A Historical Literature Review – Dr. Jason West [Internet]. [cited 2022 Feb 19]. Available from: https://jacobiem.org/wellens-syndrome-a-historical-literature-review-dr-jason-west/
  12. Rhinehardt J, Brady WJ, Perron AD, Mattu A. Electrocardiographic manifestations of Wellens’ syndrome. Am J Emerg Med. 2002;
  13. Smith SW, Dodd KW, Henry TD, Dvorak DM, Pearce LA. Diagnosis of ST-elevation myocardial infarction in the presence of left bundle branch block with the ST-elevation to S-wave ratio in a modified sgarbossa rule. Ann Emerg Med. 2012;
  14. Sgarbossa Criteria • LITFL • ECG Library Diagnosis [Internet]. [cited 2022 Feb 19]. Available from: https://litfl.com/sgarbossa-criteria-ecg-library/
  15. Sgarbossa Criteria – MEDZCOOL – YouTube [Internet]. [cited 2022 Feb 19]. Available from: https://www.youtube.com/watch?v=oLFJy1e9WWI&t=135s
  16. STEMI Equivalents — Maimonides Emergency Medicine Residency [Internet]. [cited 2022 Feb 19]. Available from: https://www.maimonidesem.org/blog/stemi-equivalents-1

 

 

 

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A Case of Smoke Inhalation Injury

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

Emmanuel Hebert

MD Candidate, Class of 2022

Dalhousie Medicine New Brunswick

Reviewed by Dr. Matthew Greer

Copyedited by Dr. Mandy Peach

Case

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

Past Medical History: Unremarkable

Medications: No prescriptions medications.

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

Figure 1: First degree burns on the back.

 

Initial bloodwork:

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

 

What is the differential diagnosis of dysphonia?

-Acute laryngitis

-Functional dysphonia

-Tracheal Injury

-Injury to recurrent laryngeal nerve

-Caustic ingestion, smoke inhalation injury, blister chemical agents

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

 

Smoke Inhalation Upper Respiratory Tract Injury

 

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

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

 

Upper Airway

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

 

Tracheobronchial

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

 

Parenchymal Injury

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

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

 

Management

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

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

 

Indications for early intubation:

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

 

Back to the case:

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

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

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

 

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

 

Key Takeaways

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

 

References:

 

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

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

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

 

 

 

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Approach to Medical Abortion Complications in the ED

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

Victoria Mercer

MD Candidate | Class of 2023
Dalhousie Medicine New Brunswick

Case:

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

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

Brief Review of Medical Abortion

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

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

Expectations vs complications

Bleeding

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

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

Cramping & Pain

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

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

Fever

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

Pearl:

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

Approach to Patient in ED After a Medical Abortion

 

 

Case Continued:

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

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

 

References

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

 

 

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Allergic Acute Coronary Syndrome (Kounis Syndrome)

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

Amar Bhardwaj CC3

Dalhousie Medicine New Brunswick

Class of 2022

Reviewed and edited by Dr. Kavish Chandra

Copyedited by Dr. Mandy Peach

 

Case presentation

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

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

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

 

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

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

 

Kounis syndrome

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

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

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

Type I:

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

Type II:

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

Type III:

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

 

Presentation

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

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

 

Kounis syndrome is a clinical diagnosis.

Management

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

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

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

Summary

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

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

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

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

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

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

 

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A Case of Pneumomediastinum

A Case of Pneumomediastinum: A Medical Student Clinical Pearl

Reviewed by Dr. Maria Kovalik

Copyedited by Dr. Mandy Peach

 

Nick Ellingwood, Med II

Dalhousie Medicine New Brunswick (DMNB)

 

Case

A 16 year-old male presented to the emergency department complaining of shortness of breath which started 3 days prior. He stated that he was unable to take a deep breath. The patient described a sore throat with a productive cough. The patient also revealed that he was having some generalized chest tightness which did not radiate and was non-pleuritic. The patient was also experiencing some diarrhea as well as nausea when he eats. The patient denied any abdominal pain, vomiting, dysphagia, or fever. He had no past medical or surgical history and taking no medications.

On Examination:

Vitals: Temp=36.7oC, HR=126, RR=24, BP=100/62, O2 Sat=95% The patient was sitting comfortably but did appear to be dyspneic.  He was of normal body habitus.

On examination, upon palpation there was crepitus in the lower neck, supraclavicular region, and shoulder region on both sides. There was diffused crackles upon auscultation over the anterior and posterior chest wall. Good air entry into the base of both lungs and no wheezing. There was a normal S1 and S2 with no additional heart sounds or murmurs. Abdomen was soft and non-tender with normal bowel sounds.

A nasopharyngeal swap, chest X-ray, cervical X-ray, CBC, electrolytes, creatinine, urea, random glucose were ordered.

Figure 1. Chest X-ray showing extensive subcutaneous emphysema along the chest wall and lower neck and a pneumomediastinum. There is bilateral perihilar opacities but no pneumothorax or pleural effusion.

Figure 2. Cervical X-rays showing subcutaneous emphysema in the supraclavicular and lower neck regions as well as the retropharyngeal region extending beyond the angle of the mandible.

Etiologies of Pneumomediastinum1,2:

  • Acute asthma exacerbations
  • Covid-19 or other lower respiratory infections
  • Injury to thoracic cavity or airways from surgery, trauma, inhalation of drugs, or Valsalva maneuvers
  • Perforated esophagus (Boerhaave syndrome)

 

Case Continued:

A CT chest was ordered to evaluate the extent of the pneumomediastinum and subcutaneous emphysema and rule out severe etiologies such as esophageal and bronchi rupture which were not present. The nasopharyngeal swap came back negative for Covid-19 but positive for another coronavirus. The bloodwork showed leukocytosis (25×109/L) but was otherwise unremarkable. The diagnosis of pneumomediastinum secondary to coronavirus infection was made.

Pathophysiology:

As seen in Figure 3, a pneumomediastinum can result from air escaping from small alveolar ruptures into the surrounding bronchovascular sheath. Air then travels along a pressure gradient through the bronchovascular sheath to the hilum and builds up in the mediastinum.3 From there, air can freely move subcutaneously to the chest wall, upper limbs, and neck. Less commonly, air will directly escape into the mediastinum from a more central structure such as the upper respiratory tract or the esophagus.

Figure 3. Pathophysiology of pneumomediastinum and subsequent subcutaneous emphysema.

https://www.uptodate.com/contents/image/print?imageKey=PEDS%2F111129&topicKey=6352&search=pneumomediastinum&rank=1~111&source=see_link

 

Additional Exam Findings:

Hamman’s sign is described as a crunching or rasping sound heard over the precordium that is synchronous with systole and tends to be best heard with the patient in the left lateral decubitus position. This sign can be positive in up to 50% of patients with pneumomediastinum and is specific for pneumomediastinum or pneumopericardium4,5.

PoCUS Findings:

Firstly, in a pneumomediastinum the visualization of the cardiac structures is commonly obstructed by the presence of an “air gap” which is characterized by diffused A-lines anterior to the heart when in the parasternal and apical views. This can also be present in pneumothorax; however, the key difference is that in a pneumothorax the cardiac structures will be visualize during diastole when the heart dilates and pushes the pleural air to the side. In a pneumomediastinum, the air gap will vary with the respiratory cycle (not the cardiac cycle such as in a pneumothorax) because during inspiration the lungs will expand and push the air in the mediastinum cranially allowing the cardiac structures to be visualized6.

There are other clinical tools that can be used to differentiate a pneumomediastinum and a pneumopericardium like ECG changes. However, they can also be easily differentiated using PoCUS because the cardiac structures can’t be visualized in the subxiphoid view in a pneumopericardium. In contrast, the absence of air between the diaphragm, pericardium and myocardium allows the cardiac structure to be visualized in the setting of a pneumomediastinum as seen in Figure 47.

Figure 4. PoCUS images showing a pneumomediastinum where box A (subxiphoid view) shows cardiac structures. The parasternal long (B), parasternal short (C), and apical (D) views all show diffuse A-lines suggesting the presence of the air superficial to the heart. These findings would suggest a pneumomediastinum7.

 

Treatment:

  • Pneumomediastinum normally follows a benign course and is self-limiting
  • Some patients undergo bronchoscopy or esophagogram to rule out airway or esophageal injury
  • Admission is recommended to observe for complications because pneumopericardium and pneumorachis can arise8,9
  • Supplemental oxygen is given to help promote gas reabsorption
  • Simple analgesics are used for pain management as needed

 

Case Conclusion:

The patient was on 4L/min of oxygen while in hospital, and his symptoms significantly improved. Repeat chest X-ray showed improvement in pneumomediastinum and subcutaneous emphysema and he was discharge after 3 days. A chest X-ray 10 days later showed minimal subcutaneous emphysema, and the patient had no symptoms.

Clinical Pearls:

  • Pneumomediastinum is rare but something to keep in your differential for chest pain and SOB especially in young thin males
  • There are some life-threatening etiologies of pneumomediastinum that must be ruled out
  • There are some specific PoCUS findings for pneumomediastinum that can help with your diagnosis
  • The treatment for pneumomediastinum is rest, simple analgesics, and oxygen

 

References:

1: Ojha S, Gaskin J. Spontaneous pneumomediastinum. BMJ Case Rep. 2018;2018:bcr2017222965. Published 2018 Feb 11. doi:10.1136/bcr-2017-222965

2: Spontaneous pneumomediastinum in children and adolescents – UpToDate [Internet]. [cited 2021 Dec 17]. Available from: https://www.uptodate.com/contents/spontaneous-pneumomediastinum-in-children-and-adolescents?search=pneumomediastinum&source=search_result&selectedTitle=1~111&usage_type=default&display_rank=1

3: Ivan Macia, Juan Moya, Ricard Ramos, Ricard Morera, Ignacio Escobar, Josep Saumench, Valerio Perna, Francisco Rivas, Spontaneous pneumomediastinum: 41 cases, European Journal of Cardio-Thoracic Surgery, Volume 31, Issue 6, June 2007, Pages 1110–1114

4: Sahni S, Verma S, Grullon J, Esquire A, Patel P, Talwar A. Spontaneous pneumomediastinum: time for consensus. N Am J Med Sci. 2013 Aug;5(8):460-4. doi: 10.4103/1947-2714.117296. PMID: 24083220; PMCID: PMC3784922.

5: Alexandre AR, Marto NF, Raimundo PHamman’s crunch: a forgotten clue to the diagnosis of spontaneous pneumomediastinumCase Reports 2018;2018:bcr-2018-225099.

6: Ng L, Saul T, Lewiss RE. Sonographic evidence of spontaneous pneumomediastinum. Am J Emerg Med. 2013 Feb;31(2):462.e3-4. doi: 10.1016/j.ajem.2012.08.019. Epub 2012 Nov 15. PMID: 23158605.

7: Zachariah, S., Gharahbaghian, L., Perera, P., & Joshi, N. (2015). Spontaneous pneumomediastinum on bedside ultrasound: case report and review of the literature. The western journal of emergency medicine, 16(2), 321–324. https://doi.org/10.5811/westjem.2015.1.24514

8: Vanzo V, Bugin S, Snijders D, Bottecchia L, Storer V, Barbato A. Pneumomediastinum and pneumopericardium in an 11-year-old rugby player: a case report. J Athl Train. 2013 Mar-Apr;48(2):277-81. doi: 10.4085/1062-6050-48.1.11. Epub 2013 Feb 20. PMID: 23672393; PMCID: PMC3600931.

9: Belotti EA, Rizzi M, Rodoni-Cassis P, Ragazzi M, Zanolari-Caledrerari M, Bianchetti MG. Air within the spinal canal in spontaneous pneumomediastinum. Chest. 2010 May;137(5):1197-200. doi: 10.1378/chest.09-0514. PMID: 20442120.

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Paediatric Supracondylar Fractures

Paediatric Supracondylar Fractures – A Medical Student Clinical Pearl

 

Reviewed by Dr. Joanna Middleton

Copyedited by Dr. Mandy Peach

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

Relevant Case:

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

Problem:

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Case Resolutions:

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

Conclusion

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

References

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

 

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