Peritonsillar Abscess Considerations and Treatment

Flimsy on Quinsy: Considerations and procedures to help diagnose and treat peritonsillar abscess  

Author: Iain McPhee- PGY1

Case study:

A 30 y.o. female presented to the emergency department with a 2-3 day history of sore throat, a unilateral, right sided oral pain that was worsening, and mild right ear ache. Although she was able to swallow food and liquid with discomfort, she reported an increased pooling of saliva in her mouth. She became more concerned when she noticed voice changes and decided to come to the hospital. 

On exam, she looked well and her vitals were within normal limits. On examination of the oral cavity there was a noted mild deviation of the uvula to the left. There was clearly demarcated erythema of both the hard palate and soft palate on the right side. Her right tonsil was only mildly enlarged and the presence of tonsillar stones were appreciated bilaterally. There was very mild fluctuance when palpating the junction between the hard and soft palate. There was an obvious dysphonia (Hot potato voice).

Background:

Peritonsillar abscess (PTA) (Quinsy) and peritonsillar cellulitis (PTC) are often indistinguishable, sharing similar clinical signs and symptoms (1). As management differs depending on the condition, several aspects warrant consideration in the differentiating process

Considerations

  1. Assess for severe upper airway obstruction
    • Look for signs of trismus, suprasternal retractions and anxious appearance. If present consider airway management.
  2. Computed tomography of the neck
    • Consider if you suspect signs of deep neck infection like a retro or parapharyngeal abscess. The CT scan should be obtained with contrast to help identify an abscess (4)
  3. Ultrasound guided exam 
    • Intraoral ultrasound has been shown to be a superior method to both diagnose and assist in the execution peritonsillar abscess drainage when compared to classic landmark-based needle aspiration (2,3). 
  4. Time
    • In the absence of a significant/apparent fluctuating mass in the mouth, consideration of the amount of time the symptoms have been present can help distinguish between the two conditions. Peritonsillar cellulitis is considered a transition phase of peritonsillar inflammatory process which leads to abscess formation (1). Look for 1-2 day history of symptoms as peritonsillar cellulitis, Abscesses are more likely to form between 2-8 days.

Algorithm: Approach to diagnosis and treatment of peritonsillar abscess in the emergency department

https://www.uptodate.com/contents/image?csi=59e98f58-4a45-4ff2-b021-31528346c088&source=contentShare&imageKey=EM%2F112062

Intraoral Ultrasound approach to drainage (as described on emdocs)

http://www.emdocs.net/unlocking-common-ed-procedures-peritonsillar-abscess-drainage/

  1. Use intracavitary probe with cover (Fig 1).
    • Examine affected area and locate abscess 
    • Also locate depth of carotid artery and any potential vascular anatomy anomalies (Fig 2).

      Figure 1: Intracavitary Probe with cover

      Figure 2: Anechoic abscess and carotid artery highlighted in red

       

  2. Analgesia/anesthesia
    • Consider IV analgesia, anxiolytics
    • Anesthetize oral cavity using topical spray like cetacaine or nebulized lidocaine
    • Inject lidocaine with epinephrine into the area of abscess with 18g needle with cut sheath (Fig 3).

      Figure 3 : Scalpel with taped guard and

  3. Optimize Abscess visualization 
    • Insert laryngoscope blade to a depth that is comfortable for the patient. Ask patient to hold laryngoscope (Fig 4)

      Figure 4: Laryngoscope blade optimizing view

  4. Drainage
    • Once adequate visualization is achieved, approach superior pole of abscess with sheathed spinal needle and continuously aspirate when advancing until pus is reached (Fig 5).
    • Consider incision with scalpel with protective guard and used 
    • Insert curved hemostat into abscess space to break up remaining loculations

      Figure 5: Anatomical picture showing superior pole

 

References

  1. Mohamad I, Yaroko A. Peritonsillar swelling is not always quinsy. Malays Fam Physician. 2013 Aug 31;8(2):53-5. PMID: 25606284; PMCID: PMC4170468.
  2. Costantino TG, Satz WA, Dehnkamp W, Goett H. Randomized trial comparing intraoral ultrasound to landmark-based needle aspiration in patients with suspected peritonsillar abscess. Acad Emerg Med. 2012 Jun;19(6):626-31. doi: 10.1111/j.1553-2712.2012.01380.x. PMID: 22687177.
  3. Froehlich MH, Huang Z, Reilly BK. Utilization of ultrasound for diagnostic evaluation and management of peritonsillar abscesses. Curr Opin Otolaryngol Head Neck Surg. 2017 Apr;25(2):163-168. doi: 10.1097/MOO.0000000000000338. PMID: 28169864.
  4. Galioto NJ. Peritonsillar abscess. Am Fam Physician. 2008 Jan 15;77(2):199-202. PMID: 18246890.

Procedures and Algorithms

  1. http://www.emdocs.net/unlocking-common-ed-procedures-peritonsillar-abscess-drainage/
  2. https://www.uptodate.com/contents/image?imageKey=EM%2F112062&topicKey=EM%2F6079&search=peritonsillar%20cellulitis&rank=1~19&source=see_link

 

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A Case of Abdominal Pain in the Elderly – EM Reflections March 2022

Thanks to Dr. Paul Page for leading this month’s discussions

All cases are imaginary but highlight important learning points.

Authored and Copyedited by Dr. Mandy Peach

Case

An 82 yo male presents to the ED via EMS with 1 day of abdominal pain that started in the late evening. He describes feeling well all day, eating a healthy size dinner and then having sudden onset abdominal pain and distension just before bedtime. He can’t describe or localize the pain but states it is a ‘hard pain’ and has been associated with 2 episodes of nausea/vomiting. He doesn’t think he has had a fever. He is unsure of his last bowel movement and complains of frequent constipation. When asked about urinary changes he describes what sounds like a long-standing history of issues with urinary hesitance. He is unsure if there has been any acute change. He thinks there is no history of abdominal surgeries but “he’s been around a long time”. He is a lifelong non smoker.

PMH: DLP, HTN

Meds: Atorvastatin, Ramipril

Vitals: BP 110/60 HR 102 RR 18 O2 97% RA T – 36.5

On exam he appears in mild discomfort, with his eyes closed. His abdomen is mildly distended. He has generalized tenderness throughout the abdomen, no guarding or peritonitis. The testicles and inguinal region appear normal.

What are some barriers to assessing abdominal pain, or any presentation, in the geriatric patient?1,2

  • History may be difficult to intrepret, sometimes with vague symptoms
  • History may be difficult to obtain due to physical deficits like hearing loss
  • Vitals are not reliable – most patients are on beta blockers so their heart rate may not be elevated, and ‘normal’ blood pressure may actually be hypotensive for a geriatric patient who will often run much higher at baseline.
  • Blunted immune response – they may not illicit the typical fever or elevated WBC that we often count on to lead us to infectious/septic processes.
  • Decreased abdominal wall muscles lead to less guarding or rebound on exam – * peritoneal signs are often absent
  • Shrinkage of omentum leads to decreased containment of intraabdominal process
  • Higher rate of perforation and ischemic gut due to chronic issues like atheroscleoris and low flow states

He doesn’t look to be terribly unwell, you plan to treat his pain and nausea and order some labs.

What would be the drug of choice for abdominal pain in the elderly2?

Hydromorphone as it is not renally excreted.

You are ordering your labs – CBC, Cr, electrolytes, LFT’s, bilirubin, lipase and a urinanalysis.

Should you order a VBG and lactate in this man with ‘normal’ vitals and a non-specific abdominal exam2?

If the patient is presenting with pain out of proportion (ie. Ischemia symptoms) these tests are a must. But consider in any patient with risk factors for cardiovascular disease or atrial fibrillation. Our patient has a history of dyslipidemia and hypertension – you order the additional tests and ECG.

Elderly patients have vague abdominal pain all the time – what percentage are actually surgical?

Up to 60% of cases are surgical.

The associated mortality rate of those requiring abdominal surgery is upwards of 7x greater than younger patients with similar presentations.

What are the main causes of surgical abdominal pain the elderly1,2?

  • Cholecystitis – consider when working up a septic patient with no obvious source
  • Appendicitis
  • Bowel Obstruction – femoral hernia is a commonly missed cause
  • Hernia

Your patient had already been sent for an abdominal series after they were triaged. Certainly with the history of abdominal pain with n/v obstruction is high on the differential, even in a native abdomen.

What are useful findings on abdominal series3,4?

You are looking for the following:

  • Pneumoperitoneum (but really, you should be getting a CT if this is a concern)
  • Air fluid levels seen in obstruction

Certainly, in a busy department XR is quick, cheap and has minimal radiation. In patients with repeated SBO an XR may be suffice. Findings for SBO on XR include:

  • Dilated bowel with air fluid levels
  • Proximal bowel is dilated, but distal bowel is not
  • Gasless abdomen – where there is a large amount of fluid within the bowel loops, which may underestimate the level of obstruction. There may be a ‘string of pearls’ sign in upright films where small amount of air is seen between valvulae conniventes.

The sensitivity, specificity, and accuracy are 79-83%, 67-83%, and 64-82%, respectively3 – not enough to rely on when the mortality rate is so high in this population. A normal abdominal series does not rule out any serious pathology.

Certainly CT would be the gold standard – it would give the site, severity and etiology of obstruction. Complications such as necrosis, ischemia and perforation would be identified as well as other causes for abdominal pain on your differential. In elderly patients in particular, it has been shown to be more high yield for clinical decision making2.

But a CT takes time in an overcapacity and understaffed ED. While you wait for it to be completed you grab for your ultrasound probe – specifically you are looking for signs of SBO as that is top of your differential.

What is the accuracy of PoCUS for SBO5?

Sensitivity 88%, specificity 96%

What is an approach to a SBO scan with PoCUS?

Using your curvilinear probe ‘Mow the lawn’ starting in the RLQ and cover the entire abdomen using graded compression. Take your time6.

What are the findings5,7?

  • Dilated bowel loops >2.5cm
  • Thickened bowel wall >3mm
  • ‘To and fro’ peristalsis
  • Tanga sign – triangular shaped areas of free fluid between bowel loops. Concerning for high grade obstruction

You do confirm all signs of SBO, including tanga sign which is concerning.

By now your patient is over in the scanner when you get some lab results back – although the WBC is at the upper end of normal the lactate is significantly elevated.

While the patient is in CT waiting for a porter to come back you get a call from the radiologist confirming closed loop bowel obstruction with signs of ischemia and necrosis.

Bottom line – have a low threshold to order CT in geriatric abdominal pain. They are high risk patients, with high mortality rates.

 

References and further reading

  1. Thomas, A (2018). Approach to the Geriatric Patient. CRACKCast E181. CanadiEM. Retrieved July 19, 2022 from https://canadiem.org/crackcast-e181-approach-to-the-geriatric-patient/
  2. Melady, D, Lee, J, Helman, A. Geriatric Emergency Medicine. Emergency Medicine Cases. July, 2013. https://emergencymedicinecases.com/episode-34-geriatric-emergency-medicine/. Accessed July 19, 2022
  3. Bordeianou, L & Yeh, D. (2021) Etiologies, clinical manifestations, and diagnosis of mechanical small bowel obstruction in adults. Uptodate. Accessed July 2019 from https://www.uptodate.com/contents/etiologies-clinical-manifestations-and-diagnosis-of-mechanical-small-bowel-obstruction-in-adults?search=bowel%20obstruction%20adult&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1#H2918585369
  4. Jones, J., Ramsey, MD, A. Small bowel obstruction. Reference article, Radiopaedia.org. (accessed on 19 Jul 2022) https://doi.org/10.53347/rID-6158
  5. Atkinson P, Bowra J, Lewis D. (2019). Point of Care Ultrasound for Emergency Medicine and Resuscitation.
  6. Tooma, D & Dinh, V. Abdominal Ultrasound Made Easy: Step by Step Guide. Small Bowel Obstruction. POCUS 101. Accessed July 19, 2022 from https://www.pocus101.com/abdominal-ultrasound-made-easy-step-by-step-guide/#Small_Bowel_Obstruction_Ultrasound
  7. Small Bowel Obstruction. PoCUS Atlas. Accessed July 19, 2022 from https://www.thepocusatlas.com/gastrointestinal
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A Summary of Bronchiolitis

A Summary of Bronchiolitis: A review of bronchiolitis, evidence behind various treatment regimens, and suggested admission criteria – A Resident Clinical Pearl

 Melanie Johnston, R3

Integrated FMEM, Dalhousie

Reviewed by Dr. Patricia Dutton

Copyedited by Dr. Mandy Peach

Respiratory illnesses are the second most common ED presentation for paediatric patients, particularly during the winter months, in Canada. 1,2 These paediatric patients with respiratory pathologies are at risk of rapid clinical deterioration; a thorough history and exam with careful attention to respiratory evaluation is critical. Three of the most common paediatric respiratory complaints presenting to the ED include croup, asthma, and bronchiolitis. This pearl will focus on a review of bronchiolitis, its presentation, evaluation, and the evidence behind various treatments.

What is bronchiolitis:

Bronchiolitis is a viral lower respiratory tract infection. It is characterized by obstruction of small airways cause by acute inflammation, swelling/edema, and necrosis of the cells lining the small airways.2 Airways are further narrowed by increased mucous production. The most common causes are respiratory syncytial virus (RSV), influenza, rhinovirus, adenovirus, and parainfluenza.2 These viruses are transmitted by secretions from the nose/mouth and via respiratory droplets in the air. Co-infection with multiple viruses occurs in 10-30% of hospitalized children.2

Figure 1: Pathophysiology of Bronchiolitis.3

 

Epidemiology:
RSV season generally begins in November and persists until April. Bronchiolitis generally presents with a first episode of wheezing before the age of 24 months during the winter months.2 It is the most common reason for admission to hospital in the first year of life in Canada, and more than one-third of children will be affected by bronchiolitis in their first two years of life.2

Presentation:

Bronchiolitis may present with a wide range of symptoms from mild upper respiratory tract infection symptoms (cough, rhinorrhea, fever) to respiratory distress (tachypnea, wheeze, grunting, indrawing, abdominal breathing, and retractions).4 The peak severity of illness usually occurs on day 2-3 of the illness with resolution over 7-10 days.2,6 Cough can persist in infants for up to three weeks after onset.

Pediatric populations at risk for more serious illness include:
– Age <3 months
– Infants born prematurely (<35 weeks gestation)
– Chronic lung disease
– Congenital heart disease
– Chronic neurological conditions
– Immunodeficiency
– Trisomy 21

Patients with the above risk factors are at risk of rapid clinical deterioration even if presenting early in illness with mild symptoms.2,5

Diagnosis:


The diagnosis of bronchiolitis is considered to be clinical based on history and physical exam. The illness generally begins with a 2-3 day prodrome of mild URTI symptoms including cough, fever, rhinorrhea. This may progress to tachypnea, wheeze, and signs of respiratory distress.2 If respiratory distress is interfering with feeding, there may be signs of dehydration (delayed cap refill, dry mucous membranes, no tears produced with crying). Initial assessment should focus on overall appearance, breathing, and circulation. A tool to assist in establishing a general first impression of the paediatric patients stability is the paediatric assessment triangle. Abnormalities in any domain of the triangle (appearance, work of breathing, circulation) should be noted and factored into initial workup with potential to decompensate, with abnormalities in two domains indicative of potentially serious illness.

Figure 3: Pediatric Assessment Triangle.1

Signs of respiratory distress to note on exam include:

– Tachypnea
– Intercostal/subcostal retractions
– Accessory muscle use
– Nasal flaring
– Grunting
– Colour change or apnea
– Wheezing
– Low O2 saturation (<90%)

In stratifying the severity of illness in bronchiolitis, the Royal Children’s Hospital of Melbourne has proposed the following chart to assist with assessment:

Figure 4: Stratifying severity of illness in bronchiolitis, adapted from RCHM.5

Investigations

Bronchiolitis is considered to be a clinical diagnosis. As such, the majority of patients won’t require any additional investigations. If there is diagnostic uncertainty, then the following investigations may be considered:

Management:

Bronchiolitis is a self-limiting disease with peak severity generally at day 3-4 of illness.2,5,6 Most children have mild disease and can be managed with supportive care at home. For those ultimately admitted, focus in hospital is on supportive care with assisted feeding, nasal suctioning, and oxygen therapy as needed.

Disposition:

Most children do well and the symptoms will peak by day 3-5 of illness.

Criteria for safe discharge home include:
– O2 > 90-92%
– Adequate oral hydration
– Mild respiratory symptoms
– Access to reliable follow-up care if needed.2

Criteria for hospital admission include:

– Persistent oxygen saturation <92% and requiring supplemental oxygen AND/OR
– Unable to maintain oral hydration (fluid intake 50% of normal), requiring IV or NG fluids AND/OR
– Persistent moderate-severe respiratory distress
– Apnea (observed or reported)
– Children with risk factors for severe disease (see above).2

Admission or a period of observation in the ED can be used to document feeds and monitor vital signs/oxygen status. Other considerations for admission to hospital include social circumstances, comfort of caretaker in managing child at home, distance to healthcare facility in case of deterioration, and the phase of illness.

Resources:

1. Pediatric Respiratory Illnesses, Dr Allan Shefrin. Jan 30, 2020. Accessed at https://criticallevels.ca/2020/01/30/episode-3-paediatric-respiratory-illnesses-dr-allan-shefrin/

  1. Bronchiolitis: Recommendations for diagnosis, monitoring and management of children one to 24 months of age. Canadian Pediatric Society. Friendman, J., Rieder, M., Walton, J. et al. Nov 3, 2014. Accessed at https://emergencymedicinecases.com/wp-content/uploads/filebase/pdf/CPS-guidelines-bronchiolitis.pdf.

    3. Bronchiolitis. Cleveland Clinic. Accessed online at: https://my.clevelandclinic.org/health/diseases/8272-bronchiolitis

  2. Bronchiolitis, Bottom Line Recommendations. Trekk: Translating Emergency Knowledge for Kids. October 2020. Accessed online at: https://trekk.ca/system/assets/assets/attachments/502/original/2021-01-08-Bronchiolitis_v_3.0.pdf?1610662513

    5. Bronchiolitis, Clinical Practice Guidelines. The Royal Children’s Hospital Melbourne. Accessed online at: https://www.rch.org.au/clinicalguide/guideline_index/Bronchiolitis/

    6. Bronchiolitis, Episode 59. Emergency Medicine Cases. Accessed online at https://emergencymedicinecases.com/episode-59-bronchiolitis/

    7. Bronchiolitis in children: diagnosis and management. NICE guideline. June 1, 2015. Accessed online at: https://www.nice.org.uk/guidance/ng9/resources/bronchiolitis-in-children-diagnosis-and-management-pdf-51048523717

    8. https://www.connectedcare.sickkids.ca/quick-hits/2019/8/29/volume6-efnk4-nyn48-max8h-rczlx (Pediatric assessment triangle)

    9. Bronchioitis, accessed online at: https://en.wikipedia.org/wiki/Bronchiolitis.

 

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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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Altered LOC – a case of thyroid storm; EM Reflections

Altered LOC – a case of thyroid storm; EM Reflections February 2022

Authored and Copyedited by Dr. Mandy Peach

Thanks to Dr. Joanna Middleton for leading the discussion

All cases are imaginary but highlight important learning points

Case

An elderly male is brought to the ED by EMS after being found wandering the streets downtown. A local resident was concerned and called 911. He looks disheveled and is dressed in light clothing despite the cold weather. He has no identification. He is agitated but not aggressive. He is speaking short sentences, with recognizable words, but is nonsensical. He can give no identifying information.

His vitals are 90/62 HR 132 RR 22 O2 93% RA T – 40.1°C.  Gluc 12

On exam he has no obvious neurological deficits but will not follow command for strength or coordination testing. He walked unaided into the department. His pupils are 3mm and reactive bilaterally. He will not follow your finger for oculomotor testing. He does have some dried blood on his right ear –  there appears to be a scalp laceration superior to the ear. There are no other signs of head injury. His neck appears to be supple as you draw his attention to things in the room. Cardiac, abdominal and skin exam are non-contributory. You hear expiratory crackles to the right lung base.

Patients with an altered level of consciousness, especially in the geriatric population, are becoming increasingly more common. What is an easy mnemonic to remember the differential1?

You order a broad scope of investigations including a tox screen, TSH, LFT’s and coags, VBG, blood and urine cultures and CXR.

Is a CT head always a requirement6?

No, CT brain scan should not be used routinely but should be considered in patients with the following indications:

New focal neurological signs
Reduced level of consciousness not adequately explained by another cause
History of recent falls
Head injury
Anticoagulation therapy.

While that is pending, what is your approach to management?

From an airway perspective they are talking, they are maintaining their oxygen saturations. There is borderline hypotensive and tachycardia with a fever.

Initially you decide to cover for sepsis, potentially a respiratory source given your findings on exam. You obtain bilateral IV access, start fluids and antibiotics post cultures. Tylenol is given for fever. You apply oxygen as saturations are low 90’s.

Although infectious causes are common there are a vast number of presentations to consider with a febrile, altered patient2.

  • Heat stroke
  • CNS causes other than infectious: ICH, Stroke, Status Epilepticus
  • Thyroid storm
  • Lithium toxicity
  • Salicylate toxicity
  • Anticholinergic toxicity
  • Alcohol and Benzo Withdrawal
  • Malignant Hyperthermia
  • Neuroleptic Malignant Syndrome
  • Serotonin Syndrome

Chances are this is sepsis so you initiate your therapy and cognitively unload yourself.

Portable CXR is done showing potentially a slight haziness in the right lower lobe. No pulmonary edema. It’s not a slam dunk infiltrate, but common things being common you still suspect sepsis.

The VBG comes back first – its normal. WBC is also back and it is upper end of normal – unexpected given how febrile this patient was. Now you’re starting to question your diagnosis – you go back to your differential for a febrile, altered patient. You decide to add lithium level to your work up as well LFT’s and extended lytes.  Heat stroke is unlikely given the cool weather ongoing this week. Otherwise, you can consider CT head for CNS causes but the remainder will require some sort of collateral history.

While you are mulling this over there is a call from the lab – they are giving a verbal for a critically low TSH level and critically high T4 levels.

You are worried this patient is in thyroid storm.

What are signs/symptoms of thyroid storm3,5?

  • High fever
  • Altered mentation: ranges from agitation and delirium to stupor and coma
  • Cardiovascular instability: tachycardia (often exceeding 140 bpm), hypotension and potentially arrythmia and cardiovascular collapse
  • GI/hepatic symptoms – nausea/vomiting, abdominal pain

 

Physical exam can reveal the following:

  • Goiter
  • Lid lag
  • Tremor
  • Warm, moist skin
  • Ophthalmopathy4 (in presence of Grave’s disease)

Does the degree of hyperthyroidism matter? Ie. The severity of the lab disturbance3?

No, the levels of TSH and and T4/T3 are typically similar to those seen in uncomplicated thyrotoxicosis.

Are there any other lab derangements that would help point in the direction of thyroid storm3?

  • mild hyperglycemia due to catecholamine-induced inhabitation of insulin release and increased breakdown of glucose stores
  • mild hypercalcemia due to hemoconcentration and increased bone resorption.
  • abnormal liver function tests as thyroid hormones are metabolized in the liver
  • leukocytosis or leukopenia

Given that lab values can be similar to thyrotoxicosis are there any criteria to diagnose thyroid storm vs impeding thyroid storm?

No validated criteria exist, however there are scoring systems in circulation similar to this one3.

A value > 45 confirms thyroid storm, a value between 25-45 is concerning for impeding thyroid storm.

You score your patient at 65, assuming that the pneumonia is the precipitating factor. You feel confident thyroid storm is the diagnosis.

Where you wrong to initiate treatment for sepsis5?

Typically for thyroid storm the patient has a history of hyperthyroidism but is tipped into instability with a precipitating factor. Given your clinical findings and CXR this patient potentially has pneumonia that precipitated his presentation. However, if infection doesn’t seem to be the most likely trigger it is not necessary to cover with antibiotics. Consider others causes.

Other than infection what are other risk factors for thyroid storm3,5?

  • Recent surgery
  • Trauma
  • Iodine load ie. Initiating amiodarone treatment
  • Pregnancy/toxemia of pregnancy
  • PE
  • Acute MI
  • DKA
  • Hyperemesis
  • CVA

Your patient is becoming increasingly agitated – what is the management plan5?

Benzos are the drug of choice to manage agitation in this patient. Other supportive therapies include fluids, cooling and monitoring and treating electrolyte/glucose disturbance as needed. However now that the diagnosis is confirmed, treating the cause of the agitation can now be initiated.

What is the treatment for thyroid storm? And the order given?

You reassess your patient after the tylenol, fluid bolus, benzos and antibiotics.

BP 102/62 HR 120, RR20 O2 98% on 1L NC, 39.9°C

You commence cooling and begin beta-blockade with propranolol. You continue fluids and plan to treat with methimazole as currently the patient is not in cardiovascular collapse. You treat with potassium iodide 1 hour later. ICU are now there to do a consult and admit.

Take home points –

  • Consider a broad differential with any altered patient, remember AEIOU
  • A febrile, altered patient isn’t always sepsis! See this great algorithm for differential as well as treatment

  • Untreated thyroid storm has a high mortality – add TSH to your investigations and remember the order of treatment matters to prevent worsening thyrotoxicosis.

 

References & further reading

  1. Morgenstern, J. 2016. First10EM AEIOU TIPS mnemonic for altered mental status. Accessed June 21, 2022 from https://first10em.com/unconscious/first10em-aeiou-tips-mnemonic-for-altered-mental-status/
  2. Helman, A. Long, B. Khatib, N. Strayer, R. Hensley, J. Foohey, S. Petrosoniak, A. EM Quick Hits 36 – Surviving Sepsis, Angle Closure Glaucoma, Bougies, Frostbite, Hot/Altered Patient, Central Cord Syndrome. Emergency Medicine Cases. March 2022. https://emergencymedicinecases.com/em-quick-hits-march-2022/. Accessed [June 21, 2022].
  3. Ross, D (2021). Thyroid Storm. UptoDate. Accessed June 21 2022 from https://www.uptodate.com/contents/thyroid-storm?search=thyroid%20storm&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1#H57436952
  4. Image from https://www.mayoclinic.org/diseases-conditions/graves-disease/symptoms-causes/syc-20356240
  5. 2017. Thyroid and Adrenal Disorders. CRACKCase E128. CanadiEM. Assessed July 6, 2022 from https://canadiem.org/crackcast-e128-thyroid-adrenal-disorders/
  6. Altered Mental Status – Delirium. Chang A, Marsden J. 2020. Point of Care Emergency Summary, BC Emergency Medicine Network.Assessed July 6, 2022 from https://www.bcemergencynetwork.ca/clinical_resource/altered-mental-status-delirium/
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A case of Herpetiform Keratitis- Clinical evaluation and important considerations.

A case of Herpetiform Keratitis- Clinical evaluation and important considerations: A Resident Clinical Pearl

Bonnie He, PGY1

Ophthalmology, Dalhousie University

Reviewed by: Dr. Cherie Adams

Copyedited by: Dr. Mandy Peach

Case

A 68-year-old female presented to SJRH Emergency Department with a three-day history of atraumatic worsening of right eye pain, photophobia, and decreased vision. She denied any experience of flashing lights or “curtain falling”. She reported a long-standing history of glaucoma for which she was previously prescribed brimonidine (alpha-agonist) ophthalmic drops and was prescribed travoprost (prostaglandin) ophthalmic drops approximately one week prior to presentation. Additional ophthalmologic history revealed used of glasses, but not contact lenses, and bilateral cataract surgery two years previously. Of particular note, she recounted an episode of “sores from her upper lip along the side of her nose to right lower eyelid” in the past for which she was treated with oral valacyclovir. Further history positive for hypertension, for which she is prescribed ramipril, and type 2 diabetes mellitus, for which is is prescribed metformin. She is a retired schoolteacher, non-smoker, social drinker and denies any recreational drug use.
Visual acuity from 20 feet with spectacle correction revealed was 20/100 on the right (OD) and 20/30+1 on the left (OS). Her intraocular pressures were OD 17 and OS 19. Examination revealed mild upper and lower eyelid edema and moderate conjunctival injection. Fluorescein staining of the right cornea revealed four small dendritic epithelial defects (Figure 1) at about the 6 o’clock position. External and slit lamp examination of the left eye was normal. Fundoscopic examination to check the optic disc, macula, retinal vessels, and periphery were deferred.

Figure 1A: 4 small dendritic epithelial lesions can be seen at the 6’oclock position.

 

Figure 1B: Classic dendritic corneal epithelial lesions 17.

OPHTHALMOLGIC ASSSESSMENT:

Ocular complaints are common in emergency care settings. Yet, the quantity and quality of ophthalmology education varies significantly across Canada, with both medical students and residents report receiving insufficient ophthalmic medical education from medical education curricula.1-3
Proper history and physical examination taking skills are crucial to the appropriate management of patients with a red eye. The American Academy of Ophthalmology recommends the 8-point physical exam as a systematic approach to any eye problems:

  1. Visual acuity
    • Position the patient 20ft or 6m away from the Snellen chart to test for distance vision
    • Document whether it is their best corrected visual acuity, (ie. did they have their glasses or contact lens on at the time of the exam)
  2. Pupils
    • In dim room light, check for:
      1. Direct response by looking for pupil constriction in the eye being shined
      2. Consensual response by looking for pupil constriction in the other eye (eye that is not being shined)
  • Rapid Afferent Pupillary Defect (RAPD) with the swinging light test by shining light back and front between eyes
  1. Extraocular motility and alignment
    • Conduct a “H test” to test for the 9 cardinal positions of gaze by tracing out the letter “H” in the air while monitor their eyes for 3 S’s: speed, smoothness, and symmetry
    • Ask patient to follow your finger with their eyes while keeping their head still in the center and note for any double vision at certain gazes
  2. Intraocular pressure
    • The Icare tonometer requires no local anesthetic
    • Insert probe into tonometer and anchor the tonometer to the seated patient’s eyebrow.
    • Slowly bring tonometer probe towards patient light until the light turns green – now you’re ready to press the button that will automatically measure the patient’s intraocular pressure
  3. Confrontation visual fields
    • At about 1 arm’s-length away, test each eye individually by holding up 1 or 2 fingers and ask patient how many fingers they see
    • Ask patient to close their OS and fixate on your nose. Close your OS to assess with your open OD.
    • To check OS, ask the patient to close their OD and fixate on your nose. Close your OD to assess with your open OS.
  4. External examination
    • Assess for any obvious globe rupture, ecchymoses, deformities or lesions around the eye
    • Check to see if there’s any ptosis (lid drooping)
  5. Slit lamp examination (watch this video to learn how to perform a slit lamp exam: https://www.youtube.com/watch?v=gHW5OYj1Gf8
    • Assess for the following structures
    • Lids/lashes/lacrimal system: edema, erythema, lesions
    • Conjunctiva/sclera: injection, subconjunctival hemorrhage
    • Cornea: foreign body, fluorescein stain + cobalt blue light to assess corneal integrity (ie. corneal abrasions, herpetic dendrites), Seidel test (leakage of aqueous humour)
    • Iris: round (normal) vs. peaked (abnormal)
    • Anterior chamber: any hyphema, hypopyon, cells, flare
    • Lens: opacity
  6. Fundoscopic examination
    • In the emergency department, fundoscopy is typically undertaken in the undilated eye.
    • May consider dilating the eye with tropicamide (dilating drop) to visualize the back of the eye with the slit lamp or direct ophthalmoscope
    • Assess for the following structures:
      1. Optic nerve: cup-to-disc ratio, pallor, symmetry between eyes
      2. Macula: foveal light reflex
  • Vessels: Arteriovenous (AV) nicking, silver or copper wiring,
  1. Periphery: bleeding

DISCUSSION:

Given the patient’s endorsed history suggestive of ipsilateral V2 herpes zoster and classic dendritic corneal lesions, the leading differential diagnosis for her acute on chronic ocular pain in this case would be zoster keratitis, though herpes keratitis should also be considered, particularly in patients with identified history and recent episode of orolabial cutaneous HSV. Interestingly, she was started on travoprost for her glaucoma a week prior to her presentation. Topical ocular hypotensive agents, including travoprost, are known to have a myriad local and systemic side effects including: superficial punctate keratitis, corneal erosion, bradycardia, hypotension, and bronchoconstriction, are common.4,5 However, of particular interest in this case,  multiple clinical and animal studies have reported that topical prostaglandins for ocular hypertension are culprits  associated with herpes simplex virus (HSV) keratitis or varicella-zoster virus (VZV) keratitis.6-13 It is thought that prostaglandin analogues such as travaprost may induce the reactivation of HSV keratitis by releasing endogenous prostaglandins in the iris and ciliary muscles.9,14-16 Therefore it could also be very well possible that she may have developed HSV keratitis.

 

Irrespective of which differential was truly causing this patient’s symptoms the antiviral treatment for zoster ophthalmicus and HSV keratitis are the same: valocylcovir 1g TID PO x 7 days (or acyclovir 800mg po five times daily if cost of valcyclovir is prohibitive) and arrangements were made for next-day ophthalmologist consultation.

 

BOTTOM LINE:

Always take a thorough ophthalmologic history for patients with ocular complaints, including complete medication history.

Always ask about contact lens use in a history in any patient with a painful red eye.

Always conduct a complete physical exam for patients with ophthalmologic complaints using the AAO 8-point framework described above.


REFERENCES

  1. Sim D, Hussain A, Tebbal A, Daly S, Pringle E, Ionides A. National survey of the management of eye emergencies in the accident and emergency departments by senior house officers: 10 years on—has anything changed? Emerg Med J. 2008;25(2):76-77. http://emj.bmj.com/content/25/2/76.abstract. doi:10.1136/emj.2007.049999.
  2. Noble J, Somal K, Gill HS, Lam W. An analysis of undergraduate ophthalmology training in Canada. Canadian Journal of Ophthalmology. 2009;44(5):513-518. http://www.sciencedirect.com/science/article/pii/S0008418209801130. doi:https://doi.org/10.3129/i09-127.
  3. Gostimir M, Sharma RA, Bhatti A. Status of Canadian undergraduate medical education in ophthalmology. Canadian Journal of Ophthalmology. 2018;53(5):474-479. http://www.sciencedirect.com.ezproxy.library.ubc.ca/science/article/pii/S0008418216309553. doi:https://doi-org.ezproxy.library.ubc.ca/10.1016/j.jcjo.2017.11.015.
  4. Inoue K. Managing adverse effects of glaucoma medications. Clinical ophthalmology (Auckland, N.Z.). 2014;8:903-913. https://pubmed.ncbi.nlm.nih.gov/24872675 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4025938/. doi:10.2147/OPTH.S44708.
  5. Anwar Z, Wellik SR, Galor A. Glaucoma therapy and ocular surface disease: current literature and recommendations. Curr Opin Ophthalmol. 2013;24(2):136-143. doi:10.1097/ICU.0b013e32835c8aba [doi].
  6. Kroll DM, Schuman JS. Reactivation of herpes simplex virus keratitis after initiating bimatoprost treatment for glaucoma. Am J Ophthalmol. 2002;133(3):401-403. doi:S0002939401013605 [pii].
  7. Wand M, Gilbert CM, Liesegang TJ. Latanoprost and herpes simplex keratitis. Am J Ophthalmol. 1999;127(5):602-604. doi:S0002939499000501 [pii].
  8. Alm A, Grierson I, Shields MB. Side effects associated with prostaglandin analog therapy. Surv Ophthalmol. 2008;53 Suppl1:93. doi:10.1016/j.survophthal.2008.08.004 [doi].
  9. Soomro MZ, Moin M, Attaulla I. Latanoprost and Herpetic Keratitis. Pakistan Journal of Ophthalmology. 2011;27(4).
  10. Kothari MT, Mehta BK, Asher NS, Kothari KJ. Recurrence of bilateral herpes simplex virus keratitis following bimatoprost use. Indian J Ophthalmol. 2006;54(1):47-48. doi:10.4103/0301-4738.21617 [doi].
  11. Ekatomatis P. Herpes simplex dendritic keratitis after treatment with latanoprost for primary open angle glaucoma. Br J Ophthalmol. 2001;85(8):1008-1009. doi:10.1136/bjo.85.8.1007a [doi].
  12. Morales J, Shihab ZM, Brown SM, Hodges MR. Herpes simplex virus dermatitis in patients using latanoprost. Am J Ophthalmol. 2001;132(1):114-116. doi:S0002939401010121 [pii].
  13. Villegas VM, Diaz L, Izquierdo NJ. Herpetic keratitis in a patient who used two different prostaglandin analogue ophthalmic solutions: a case report. P R Health Sci J. 2008;27:348+. https://link.gale.com/apps/doc/A189052227/HRCA?u=anon~6a050068&sid=googleScholar&xid=2c140d29.
  14. Dios Castro E, Maquet Dusart JA. Latanoprost-associated recurrent herpes simplex keratitis. Arch Soc Esp Oftalmol. 2000;75(11):775-778.
  15. Gordon YJ, Yates KA, Mah FS, Romanowski EG. The effects of Xalatan on the recovery of ocular herpes simplex virus type 1 (HSV-1) in the induced reactivation and spontaneous shedding rabbit models. J Ocul Pharmacol Ther. 2003;19(3):233-245. doi:10.1089/108076803321908356 [doi].
  16. Kaufman HE, Varnell ED, Toshida H, Kanai A, Thompson HW, Bazan NG. Effects of topical unoprostone and latanoprost on acute and recurrent herpetic keratitis in the rabbit. Am J Ophthalmol. 2001;131(5):643-646. doi:S0002939400009107 [pii].
  17. Yu, Hubert (2019) Canadiem Medical Concepts: Approach to Corneal Disorders in the ED

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