Back to School – Back-to-Back Asthma Attacks


Resident Pearl by Dr. Rosario Hernandez Barba

FM PGY1

Dalhousie University

Reviewed by Dr. B Ramrattan

Copy Edited by Dr. J Vonkeman

Pdf Download: EMSJ Back to School – Back-to-Back Asthma Attacks – RHernandezBarba


Background

Asthma is a common chronic respiratory condition characterized by reversible airway inflammation and bronchoconstriction. Asthma affects people of all ages, but often is diagnosed in childhood from as early as 12months of age. Key symptoms include coughing, wheezing, shortness of breath, and chest tightness (Trottier et.al, 2021). Acute asthma exacerbations in children and youth are frequent presentations in the emergency department. Triggers for asthma exacerbations include: pollutants, allergens, respiratory infections, exercise, and cold air. (Trottier et.al, 2021). Appropriate and rapid assessment of respiratory distress in the emergency department can guide efficient treatment for patients of all ages.


Evaluation

  • Vital signs
  • PRAM score
  • +/- bedside spirometry ( FEV)

 

PRAM – a rapid assessment of asthma symptom severity (Ducharme, 2008)

  • 5 criteria 12-point scoring tool
  • Watch then listen!
  1. Vitals – O2 saturation
    • Measured with the patient on room air.
  2. Suprasternal retractions
    • Visible indrawing

  1. Scalene muscle retraction
    • Palpable contraction of deep cervical muscles on lateral neck.

  1. Air entry – Lung fields matter
    • Determine rating using the most severely affected lung.
    • Lung fields: Right anterior, right posterior, left anterior, left posterior.
  1. Wheezing – Lung auscultation zones matter
    • Determine rating with least 2 affected auscultation zones. Use the 2 most severely affected.
    • Auscultation zones: RUL, RML, RLL, LUL, LLL

 

Other indicators of severity include: (Trottier et. al, 2021)

  • Nasal flaring
  • Reduced activity level
  • Inability to speak in full sentences, inability to feed (infant)
  • Decreased level of alertness
    • Clinical features of cerebral hypoxemia
    • Sign of impending respiratory failure

 

Bedside Spirometry (Trottier et.al, 2021)

  • Can be used as an objective measure of airway obstruction and severity of exacerbation to guide management.
  • Although recommended by the Canadian Pediatric Society, it requires patient cooperation for reliability.
  • FEV1 is often not measured before initiation of bronchodilators.

 


Management

 

Critical Bedside Actions (Ducharme, 2008)

  1. Ensure oxygenation.
    • Goal is to keep oxygen saturation >92%
  2. Administer bronchodilators:
    • Salbutamol (SABA) +/- Ipratropium (SAMA)
  3. Systemic corticosteroids to relieve inflammation.
    • Mild exacerbation: Corticosteroids are optional.
    • Consider oral steroids if risk factors for severe asthma.
  4. Serial reassessments to monitor response to therapy.

Clinical Pathways

  • Use a clinical pathway for management according to severity. Order the pediatric asthma order set for correct dosing based on age. (Lewis, 2021)
  • See Clinical Pathways for Asthma Exacerbation for management according to severity

Medical Management (Trottier, et.al, 2021)

  1. Oxygen – treat hypoxemia urgently with facemask or nasal cannula.
  2. Bronchodilator – Short acting beta2-agonist: Salbutamol
    • A metered-dose inhaler (MDI) with an aero chamber is the more efficient than a nebulizer for bronchodilator delivery.
    • The dose and frequency of therapy depends on the severity of the presentation and the response to treatment.
    • In Severe presentations – continuous administration may have a better bronchodilator effect than intermittent therapy. Used if response to conventional treatment is poor.
    • Side effects: are generally well tolerated.
    • Inappropriately escalating doses can cause increased lactic acid and compensatory hyperventilation which can be confused with asthma deterioration.
  3. Bronchodilator – Short acting anticholinergic: Ipratropium
    • If Moderate-Severe: Adjunctive therapy to Salbutamol
    • Reduces hospital admission rates, risk of nausea and tremor, and improves lung function.
  4. Corticosteroids PO/IV: methylprednisolone
    • If Moderate-Severe: ALL patients should receive steroids as part of their initial treatment.
    • Mild: no clear evidence to support routine use of oral corticosteroids. Use clinical picture and patient history of repeated salbutamol doses to guide management.
  5. Magnesium Sulphate IV
    • If Moderate-Severe: patients with incomplete response to conventional therapy during the first 1-2 hours
    • Side effects: hypotension and bradycardia
      • Initiation requires consultation with a pediatrician.
      • Cardiorespiratory monitoring

Reassess

  • While initiating management, obtain a focused asthma history from caregivers including:
    • Triggers
    • Current medications
      • Amount of rescue inhaler use
      • Systemic steroid use
    • Previous events and admissions, including ICU and intubation.
    • Comorbidities
  • Reassess after 1 hour if mild, more frequently if moderate- severe
  • Communicate with parents.

 

Figure 5 Medications and dosages for acute asthma treatments for children > 1y (CPS.ca)

Management of Impending Respiratory Failure: (Trottier, et.al, 2021)

  • Confused, lethargic, cyanotic, decreasing respiratory effort.
  1. CALL FOR HELP: PICU, anesthesia (or best provider for intubation if needed)
    • Cardiopulmonary monitors
    • Start IV lines x2.
    • Labs: CBC, lytes, VBG
  2. Oxygen – 100% non-rebreather mask
    • Support ventilation if required.
  3. Bronchodilators – nebulized salbutamol and ipratropium
  4. Corticosteroids – IV/IM
  5. Magnesium Sulfate – IV
  6. Consider other medications with pediatric consultation:
    • IV salbutamol
    • Heliox
    • Ketamine
    • Anesthetic gases.
  7. Consider non-invasive ventilation until help arrives.
  8. CXR if possible – r/o other causes of respiratory failure
  9. Be ready for rapid sequence intubation.
  10. Reassess and COMMUNICATE
  • Try to avoid intubation unless the patient becomes bradycardic and pCO2 is HIGH
  • ALWAYS chat with peds ICU before intubating

 


Bottom Line

  • Assess the severity of the asthma exacerbation using PRAM scores.
  • Initiate treatment promptly to relieve bronchoconstriction.
    • Regardless of severity, salbutamol is first line to relieve bronchoconstriction.
    • When in doubt, take the blue puffer out.
  • Know when to call for help!
  • Continuous reassessment and monitoring are key throughout their stay to adjust treatment.
  • Communicate with children and their parents throughout.

 


References

  1. Ducharme, F. M., Chalut, D., Plotnick, L., Savdie, C., Kudirka, D., Zhang, X., Meng, L., & McGillivray, D. (2008). The Pediatric Respiratory Assessment Measure: A Valid Clinical Score for Assessing Acute Asthma Severity from Toddlers to Teenagers. The Journal of Pediatrics, 152(4), 476–480.e1. https://doi.org/10.1016/j.jpeds.2007.08.034
  2. Lewis,D. (2021, March). Emergency Medicine Saint John. Asthma Pediatrics | Department of Emergency Medicine | Saint John (sjrhem.ca)
  3. Trottier, E. , Chan,K., Allain,D., Chavin-KImoff,L. (2022, May). Managing an acute asthma exacerbation in children. Canadian Paediatric Society. Managing an acute asthma exacerbation in children | Canadian Paediatric Society (cps.ca)
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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?16106625135. 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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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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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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Chest tube insertion – Pigtail

Pigtail Catheter Insertion Procedure

EMSJ Faculty Pearl

Dr. Paul Frankish & Dr. Matt Greer

Updated April, 2023


See Video of Pigtail Catheter Insertion Here


Equipment Update: 

Adults: Trauma carts should be stocked with 28Fr, 24Fr, 20Fr standard chest tubes and 14Fr pigtail catheter kits. It is recommended that we discontinue stocking larger sized chest tubes (32Fr, 36Fr) and Cook 9Fr pneumothorax set with metal trochar/needle.

Pediatrics: PALS carts should be stocked with 10Fr seldinger kits, 14Fr pigtail catheter kits and 20 Fr standard sized chest tubes.


  1. Obtain informed consent if possible, obtain all supplies needed, have drainage system opened and ready to go.
  2. Confirm 3-way stopcock attached to tube, then insert obturator through this 2. Sterile prep, drape, gown/glove.
  3. Identify triangle of safety (5th IC, mid axillary, pectoralis). – or use PoCUS to guide site safety and depth (DL)
  4. Anesthetize skin, subcutaneous, rib, intercostal, and pleura. Consider procedural sedation.

May need up to 20 cc of local, consider refreezing with larger spinal needle, withdraw until the air bubbles stop to freeze the pleura


5. Insert large “seeker” needle at desired IC space, with fluid filled syringe attached, withdraw as you go.


Note the depth when you get air bubbles for when you dilate the tract


6. Slide over superior aspect of rib and stop when you withdraw air bubbles/fluid.
7. Detach syringe and insert guidewire through needle. There should be no resistance. Only about 10 cm inside the thoracic cavity is required. Remove needle while leaving the guide-wire in place.
8. Make a small incision with 11-blade alongside guidewire, then dilate to required depth with dilator, then insert pigtail with obturator over wire to appropriate depth.


Remove the obturator once tube is within pleural cavity, then advance pigtail into chest


9. Insert as far as possible until resistance is felt to ensure all fenestrations are within the thoracic cavity.


You can always pull it back out if it’s in too far


10. Attach tubing extension, then to either Heimlich valve or underwater seal/wall suction.


Heimlich valve function is unidirectional. Attach blue end to chest tube


11. Suture in place as per usual chest tube technique. Ensure dressing optimizes skin seal (sticky/occlusive).
12. Confirm placement with chest x-ray.


 

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A life threatening case of Hiccups

A life threatening case of Hiccups – A Resident Clinical Pearl

Mark McGraw, PGY3 FMEM program,  Dalhousie University Saint John

Reviewed by Dr. Luke Taylor

Copyedited by Dr. Mandy Peach

Introduction:

Its mid morning on an acute shift in the emergency department and you hear a familiar but somewhat out of place sound coming from around the corner. You look up to see the triage nurse walking in a middle-aged male patient who is hiccuping constantly. The patient looks unwell and is pale, but he is able to walk into the department without assistance. The triage nurse asks the charge doc where she should place the patient. He has had intractable hiccups for over a week and has been unable to sleep or eat anything. His chief complaint is hiccups and weakness. She notes he also has a small infected cyst on his back that is being treated with Keflex from one of the local surgeons and had a subjective fever at home. Vitals on triage were normal but she was concerned because he just didn’t look right. You suggest he take a trauma bed and state you’ll see him now based on his appearance and wonder to yourself how often a trauma bed is taken up with someone who has a chief complaint of hiccups….

A little background:

Hiccups are a bit of a physiologic anomaly and appear to have no protective effect or evolutionary purpose. Hiccups can be found early in life and are can be found as early as the second trimester of pregnancy. The incidence of hiccups in the general pediatric and adult population is unknown but its fair to say the majority of people have experienced them at some point in their lives. To most, hiccups are nothing more than a brief annoyance or embarrassing distraction but in some cases they can herald sinister pathologies.

Hiccups result from inappropriate closure of the glottis through a reflex arc that consists of the phrenic nerve, vagus nerve, and thoracic sympathetic chain. During inspiration our glottis remains patent allowing unimpeded airflow into the lungs. The hiccup reflex triggers glottis closure, typically triggered during the swallowing to prevent aspiration, about 30 milliseconds after the onset of inspiration resulting in a rush of air against a closed glottis.

The majority of problematic hiccup cases arise from stimulation, inflammation, or injury to nerves of the afferent reflex arc. Two of the most common causes of benign hiccups are gastric distension from eating a large amount of food or consuming carbonated beverages and relaxation of the glottis due to alcohol ingestion.

The differential for hiccups is broad. UpToDate lists over 50 items on its differential for persistent/intractable hiccups grouped as CNS disorders, vagus/phrenic irritation, GI disorders, thoracic disorders, CV disorders, toxic/metabolic causes, postoperative, drug induced, and psychogenic.

Hiccups under 48 hours

In patients with hiccups lasting less than 48 hours and without red flag symptoms or other warning signs it is reasonable to try physical maneuvers to stop hiccups. The goal of all these maneuvers is stimulation/irritation of the afferent reflex arc.

• Breath holding or Valsalva maneuvers (increasing hypercapnia),
• Sipping or gargling cold water (nasopharynx irritation)
• Swallowing a spoonful of dry sugar (nasopharynx irritation),
• Pulling a patient’s knees to his/her chest and having them lean forward (decrease diaphragmatic pressure)

Hiccups over 48 hours

There is little quality evidence on the treatment of hiccups. In general, if an etiology is suggested from the history and physical target treatment, i.e. using a PPI in patients with underlying GERD, should be considered.

A 2015 systematic review suggested the use of baclofen and gabapentin as first line agents in treating hiccups with metoclopramide and chlorpromazine used as second line agents. A follow up systematic review in 2017 published in the journal of emergency medicine found that only baclofen and metoclopramide had randomized control trials supporting their efficacy. Baclofen was found to be particularly effective for treatment of intractable hiccups associated with stroke.

Treatment options:

• Baclofen 5 to 10 mg PO TID,
• Gabapentin 100 to 400mg PO TID,
• Metoclopramide 10mg PO TID or QID,
• Chlorpromazine 25mg PO TID,

A recent case report published in the American Journal of Emergency Medicine (Kocak et al., 2020) demonstrated almost immediate termination of hiccups in a patient following a subdermal injection of lidocaine and thiocolchicoside into the sternocleidomastoid muscle and epigastric region.

 

 

Back to our case

Our patient settles into a bed in the trauma bay and his repeat vitals show a declining blood pressure and increasing heart rate. His only complaint at this time continues to be his persistent hiccups. Cardiac, respiratory, abdominal and CNS exams are unremarkable. When you assess the “small lump” on his back you find an area of erythema extending from the superior tip of his scapula to his L1/L2 region inferiorly with a large softball size nodule around the lateral border of his scapula. You initiate empiric therapy with pip/tazo and clindamycin and call for an urgent CT scan and surgical consult.

While prepping for the scan the patient asks about treatment for his hiccups. You decide to try metoclopramide 10mg IV, which does nothing to alleviate his hiccups. His CT scan confirms a massive abscess extending from his deltoid muscle to his obliques with infiltration into the muscle and fascia. He is taken to the OR by a team of 3 surgeons for emergent debridement of his necrotizing fasciitis. After a brief stay in the ICU he is transferred to the surgical floor where you find out his hiccups have resolved.

Summary
The next time you are working in the emergency department and a patient presents with hiccups here are a few helpful points to remember:

• Patients with hiccups lasting less than 48 hours in the absence of red flag / systemic symptoms typically do not require medical workup or treatment.
– Physical maneuvers to terminate hiccups may provide relief for patients in the ED.
• Patients with persistent hiccups over 48 hours warrant a full physical exam and laboratory studies tailored to the patient’s history as hiccups may be the initial manifestation of an underlying neoplasm, infection, or metabolic disorder.
• If no underlying etiology is found there is reasonable evidence to support empiric treatment with metoclopramide 10mg PO TID or baclofen 5 to 10mg PO TID.
• In patients with persistent hiccups secondary to another disease process empiric treatment may be a useful adjunct while the underlying cause is addressed.

 

References

Polito NB, Fellows SE. Pharmacologic Interventions for Intractable and Persistent Hiccups: A Systematic Review. J Emerg Med. 2017 Oct;53(4):540-549. doi: 10.1016/j.jemermed.2017.05.033. PMID: 29079070.
Steger M, Schneemann M, Fox M. Systemic review: the pathogenesis and pharmacological treatment of hiccups. Aliment Pharmacol Ther. 2015 Nov;42(9):1037-50. doi: 10.1111/apt.13374. Epub 2015 Aug 25. PMID: 26307025.
Kocak AO, Akbas I, Betos Kocak M, Akgol Gur ST, Cakir Z. Intradermal injection for hiccup therapy in the Emergency Department. Am J Emerg Med. 2020 Sep;38(9):1935-1937. doi: 10.1016/j.ajem.2020.03.044. Epub 2020 Mar 25. PMID: 32245702.
Chang, F. Y., & Lu, C. L. (2012). Hiccup: mystery, nature and treatment. Journal of neurogastroenterology and motility, 18(2), 123–130. https://doi.org/10.5056/jnm.2012.18.2.123
Image of reflex arc: http://blog.clinicalmonster.com/2017/03/23/so-bored-i-hiccuped/
Marion, DW. Hiccups. In: UpToDate, Post, TW (Ed), UpToDate, Waltham, MA, 2020.

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Carbon Monoxide Poisoning

Carbon Monoxide Poisoning – A Medical Student Clinical Pearl

Mitchell McDonough

DMNB, Class of 2022

Reviewed by Dr. Rachel Goss

Copyedited by Dr. Mandy Peach

Case

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

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

Differential for Confusion

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

Stroke/CNS structural lesion/Head Injury

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

Intoxication/withdrawal
• Alcohol
• Drugs
• Carbon Monoxide

Investigations

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

Pertinent Arterial Blood Gas Values for our patient:

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

 

Carbon Monoxide Poisoning Overview

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

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

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

Clinical Presentation

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

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

 

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

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

Diagnosis

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

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

Treatment

Treatment of patients with suspected carbon monoxide poisoning include:

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

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

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

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

Case Conclusion

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

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

References

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

 

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Lung PoCUS – Podcast

Lung PoCUS in Pediatric Emergency Medicine – Podcast

PoCUS Fellowship Clinical Pearl (RCP) May 2020

Dr. Mandy Peach (Emergency Physician and Dalhousie PoCUS Fellow, Saint John, NB, Canada)

Reviewed by Dr. David Lewis

 


Extract:

“My name is Mandy Peach and I am Emergency Physician at the Saint John Regional Hospital in Saint John, New Brunswick. I’m currently completing a PoCUS Fellowship and a pediatric rotation through the IWK Emergency Department in Halifax…….

What is the evidence for the use of PoCUS and diagnosing pediatric pneumonia. Well trained PoCUS Physicians can identify pneumonia with a sensitivity of 89% and a specificity of 94%, compared community-acquired pneumonia chest x-ray has a sensitivity of 69% and a specificity of 100%, if you see it great…. but what about early bacterial pneumonia and this case PoCUS has the upper hand, and if you consider consolidations behind the heart that can be visualized on PoCUS and obscured on chest x-ray – PoCUS 2  chest x-ray zero. So clearly it’s a useful tool to have when trying to differentiate between bacterial pneumonia that requires treatment and viral causes that would indicate conservative management. So how do we actually ultrasound the lungs…..the first step is to make the kid comfortable scan them in a position of comfort for example and their parents arms what the patient touch the ultrasound gel or the probe so it’s less of a scary thing maybe play their favourite music or YouTube video on the background or give them their favourite or snack do you want to choose a high frequency linear probe and scanning the longitudinal plane ……….”

 

Listen to the Podcast for some useful tips on performing and interpreting lung ultrasound in the pediatric population.

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Whose Line is it Anyway? – PoCUS in a Patient with Dyspnea

Medical Student Clinical Pearl – March 2020

Nguyet (Na) Nguyen

MD Class of 2021
Memorial University of Newfoundland

Reviewed and Edited by Dr. David Lewis

All case histories are illustrative and not based on any individual


 

Case Report

ID: 60 y/o M with dyspnea presenting to the ED late evening

HPI: Patient complained of increasing SOB starting the morning on day of presentation, with a worsening 3 days of non-productive cough. No chest pain or other cardiac features. No complaint suggestive of URTI or GI illness. Patient was given Atrovent and Ventolin en route by EMS, and was allegedly moving more air into his lungs after this intervention. Patient reports no ankle swelling, paroxysmal nocturnal dyspnea, but reports using 2 pillows to elevate himself when sleeping. Patient reports no fever, unexplained weight loss or fatigue.

Past medical history includes chronic back pain, DM, atrial fibrillation, peripheral DM-related ulcers, chronic kidney disease, BPH, colon cancer with hepatic metastases. Past surgical history significant for 5x CABG, liver and colon resection.

His medications are amitriptyline 10mg PO qhs, acetaminophen 650mg PO BID, dutasteride 0.5mg PO daily, ferrous sulfate 300mg PO daily, furosemide 40mg PO BID, metformin 500mg BID, pantoprazole 40mg PO BID, pregabalin 150mg PO BID, primidone 125mg PO daily, rosuvastatin 40mg PO qhs, rivaroxaban 15mg PO daily.

He has a distant 10 pack-years smoking history, drinks alcohol occasionally, and does not use recreational drugs. The patient lives with his wife in their own home.

Physical exam: Patient was markedly pale, non-diaphoretic, in tripod position with increased work of breathing. His temperature was 36.9, regular pulse rate at 105, respiratory rate 22, oxygen saturation 90% on room air and a nebulizer mask through which he was receiving aerosolized Atrovent and Ventolin. His BP was 125/78mmHg.

Cardiovascular exam revealed distant S1S2 in a chest with no visible deformity. His JVD was at the level of the sternal angle, there was no pedal edema bilateral. Capillary refill was 3 seconds bilateral at the thumbs. Percussion revealed no focal dullness, however on auscultation, basal crackles were heard more prominently in the right lung base, though also present on the left. There were also wheezes noted in the upper lobes heard in the anterior chest. Abdomen was soft, non-distended, non-tender. Neurological exam unremarkable.

Investigations: ECG showed sinus tachycardia with a LBBB, bloods drawn for routine labs, VBG, lactate, CXR ordered.

Differential diagnosis: AECOPD vs congestive heart failure.

PoCUS (Arrival Time + 10 mins): B-lines were observed in both lungs when a curvilinear probe was placed over different areas of the anterior chest. A small pleural effusion was also noted at the bottom of the right lung. B-lines represent increased fluid in an area of the lung, and given different clinical contexts maye represent pulmonary edema, pneumonia, or pulmonary contusion. In this case the most likely explanation for bilateral diffuse B-Lines is CHF and Pulmonary Edema. 

Working Diagnosis (Arrival Time + 10 mins): CHF and Pulmonary Edema

Management (Arrival Time + 15 mins): Pending transfer fo CXR and results of investigations the patient was treated with intravenous diuretics. He passed 500mls of urine and his symptoms improved considerably.

 

Investigations Results (Arrival Time + 45 mins): leukocytes 6.4, hemoglobin 83, platelet 165, sodium 140, potassium 5/0, chloride 101, creatinine 120, urea 11.7, glucose 17.0. Venous blood gas showed pH 7.31, pCO2 555, HCO3- 28 and lactate 2.7.

CXR (Arrival Time + 45 mins):

CXR was similar to above, this image is from: https://radiopaedia.org/cases/acute-pulmonary-oedema-6

 

Final impression: Congestive heart failure


What are B Lines?

These are the ultrasound equivalent of Kerley-B lines often reported on chest X-ray, which indicate edema in the lungs. For an exam to be positive (i.e indicative of pathology), one needs to see a minimum of 3 B-lines per view. B-lines look like flashlight beams traveling undisrupted down the entire ultrasound screen, as seen in the images above obtained during the exam.

These need to be distinguished from other artifacts such as ‘A-lines’ and ‘comet tails’. A-lines are seen in normal lungs. These are ‘repetitive reverberation’ artifacts of the normal pleura in motion. (Figure 1)(1)

‘Comet tails’- reported first by Lichenstein et al. in 1998 (although he was describing B-Lines in this paper) (Figure 2) (1), are ‘short, hypoechoic artifacts’ that only descend vertically partially down the screen. These are normal lung artifacts. This paper explains “a common misunderstanding in lung ultrasound” nomenclature that stems from Lichtenstein’s original paper.

Download pdf

 

From: https://www.mdedge.com/emergencymedicine/article/96697/imaging/emergency- ultrasound-lung-assessment

 


More on Comet Tails Artifact in this post from LitFL:

Comet tail artefact

 


 

Protocols

There are multiple protocols that guide the ultrasound technique (4) , some of which are:

  • Lichenstein et al (1998): longitudinal scans of anterior and lateral chest walls of patients in semi- recumbent position. Positive test defined as bilateral multiple B-lines diffuse anterolateral or lateral. The protocol had reported sensitivity (true positive) of 100%, and specificity (true negative) 92% for cardiogenic pulmonary edema. Blue Protocol (2015)
  • Liteplo et al (2008): anterior and lateral chest walls with patient supine: each chest divided into 4 zones (anterior, lateral, upper and lower). Positive test: pathologic pattern found in >1 zone on each side, with both sides involved.
  • Volpicelli et al. (2008): longitudinal scans of supine patients with chest divided into 11 areas (3 anterior R, 3 lateral R, 2 anterior L, 3 lateral L) to obtain score 0-11. Scores strongly correlated with radiologic and BNP (lab marker of CHF) at presentation.

 

 


 

What is the Evidence?

Al Deeb et al. conducted a systematic review and analysis of prospective cohort and prospective case-control studies in the ED, IDU, inpatient wards and prehospital settings (n = 1075). This was published in Acad Emerg Med (2014), which reported a sensitivity of 94.1% for using B-lines to diagnosis acute cardiogenic pulmonary edema (ACPE), and a specificity of 92.4% for patients with a moderate- high pretest probability for ACPE.

The SIMEU Multicenter study reported in 2015 reported a significantly higher accuracy (97% sensitivity and 97.4% specificity) with an approach incorporating lung ultrasound (LUS) in differentiating acute decompensated heart failure (ADHF) and non-cardiac causes of acute dyspnea, compared to approaches using the initial clinical workup (past medical history, history of presenting illness, physical examination, ECG, ABG), chest X-ray alone and natriuretic peptides.

Martindale et al. reported in 2016 (Academic Emergency Medicine) high positive likelihood ratio of pulmonary edema observed on lung ultrasound and low negative likelihood ratio of B-line pattern on lung US in affirming the presence of acute heart failure, after a systematic review and analysis of 57 prospective and cross-sectional studies (n = 1,918).

A useful Systematic Review “Emergency department ultrasound for the detection of B-lines in the early diagnosis of acute decompensated heart failure: a systematic review and meta-analysis ” from McGivery et al from SJRHEM (7), was published in 2018.


 

Learning Point

For a patient presenting to the ER with dyspnea, using PoCUS to observe 3 or more B-lines in two bilateral lung zones +/- pleural effusion can rapidly guide an accurate diagnosis of acute congestive heart failure.


 

References

  1. Taylor, T., Meer, J., Beck, S. Emerg Med. (2015) https://www.mdedge.com/emergencymedicine/article/96697/imaging/emergency- ultrasound-lung-assessment Last accessed Feb 29, 2020
  2. Lee, FCY, Jenssen, C., Dietrich, CF Med Ultrason (2018); 20(3): 379-384
  3. Ang SH. & Andrus P Curr Cardiol Rev. 2012 May; 8(2): 123-136https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3406272/
  4. Al. Deeb M., Barbic S., Featherstone R., Dankoff J., Barbic D. Acad Emerg Med 2014 Aug; 21(8): 843-52 https://www.ncbi.nlm.nih.gov/pubmed/25176151
  5. Pivetta E et al. Chest. 2015 Jul; 148(1): 202-210 https://www.ncbi.nlm.nih.gov/m/pubmed/25654562/
  6. Martindale JL, Wakai A, Collins SP, Levy PD, Diercks D, Hiestand BC, Fermann GJ, deSouza I, Sinert R, Acad Emerg Med. 2016 Mar; 23(3): 223-242 https://www.ncbi.nlm.nih.gov/pubmed/26910112
  7. McGivery K, Atkinson P, Lewis D, et al. Emergency department ultrasound for the detection of B-lines in the early diagnosis of acute decompensated heart failure: a systematic review and meta-analysis. CJEM. 2018;20(3):343‐352. doi:10.1017/cem.2018.27

 

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Lung Ultrasound in the Evaluation of Pleural Infection

Lung Ultrasound in the Evaluation of Pleural Infection

Resident Clinical Pearl (RCP) July 2019

Yazan Ghanem PGY5 Internal Medicine, Dalhousie University

SJRHEM PoCUS Elective

 

Reviewed and edited by  Dr. David Lewis.

 


CASE: MR. WHITE

 

83 year old male with known past medical history of mild cognitive impairment (lives alone in assisted living). Two weeks prior to current presentation, he was admitted with community acquired pneumonia and discharged after 2 nights of hospital stay on oral antibiotics.

He is now presenting with 5 days history of worsening dyspnea, fever, fatigue and reduced oral intake. Vital signs are: Temperature 38.4 C; heart rate 80/min; Blood pressure 121/67; Respiratory rate 28/ minute; Oxygen saturation 90% on room air. His chest exam showed reduced air entry and dullness to percussion in the right hemithorax.

CXR:

 

Bedside POCUS:

 

Pleural fluid analysis:

•       WBC – 22,000 cells per uL

•       LDH – 1256 Units / L

•       Glc – 2.2 mmol / L

•       pH – 7.18

•       Gram Stain – Neg

 

Next steps in management?

 

A – 14 Fr pleural drain + Start IV Levofloxacin

 

B – 28 Fr pleural drain + Start Ceftriaxone / Azithromycin

 

C – 14 Fr pleural drain + Start Piperacillin – Tazobactam

 

D – Start Ceftriaxone / Azithromycin + Repeat CXR in 1 week

 

 

(See end of page for answer )

 


 

Normal Thoracic Ultrasound:

Thoracic Ultrasound is limited by bony structures (ribs and scapulae) as well as by air within lungs (poor conductor of sound waves).

With the transducer held in the longitudinal plane:

1 –     Ribs are visualized as repeating curvilinear structures with a posterior acoustic shadow.

2 –     Overlying muscle and fascia are seen as linear shadows with soft tissue with soft tissue echogenicity.

3 –     Parietal and visceral pleura is visualized as a single echogenic line no more than 2 mm in width which “slides” or “glides” beneath the ribs with respiration. Two separate lines can be seen with a high frequency transducer.

4 –     Normal aerated lung blocks progression of sound waves and is characterized by haphazard snowstorm appearance caused by reverberation artifact.

5 –     Diaphragms are bright curvilinear structures which move with respiration. Liver and spleen have a characteristic appearance below the right and left hemi diaphragms respectively.

 

 


Pleural Effusion:

Ultrasound has higher sensitivity in detecting pleural effusions than clinical examination and chest X-Ray.

On Ultrasound, pleural effusions appear as an anechoic or hypoechoic area between the visceral and parietal pleura that changes in shape with respiration. Atelectatic lung tissue appear in the far field as flapping or swaying “tongue-like” echodensities.

Ultrasound morphology:

1-     Anechoic Effusion: Totally echo-free (Could be transudative or exudative)

2-     Complex Non-septated: Echogenic appearing densities present (fibrinous debris). Always exudative.

3-     Complex Septated: Septa appear in fluid. Always exudative.

 

 


Parapneumonic Effusions and Empyema:

Ultrasound is superior to CT in demonstrating septae in the pleural space. However, CT is recommended for evaluation of complex pleuro-parenchymal disease and loculated pleural collections if drainage is planned: There is no correlation between ultrasound appearance and the presence of pus or need for surgical drainage; however, the presence of a septated appearing parapneumonic effusion correlate with poorer outcomes (longer hospital stay, longer chest tube drainage, higher likelihood for need for fibrinolytic therapy and surgical intervention.

Parapneumonic effusions appear as hyperechoic (with or without septae) on ultrasound.

 


Pulmonary Consolidation:

Pulmonary consolidation is sonographically visible in the presence of a pleural effusion that acts as an acoustic window or if directly abutting the pleura.

It appears as a wedge-shaped irregular echogenic area with air or fluid bronchograms.

 


 

Back to Mr. White

 

Next steps in management?

 

A – 14 Fr pleural drain + Start IV Levofloxacin

 

B – 28 Fr pleural drain + Start Ceftriaxone / Azithromycin

 

C –14 Fr pleural drain + Start Pipercillin- Tazobactam

 

D – Start Ceftriaxone / Azithromycin + Repeat CXR in 1 week

 

Rationale:

Complicated parapneumonic effusions should be managed with drainage and antibiotics that will treat anaerobic infection. An alternative would be a combination of Ceftriaxone and Metronidazole (No pseudomonas coverage). Levofloxacin alone does not add any anaerobic coverage. Azithromycin has poor penetration into loculated pleural collections.

 


 References

 

British Thoracic Society – Pleural Disease Guideline – 2010

https://thorax.bmj.com/content/65/8/667

 

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