Greenstick and Torus fractures

Torus Fractures (Buckle/Cortical Fractures)

Torus fracture is an injury of the cortex on the non-compressive side of the bone with an intact cortex on the tension side. Torus is derived from Latin (tori) meaning a swelling or protuberance. Deformity should not occur in torus fracture because the periosteum and cortex are intact on the side of the bone opposite to fracture. The distal end of the radius is the most common site for a torus fracture. Compressive forces often result in a bulging or buckling of the periosteum rather than a more complete fracture line. these injuries usually involve the metaphysis. A simple torus fracture will not produce a visible deformity to the shape of the extremity; however, there is typically soft tissue swelling and point tenderness over the bony injury. 

Radiographically, the torus fracture may be subtle. Carefully inspect the contour of the metaphyseal flare. Any asymmetry, bulging, or deviation of the cortical margin indicates a torus fracture. Soft tissue swelling is also usually evident. Torus fractures are not associated with angulation, displacement, or rotational abnormalities, so reduction is not necessary. Treat by splinting in a position of function fracture clinic follow-up within 1 week. 

https://radiopaedia.org/cases/torus-fracture-1

Greenstick Fractures
A greenstick fracture is characterized by cortical disruption and periosteal tearing on the convex side of the bone, with an intact periosteum on the concave side of the fracture. Greenstick fractures are more stable and somewhat less painful than complete fractures because the area of intact periosteum limits bony displacement. The need for reduction is determined by the degree of angulation of the fracture, the age of the child, and the anatomic location of the injury.

https://radiopaedia.org/cases/radius-and-ulna-greenstick-fractures

Posted by:

              

     Lakshay Chanana

     

     Speciality Doctor

     Northwick Park Hospital

     Department of Emergency Medicine

     England

     @EMDidactic

Basic Asthma Management (Coreem)

Definition: An episode of wheezing, chest tightness or coughing resulting from variable airflow obstruction that is reversible. Underlying exacerbations is a chronic inflammatory disorder of the airways.

Epidemiology:

• 1 million Americans suffer from asthma
• 75 million ED visits/year
• 456,000 hospitalizations in the US (Akinbami 2011)

Pathophysiology:

• Stimuli (allergen and non-allergen) induce bronchoconstriction
• Bronchoconstricting stimuli result in edema, inflammation, airway smooth muscle hypertrophy and mucous production.
• Long-term permanent structural airway remodeling can develop
• Airway inflammation limiting airflow is the common final pathway

Symptoms:

• Wheezing
• Cough
• Dyspnea
• Chest tightness
• Shortness of Breath

Physical Exam

• Wheezing
• Tachypnea
• Tachycardia
• Retractions
• Use of accessory respiratory muscles
• Speaking in short sentences

Immediate Management:

Basics: ABCs with a focus on breathing. Supplementary O2 typically not needed in mild to moderate exacerbations.

Inhaled Beta2 Agonist (i.e. albuterol)

• Mechanism: Stimulate beta2 receptors in lungs leading to bronchodilation
• Nebulized albuterol solution
  • Dose:5 mg every 10-20 min
  • Can be paired with an inhaled anticholinergic
• Albuterol metered-dose inhaler (MDI)
  • Equally effective to nebulized solution in mild exacerbations (Newman 2002, Cates 2013)
  • Dose: 6-12 puffs every 10-20 min
• Side effects: tachycardia (beta1 stimulation), tremors, lactic acidosis (Lewis 2014)

Inhaled Anticholinergic (i.e. Ipratropium)

• Mechanism: Override smooth muscle constriction and secretory consequences of parasympathetic nervous system. Block reflex bronchoconstriction.
• Dose: 0.5 mg every 10-20 min (up to 3 doses)
• Impact: In combination with beta2 agonist, may avoid hospitalization in up to 1 in 11 treated patients (Plotnick 1998).

Systemic Corticosteroids

• Mechanism: Inhibit recruitment of inflammatory cells and mediators.
• Route: Evidence suggests that oral and intravenous corticosteroids are equally efficacious in patients with mild to moderate asthma exacerbations
• Dose
  • Prednisone: 1 mg/kg (typically up to 60 mg) PO
  • Methylprednisolone sodium: 125 – 250 mg IV or IM
  • Dexamethasone: 10-20 mg PO
• Impact: Numerous studies have shown reductions in admission rates as a result of systemic corticosteroid use in the ED (Rowe 1992). The majority of patients presenting to an ED for asthma exacerbation should receive systemic steroids.

Magnesium 

• Mechanism: Bronchial smooth muscle relaxation
• Dose: 1-2 g over 30-60 min
• Impact: Modest decrease in hospital admission rate in patients refractory to standard management (Levy 2014)
• Reserved for moderate to severe exacerbations

Special Populations: Pregnancy

• Acute asthma exacerbations should be treated the same in pregnant patients as in nonpregnant patients.
• Fetal monitoring should be considered for patients with moderate to severe exacerbations in the 3rd

Diagnostics: Asthma is a clinical diagnosis and patients with mild to moderate exacerbations rarely need any testing in the ED. Diagnostic tests may be useful in patients with asthma that is refractory to standard management as detailed above or if an alternate cause of symptoms is suspected.

Pulmonary Function Tests (PFTs)

• Measure forced expiratory volume in 1 second (FEV1) or peak expiratory flow rate (PEFR)
• Most helpful when patient knows their baseline performance

Chest Radiography

• The majority of patients with asthma exacerbations that are typical for them do not need a chest X-ray performed.
• Consider X-ray in patients with more severe symptoms or those that do not resolve with standard treatment.

Lab Studies

• Rarely useful in mild to moderate (or even in severe) asthma exacerbations.
• Leukocytosis common as a result both of stress as well as steroid use
• Arterial Blood Gas
  • Do not correlate with clinical outcomes
  • Critical ABG data points (O2, CO2) can be obtained by other means (Pulse oximetry for O2, VBG for CO2)

Disposition

• Relapse after ED visits is common (up to 11% at 3 days) (Rosen’s 2014)
• Admission
  • Incomplete response based on overall clinical picture or PFTs (< 70% improvement)
  • Significant comorbidities
• Discharge
  • Airway inflammation continues after discharge and can take days to improve
  • Medications
    • Beta agonist inhaler (and demonstration of proper use). Consider giving all patients a spacer device as this improves drug delivery and thus efficacy.
    • Steroids
      • Short burst steroid treatment with prednisone for 5 days (no taper needed)
      • Dexamethasone – 2 doses on days 1 and 2 shown to be non-inferior to 5 days of prednisone in one small study (Kravitz 2011)
    • Follow-up
      • Patients should contact their physician in 3-5 days and have follow-up arranged in 1-2 weeks
      • Consider referral to an asthma specialist in patients with frequent exacerbations, frequent ED visits or frequent rescue inhaler use.

Take Home Points

• First line treatment for asthma exacerbations is inhaled beta agonists, inhaled anticholinergics and systemic corticosteroids.
• The majority of patients presenting to the ED with asthma exacerbations should be started on short-burst corticosteroids to control inflammation and prevent admission and relapse.
• Diagnostic testing is not required for the majority of patients with asthma exacerbations.

References:

1. Nowak RM, Tokarski GF: Asthma in Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 8. St. Louis, Mosby, Inc., 2014, (Ch) 73: p 941-58
2. Akinbami LJ et al. Asthma prevalence, health care use, and mortality: United States, 2005-2009. Natl Health Stat Report 2011; 32:1-14. Link
3. Newman KB et al. A comparison of albuterol administered by metered-dose inhaler and spacer with albuterol by nebulizer in adults presenting to an urban emergency department with acute asthma. Chest 2002; 121: 1036-41. PMID: 11948030
4. Cates CJ et al. Holding chambers (spacers) versus nebulisers for beta-agnonist treatment of acute asthma (Review). Cochrane Database Syst Rev 2013. PMID: 24037768
5. Lewis LM et al. Albuterol administration is commonly associated with increases in serum lactate in patients with asthma treated for acute exacerbations of asthma. Chest 2014; 145(1): 53-9. PMID: 23949578
6. Plotnick LH, Ducharme FM. Should inhaled anticholinergic be added to B2 agonists for treating acute childhood and adolescent asthma? A systematic review. BMJ 1998; 317: 971-7. PMID: 9765164
7. Rowe BH et al. Effectiveness of steroid therapy in acute exacerbations of asthma: a meta-analysis. Am J Emerg Med 1992; 10: 301-10 PMID: 1535500
8. Levy Z, Slesinger TL. Does intravenous magnesium reduce the need for hospital admission among adult patients with acute asthma exacerbations. Ann Emerg Med 2014. PMID: 25128007
9. Kravitz J et al. Two days of dexamethasone versus 5 days of prednisone in the treatment of acute asthma: a randomized controlled trial. Ann Emerg Med 2011; 58: 200-4. PMID: 21334098

This post was initially posted at coreem. Shared with permission. 

Life-Threatening Asthma (Coreem)

Background: Acute severe asthma or status asthmaticus refers to an episode of bronchoconstriction that is unresponsive to standard management. Patients with acute severe asthma will present with significant respiratory distress and it is critical to rapidly treat them to avoid significant morbidity and mortality. Patients will present with tachypnea, retractions, diaphoresis, ability to only speak 1-2 words at a time, abdominal breathing, cold extremeties. and wheezing (although the most severe may have a “quiet chest” indicating the absence of any significant air entry).

Immediate Management:

There are three main goals of immediate management of the severe asthma exacerbation:

1. Stave off intubation while your medications have time to act. Intubation is associated with increased morbidity and mortality.
2. Maximize pre-intubation parameters in case the patient doesn’t turn around and intubation is required.
3. Reverse bronchoconstriction to decrease work of breathing and prevent respiratory failure from exhaustion of respiratory muscles.

Basics: ABCs, IV, supplemental O2. Patient should be provided with all of the therapies used in mild to moderate asthma exacerbations but will require more aggressive management

Oxygenation + Respiratory Support

• Hypoxia only occurs late in a patient with a severe asthma exacerbation. Do not wait for hypoxia before supplying supplemental O2.
• Standard Nasal Cannula – Turn up to 15-20 L/min
• High-Flow Nasal Cannula (HFNC)
  • Allows for increased flow (40-60L/min of humidified O2 
  • May be difficult to administer nebulizer treatments via facemask does not fit over HFNC
• Non-Rebreather with Beta-Agnoist Reservoir
• Non-invasive Positive Pressure Ventilation (NIPPV)
  • Decreases work of breathing and improves gas exchange
  • The evidence demonstrating a benefit to NIPPV is limited but available studies do not show substantial adverse events (Pollack 1995, Soroksky 2003, Lim 2012). These studies did not include the sickest subset of patients with asthma
  • Bilevel Positive Airway Pressure (BPAP) preferred over Continuous Positive Airway Pressure (CPAP)
    • Difference in inspiratory (IPAP) and expiratory (EPAP) pressure aids in increasing tidal volume delivered
    • Start at IPAP 10 mm Hg, EPAP 5 mm Hg (or less) and titrate IPAP up (Typically no need to increase EPAP).

Intravenous Fluids

• Patients with severe asthma exacerbations have enormous insensible losses from increased respirations and work of breathing.
• Lung hyperinflation decreases pulmonary venous return, which can lead to hypotension. This is exacerbated by mechanical ventilation as the patient converts from negative pressure ventilation to positive pressure ventilation thus increasing intrathoracic pressure which can further decrease venous return.
• Aggressive IV fluids (30 cc/kg) should be given early to replete intravascular volume.

Epinephrine

• Epinephrine is a non-selective beta agonist that causes bronchodilation, vasoconstriction, increased cardiac contractility and increased heart rate
• Patients with severe asthma may have minimal benefit from inhaled beta agonists (i.e. albuterol) due to severe bronchoconstriction limiting delivery of medication to distal bronchioles.
• Intramuscular (IM) / Subcutaneous(SQ) Epinephrine
  • Dose: 300-500 mcg
  • Limited evidence demonstrates minimal significant side effects at this dose (Cydulka 1988)
• Intravenous (or Intraosseous) Epinephrine
  • More rapidly reaches target tissue than IM/SQ especially if patient hypotensive
  • Has effect of bronchodilation as well as vasoconstriction, which can reduce airway edema (Grandordy 1995)
  • Dose: 1 – 5 mcg/min and titrate to effect
  • Multiple retrospective studies demonstrate minimal adverse events with IV epinephrine (Smith 2003, Putland 2006)
• Contraindications: Epinephrine can theoretically cause uterine vasoconstriction and should be used with caution in pregnant patients.
• Terbutaline
  • Selective, parenteral beta 2 agonist that causes bronchodilation without effecting heart rate or cardiac output
  • Subcutaneous (SC) Terbutaline: 0.5 mg SC every 4 hours

Magnesium

• Mechanism: Bronchial smooth muscle relaxation
• Impact:
  • Modest decrease in hospital admission rate in patients refractory to standard management (Levy 2014). However, the sickest subset of patients were excluded from this study
  • The 3Mg trial (Goodacre 2013) demonstrated only a weak benefit to IV Magnesium in severe asthma however, this study did not include patients with life-threatening asthma.
  • In the absence of robust evidence, it is reasonable to administer magnesium to severe asthma exacerbations as there are minimal side effects of the drug and a potential for benefit
• Dose: The dose in severe asthma is not established. 2 g IV over 15 minutes is a reasonable first dose and this may be repeated

Heliox

• Mechanism: Improved laminar flow of inhaled has which may allow better airflow through the constricted airways; allows better gas exchange and transport of medications to flow down to distal airways and alveoli
• A mixture of helium and oxygen(multiple possible rations – 60:40, 70:30, 80:20). Only give the minimum FiO2 necessary to achieve goal O2saturation
• Evidence of utility limited but has not been extensively studied in the sickest subset of asthmatic patients and may still be beneficial in this group.
• Heliox may be used both via NIPPV and mechanical ventilator
• Limitation: If patient markedly hypoxic, may not give an adequate amount of FiO2.

Intubation

• Only about 2% of asthma exacerbations require intubation with 10-30% of those admitted to the ICU requiring invasive ventilation (Rosen’s 2014)
• Intubation is an inherently dangerous intervention in asthma because it does not fix the underlying problem (bronchoconstriction) and can cause dynamic hyperinflation (see below under ventilation), and rapid acidosis if respiration is not matched during RSI or post-intubation
• There is no specific vital sign, lab value or other diagnostic test result, which determines the necessity for intubation. The decision to intubate is based on a number of factors including the patients overall appearance, work of breathing, perceived ability to maintain their effort of breathing, mental status etc.
• Prior to intubation, be sure to maximize pre-oxygenation and intravascular volume
• Delayed Sequence Intubation (RSI)
  • Procedural sedation (with dissociative dose ketamine) for the procedure of pre-oxygenation
  • Useful in patients who have significant hypoxia/hypercarbia despite resuscitation and do not tolerate NIPPV to aid in pre-oxygenation
  • See the EMCrit website for full details on the procedure
• Rapid Sequence Intubation (RSI) Medications
  • There is no optimal set of agents for RSI in the severe asthmatic
  • Ketamine
    • Preferred agent because it is relatively hemodynamically stable and it has bronchodilatory properties.
    • Dose: 1-2 mg/kg
  • Paralytic
    • Common options are rocuronium and succinylcholine
    • Rocuronium offers the advantage of longer paralysis which avoids vent asynchrony early in management

Mechanical Ventilation

• Appropriate mechanical ventilation relies on ensuring that the patient has an adequate time to fully expire the delivered breath and avoid hyperinflation
• Permissive Hypercapnea: Decreasing respiratory rate and allowing PaCO2 to rise to supranormal levels.
  • This strategy avoids breath stacking which leads to hyperinflation
  • Hyperinflation leads to increased airway pressures and can lead the development of a tension pneumothorax
  • Hyperinflation can also lead to marked decrease in venous return leading to decreased cardiac output and cardiac arrest
  • Hyperinflation leads to increased pulmonary vascular resistance and right ventricular dysfunction
• Post-intubation meds (A full discussion of post-intubation care will appear in a future post)
  • Analgesia
    • Fentanyl (1-2ug/kg/hr) preferred over morphine or hydromorphone as it has minimal histamine effects
  • Sedation Options: Ketamine, propofol
  • Consider short-term paralysis if difficulty ventilating the patient
• Initial Ventilator Settings
  • RR: 6-10 breaths/min
  • VT: 6-8 ml/kg (ideal body weight
  • PEEP: 0-5 cm H2O
  • FiO2: Minimum necessary to maintain O2 sat > 93%
  • Inspiratory Flow Rate: (suggest 100-120 L/min)
• Check Plateau Pressures and maintain at < 30 mm Hg
  • Plateau pressure reflects the pressure experienced by alveoli
  • Maintaining Pplat < 30 mm Hg helps to avoid alveolar damage
  • If plateau pressure is > 30 mm Hg, consider lowering the RR and VT.

Mechanical ventilation does not fix the underlying bronchoconstriction. Be sure to continue maximal medical management.

Trouble Shooting the Ventilator

• Hemodynamic instability and hypoxia after intubation and mechanical ventilation are common and life-threatening. Rapid recognition of the underlying problem and treatment are critical
• DOPES Mnemonic – describes the most common causes of instability
  • Displacement of the endotracheal tube (ETT)
    • Direct visualization with laryngoscope preferred (US confirmation another option)
  • Obstruction of the endotracheal tube
    • Pass ETT suction catheter
  • Pneumothorax (tension)
    • Lung POCUS for lung sliding
    • Empiric needle decompression or finger thoracostomy
  • Equipment failure
    • Disconnect the vent and deliver manual BVM breaths
  • Stacked Breaths
    • Forcibly exhale patient (gently push down on anterior chest wall with two hands until no further exhalation detected)

Trouble Shooting – Severe Acidemia 

• A pH < 7.15 can lead to physiologic issues
• Check plateau pressure and if < 30 mm Hg, consider increasing ventilation (increase RR/TV)
• Invasive Treatment
  • Inhaled Anesthetics (i.e. sevoflourane)
  • Veno-Venous (VV) ECMO

Take Home Points

• Consider parenteral epinephrine in patients with severe asthma exacerbations as inhaled beta agonists are unlikely to penetrate into the distal airways.
• Intravenous epinephrine is life-saving and safe when used appropriately.
• Use NIPPV and high-flow nasal cannula to appropriately pre-oxygenate patients and avoid critical desaturations during intubation.
• Use a strategy of permissive hypercapnea for mechanical ventilation to avoid breath stacking, hyperinflation and high airway pressures. Aim for plateau pressures < 30 mm Hg.
• Use the DOPES mnemonic to troubleshoot hemodynamic instability after initiation of mechanical ventilation.

Read More:

EMCrit Podcast 15: The Severe Asthmatic

EMCrit Podcast 16: Coding Asthmatic, DOPES and Finger Thoracostomy

REBELCast: The Crashing Asthmatic

References:

Pollack CV et al. Treatment of acute bronchospasm with beta-adrenergic agonist aerosols delivered by a nasal bilevel positive airway pressure circuit. Ann Emerg Med 1995; 26(5): 552-7. PMID: 7486361

Soroksky A et al. A pilot prospective, randomized, placebo-controlled trial of bilevel positive airway pressure in acute asthmatic attack. Chest 2003; 123: 1018-25. PMID: 12684289

Lim WJ et al. Non-invasive positive pressure ventilation for treatment of respiratory failure due to severe acute exacerbations of asthma. Cochrane Database Syst Rev 2012. PMID: 23235608

Cydulka R et al. The use of epinephrine in the treatment of older adult asthmatics. Ann Emerg Med 1988; 17(4): 322-6. PMID: 3354935

Grandordy BM et al. The effect of intravenous phenylephrine on airway calibre in asthma. Eur Respir J. 1995;8:624-631. PMID: 7664864

Smith D et al. Intravenous epinephrine in life-threatening asthma. Ann Emerg Med 2003; 41(5): 706-711. PMID: 12712039

Putland M et al. Adverse events associated with the use of intravenous epinephrine in emergency department patients presenting with severe asthma. Ann Emerg Med 2006; 47(6): 559-564. PMID: 16713785

Levy Z, Slesinger TL. Does intravenous magnesium reduce the need for hospital admission among adult patients with acute asthma exacerbations. Ann Emerg Med 2014. PMID: 25128007

Goodacre S et al. Intravenous or nebulized magnesium sulphate versus standard therapy for severe acute asthma (3Mg trial): a double-blind, randomised controlled trial. Lancet Respir Med 2013; 1: 293-300. PMID: 24731521

Nowak RM, Tokarski GF: Asthma in Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 8. St. Louis, Mosby, Inc., 2014, (Ch) 73: p 941-58

This post was intially posted at coreem. Shared with permission. 

Who owns the airway?

In modern day medicine, these are countless specialties and sub-specialties that we can explore. There are fellowships on heart failure, fellowships on particular disease entities and so on. But there are some things that remain very basic such as basic airway skills that every physician must know. In contrast, who is the expert in advanced airways is a matter of debate though? Is it Emergency Medicine, Intensive Care, Anesthesia or ENT.  

Managing Airways depends a lot on local protocols and systems but in general, it is either ITU, Anesthetics or EM personnel who do this. During initial bits of my training in a missionary hospital I learned and mastered my basic and advanced airway skills. I was fortunate enough to work with some of the finest EM and ITU gurus in the country. By the end of two years, I was pretty confident about my airway skills. Particularly at Vellore, Airway was definitely an EM physicians territory and I don't recall a single day when Anesthetists were summoned to ED for any airway. Later, I moved to a corporate hospital in Hyderabad where once again - Airway was an ED doctor's forte and Anesthetist/ENT was rarely called to ED to help with airways. 

Surprisingly, a large population of EM physicians/trainees believe that Airway is best left to Anesthetists since they are experts in managing it. Well, by that logic we should stop reading ECGs, CT scans, X Rays or even doing abdomen exams as they are best done by a Surgeon who has done is 1000s of times. I guess we are getting back to those good old Casualty Medical Officer days..On the name of safety, support, courtesy and expert care we often let down EM as a stand-alone specialty. 

Arguments from those who think Anesthetists/ITU should do all Airways

They do it several times a day and a few thousand times in their residency. So they are the best!

Any seasoned ED doctor understands how you feel when you intubate a desaturating patient with a full belly and high risk of aspiration. This a common scenario in EDs and not in Operation Theatres. ED RSIs are very different from elective theatre intubations. ED intubations happen over a span of few minutes and they should be dealt with a sense of emergency (not urgency). 

Most Anesthesia trainees learn this crucial skill in a well controlled and elective environment and continue to polish it further in controlled settings whilst EM trainees learn this during Anesthetic Rotations/Emergency Department and continue to fine-tune it in A&E under the supervision of a Consultant. 

Post-intubation care is tough and we can't manage that

Really!! EM is a tough specialty and this is not a reason to call ITU/Anesthesia to manage airways. Check this out to understand "post-intubation" care. Not knowing enough and being sloppy is not a valid argument. 

We need more protocols and guidelines 

Until recently, I was a big proponent of guidelines and protocols but lately, I have been questioning and thinking if these are leading to any benefit or more harm. As clinicians, we stop thinking when using these pathways. Patients are thrown into pathways and they all get worked up in the same fashion. Same initial workup for a 20yo Chest pain and  40YO Chest Pain and 65yo Chest Pain - unnecessary blood tests, false positives, invasive testing, incidentalomas and serious harms from procedures + inappropriate utilization of resources. Hopefully, things would not be the same for "Difficult Airway Pathways". I certainly believe that we should have difficult airway pathways in ED formed in liaison with Anesthetics/ITUs but we should NOT be summoning them for every airway in ED. Emergency Departments should have their own protocols for intubation and ED should be able to decide on intubation.

The Designation Bias and "EM Mindset"

Many are of the opinion that a patient does not need intubation when GCS is 9/15 (not <8/15). Well, it is not that simple. So here is my list of those patients who needs intubation (This is not an exhaustive list):

• Respiratory Failure or Impending Respiratory Failure (Type 1 or Type 2)
• Cardiac Arrest 
• Airway Patency issues or Potential Airway compromise (Low GCS, Head Injury, Neck Masses, Stridor, Burns, Anaphylaxis)
• Anticipated Course of Care 
• Unresponsive Shock
• Raised ICP

The way EM and Anesthesia think about "Emergency Airway Management" can be very different. If Anesthetics fail the airway in the first attempt, it is called a difficult airway but if ED fails in the first attempt, it is called as incompetency. (Designation bias)

Strong Leadership and Getting Support from Colleagues

The practice of EM is extremely variable in different parts of the world. There is often an overlap with Pre-Hospital, ITU, Anesthetics. To progress as a specialty, it is important to have a quintessential group of mentors who love what they do and want to progress EM as an individual specialty. Sadly, this is not always the case and EM is governed by other specialists with little or no EM training. Once in a while, things do go wrong with high-risk procedures and having support from your colleagues is then of utmost importance. This is only possible if the whole body of senior doctors is on the same page regarding airway protocols.

Summary

Managing airway is not left to an individual specialty anymore. It is a skill shared by EM, ITU, Anesthetics, and ENT as well. 

Posted by:

              

     Lakshay Chanana

     

     Speciality Doctor

     Northwick Park Hospital

     Department of Emergency Medicine

     England

     @EMDidactic