Author: Geoff Jara-Almonte (PEM Fellow, NY Methodist Hospital) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital) and Brit Long, MD (@long_brit, EM Chief Resident at SAUSHEC, USAF)
You are working overnight covering the pediatric ED in a busy urban community hospital when you get an EMS pre-notification for a “sick asthmatic.” You quickly prepare the resuscitation room. The EMS crew rushes in a few minutes later with a young boy on the gurney. He is somnolent and in marked distress. You see on the EMS monitor that his HR is 172, last BP was 95/59, SpO2 98%. He is getting a nebulizer through a facemask. You note he is bradypneic with a markedly prolonged expiratory phase. As you move in to listen to him you hear audible inspiratory and expiratory wheezing. His eyes are closed, but he moans and opens his eyes to painful stimuli. As you transfer him to the gurney EMS gives you report: he was found unresponsive outside a local housing project. There was no family with him, en-route they gave 0.15 mg of IM epinephrine, and 2 duo-nebs with minimal improvement.
In a community emergency medicine practice asthma is one of, if not the, most common cause of critical illness in pediatric patients. Though most patients will do well, asthma is still responsible for 5,000-6,000 deaths per year. The mainstays of therapy for an acute asthma exacerbation are inhaled beta-agonists and anti-cholinergics to reduce bronchospasm and systemic steroids to reduce airway inflammation.[i]
Patients with severe life-threatening asthma who do not respond rapidly to first-line therapy should receive adjunctive therapies. No strong guidelines exist to define the order in which to administer adjunctive therapies or exact indications for each.
- Epinephrine – Given IM dose 0.01 mg/kg up to 0.3mg.
- Terbutaline – Given SQ, usual dose 0.01 mg/kg up to 0.3 mg.
- Magnesium sulfate – 50 mg/kg IV – smooth muscle relaxant – equivocal benefit, though may be beneficial in those with the most severe exacerbations.[ii]
- Heliox – Lower density gas, produces more laminar flow, thought to decrease airway resistance. Dosed in He/O2. In general want to maximize FiHe without impairing oxygenation. Only evidence of benefit in patients with severe airway obstruction.[iii]
- Ketamine – As an IV load and infusion for non-intubated patients has had reported effect in case series; however, no convincing data for efficacy.[iv]
You quickly realize that the child has severe life-threatening status asthmaticus. You give him another dose of IM epinephrine, place a line and give IV steroids, and hang magnesium sulfate. His mental status seems to improve after the epi, his eyes open spontaneously, and he is looking around. His respiratory rate is picking up. Your resident asks if you shouldn’t intubate him as he is still in severe respiratory distress.
Intubated asthmatics can be very difficult to manage because of the obstructive physiology; they are prone to breath-stacking and developing auto-peep and high airway pressures. In general, it is best to do everything to avoid intubating the severe asthmatic if at all possible. Some authors theorize intubation increases the risks of complications in the ICU.[v] Early aggressive medical therapy can often prevent an intubation.
Nevertheless the decision to intubate is made clinically and should not be delayed if deemed necessary.
Non-invasive ventilation is also sometimes used in severe asthmatics to prevent intubation. Though this has been shown to be effective in COPD, a Cochrane review found no evidence to support its efficacy in asthma.[vi],[vii]. NIH and AHA guidelines do not make any recommendations on its use.
Since he seems to be improving, you decide to hold off on intubating and call for Bi-PAP and heliox instead. As you are waiting for RT to arrive you notice that he is becoming more somnolent. His respiratory rate is slowing. You decide that he absolutely needs to be intubated. You have your nurse draw up ketamine and succinylcholine, and your resident easily intubates him. RT arrives and you place him on the ventilator.
Intubation does not actually improve the underlying pathophysiology of asthma – small airway obstruction and inflammation. It is important to continue giving bronchodilators and steroids.
Ventilator setting must be selected carefully.
- Relatively low tidal volumes decrease the risk of barotrauma.
- A slow respiratory rate with a short inspiratory time and long expiratory time minimize the risk of auto-PEEP.
- You may need to allow a degree of hypercapnia and respiratory acidosis.[viii]
You briefly relax after he is safely on the vent. Your RT sets up continuous in-line nebs, and you get a chest X-ray to confirm the tube. You start him on a ketamine infusion for sedation and are waiting to transport him up to the PICU when the nurse rushes out of the room to tell you his sats are dropping. You come in and find he has a SpO2 of 80%, and his cuff pressure is 60/35 with a heart rate of 80. The ventilator is alarming for high airway pressures. You see from the flow-curve that he has been stacking breaths.
Management of the crashing ventilated asthmatic requires recognition of auto-peep and relief of dynamic hyperinflation.
- Disconnect the patient from the ventilator circuit and allow as much passive exhalation as possible.
- A technique of “lateral chest compression” is described in which one provider compresses the ribcage laterally to force exhalation of trapped air. There are no systematic studies evaluating the effectiveness of this technique; however, several case reports and a few series support its effectiveness.[ix],[x],[xi]
- A few historic case reports describe successful manual decompression of hyperexpanded lungs in arrested patients via thoracotomy, usually with dismal outcomes.[xii],[xiii]
You disconnect him from the ventilator, and you note a prolonged exhalation. You have your resident compress his chest and note continued exhalation. You start to bag him and have your resident provide lateral chest compression after each breath. However there is still significant resistance to bagging. His sats continue to drop into the 70s, and his heart rate falls into the 40s. You remember that CPR is different in children than adults.
Pediatric basic life support differs in a few key ways from adults.
- Start chest compressions with bradycardia (hr < 60) and signs of poor perfusion, even if there is a palpable pulse.
- If no advanced airway, use a compression:ventilation ratio of 15:2 if two rescuers, and 30:2 if only one rescuer.
- Recall the differences in the pediatric airway that can make it a challenge to ventilate (large occiput, large tongue). Make sure to allow for full chest recoil.
- Outside of the hospital setting the Compression – Airway – Breathing sequence is advocated for lay-rescuers.[xiv]
You have one of your techs begin chest compressions, and your RT takes over bagging. On the monitor you notice he has developed a slow narrow complex rhythm without P waves. There are no palpable pulses. You try to remember what the recommendations for management of pediatric pulseless electrical activity are.
Management of cardiac arrest without a shockable rhythm (PEA or asystole) in children is largely similar to that in adults.
- With an advanced airway in place continue chest compressions with a rate of at least 100/min. Minimize interruptions, do not stop for ventilations.
- Ventilations are given every 6 – 8 seconds, about 8 – 10 breaths per minute.
- Epinephrine is the vasopressor of choice. The does is 0.01 mg/kg (0.1 mL/Kg of 1:10,000) up to 1mg; this is given every 3 – 5 minutes.
- There is no recommendation for the routine administration of any other drug during pediatric cardiac arrest.
- Children, especially infants, have low glycogen stores and easily become hypoglycemic. Check a blood glucose and treat hypoglycemia or empirically give dextrose.
You give him a dose of epinephrine and continue chest compressions for two minutes. You pause to check for pulses, but he is still pulseless with a wide complex rhythm. You ask your team if anyone can think of potentially reversible causes of cardiac arrest that you haven’t addressed. Your resident asks if he might have a pneumothorax.
Asthmatics are at an increased risk for spontaneous pneumothorax due to high intrapulmonary pressures.[xv],[xvi] In any crashing asthmatic have a high suspicion for pneumothorax, particularly if he or she has been receiving positive pressure ventilation. Consider lung ultrasound, or if not available, empiric decompression of both hemi-thoraces in the arrested asthmatic
High intrathoracic pressures and auto-peep also decrease venous return and may precipitate hypotension. Routine aggressive hydration is not recommended, but it is reasonable in the arrested patient.
You have difficulty auscultating breath sounds on either side, and are concerned he may have a pneumothorax. While your tech continues CPR, you and your resident each quickly perform surgical thoracostomies. Your resident reports a rush of air as she enters the pleural cavity. You find nothing on your side. She quickly places a chest tube. At the next pulse check he has a bounding femoral pulse and sinus tachycardia on the monitor. You reconnect him to the ventilator, repair your thoracostomy, and transfer him to the pediatric ICU.
[i] Hoek, Terry L. Vanden, et al. “Part 12: Cardiac Arrest in Special Situations 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.” Circulation 122.18 suppl 3 (2010): S829-S861.
[ii] Rowe BH, Bretzlaff J, Bourdon C, Bota G, Blitz S, Camargo CA. Magnesium sulfate for treating exacerbations of acute asthma in the emergency department. Cochrane Database of Systematic Reviews 2000, Issue 1. Art. No.: CD001490. DOI: 10.1002/14651858.CD001490.
[iii] Rodrigo GJ, Pollack CV, Rodrigo C, Rowe BH. Heliox for non-intubated acute asthma patients. Cochrane Database of Systematic Reviews 2006, Issue 4. Art. No.: CD002884. DOI: 10.1002/14651858.CD002884.pub2.
[iv] Jat, Kana R., and Deepak Chawla. “Ketamine for management of acute exacerbations of asthma in children.” The Cochrane Library (2012).
[v] Carroll, Christopher L., and Aaron R. Zucker. “The increased cost of complications in children with status asthmaticus.” Pediatric pulmonology 42.10 (2007): 914-919.
[vi] Ram FSF, Picot J, Lightowler J, Wedzicha JA. Non-invasive positive pressure ventilation for treatment of respiratory failure due to exacerbations of chronic obstructive pulmonary disease. Cochrane Database of Systematic Reviews 2004, Issue 3. Art. No.: CD004104. DOI: 10.1002/14651858.CD004104.pub3.
[vii] Lim WJ, Mohammed Akram R, Carson KV, Mysore S, Labiszewski NA, Wedzicha JA, Rowe BH, Smith BJ. Non-invasive positive pressure ventilation for treatment of respiratory failure due to severe acute exacerbations of asthma. Cochrane Database of Systematic Reviews 2012, Issue 12. Art. No.: CD004360. DOI: 10.1002/14651858.CD004360.pub4.
[viii] Stather DR, Stewart TE. Clinical review: Mechanical ventilation in severe asthma. Critical Care. 2005;9(6):581-587. doi:10.1186/cc3733.
[ix] Barker, P. “Resuscitation in status asthmaticus.” The Medical journal of Australia 142.3 (1985): 238-238.
[x] Fisher, Malcolm M., Anne P. Whaley, and Roger R. Pye. “External chest compression in the management of acute severe asthma—a technique in search of evidence.” Prehospital and disaster medicine 16.03 (2001): 124-127.
[xi] Fisher, MALCOLM M., C. JANE Bowey, and K. E. N. N. E. T. H. Ladd-Hudson. “External chest compression in acute asthma: a preliminary study.” Critical care medicine 17.7 (1989): 686-687.
[xii] Smolnikoff, V. P. “Total bronchospasm and lung massage.” Anaesthesia 15.1 (1960): 40-44.
[xiii] Diament, R. H., and J. P. Sloan. “Failed resuscitation in acute severe asthma: a medical indication for emergency thoracotomy?” Archives of emergency medicine 4.4 (1987): 233-235.
[xiv] Kleinman, Monica E., et al. “Part 10: Pediatric Basic and Advanced Life Support 2010 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations. “Circulation 122.16 suppl 2 (2010): S466-S515.
[xv] Williams-Johnson, J., et al. “Simultaneous spontaneous bilateral pneumothoraces in an asthmatic.” The West Indian medical journal 57.5 (2008): 508-510.
[xvi] Leigh-Smith, Simon, and Grant Christey. “Tension pneumothorax in asthma. “Resuscitation 69.3 (2006): 525-527.