EM-CCM Summary, 9/2/2014- The Sick Asthmatic - The Original Kings of County

EM-CCM Summary, 9/2/2014- The Sick Asthmatic.
Presented by Dr. Elizabeth Abram

The Case (As usual, this is a fictitious patient seen at a fictitious hospital called Janus General. Don’t believe me? I’m on staff there – see):

25 year old female with URI and asthma exacerbation. In the ED, the patient received oral steroids, nebulized albuterol and ipatropium with some improvement. Eventually, the patient required admission for persistent symptoms, when all of a sudden…

The patient became acutely short of breath!

What would you do next?

Non-Invasive Positive Pressure Ventilation (NIPPV) such as bi-pap and epinephrine IM

But if the patient continues to worsen?

Intubation

What problems arise with asthma patients once the above treatment is instituted?

Vent problems include: carbon dioxide retention, acidemia, breath stacking, hyperinflation, and high airway pressures on the ventilator.

Pathophysiology of Asthma:
REVERSIBLE IgE mediated activation of mast cells and eosinophils that produce cytokines which in turn cause release of inflammatory mediators (histamine, prostaglandins, leukotrienes). These pro-inflammatory agents cause airway hypersecretion, bronchial hyperresponsiveness (smooth muscle constriction) and airway obstruction. Clinically this translates into wheezing, shortness of breath, and cough. When the patient decompensates, bronchoconstriction results in retained volume in lungs and hyperinflation. The patient attempts to overcome this by maintaining “autoPEEP” to keep airways patent and decrease respiratory effort. This retained volume and pressure in turn decreases lung compliance.

Mainstays of treatments in the acute phase:
High level of evidence for nebulized beta-2-agonists in conjunction with nebulized anti-cholinergics, oral corticosteroids- albuterol, ipatropium, prednisone. Patients with tachypnea and respiratory distress have significant insensible loss. Patients with prolonged asthma symptoms or worsening symptoms require fluid resuscitation, especially prior to induction of intubation.

NIPPV:
BiPAP can be used as a bridge to help decrease work of breathing and generate PEEP while conventional treatments are in place. There is a paucity of evidence, but several small studies have shown that NIPPV has shown improved outcomes in the tender of fewer intubations, shorter admissions, and fewer ICU stays. There are, however, some patients for whom we can predict that NIPPV will not help. These are patients with worsening mental status, rising level of PCO2, vomiting, agitation, or worsening tachycardia, hypoxemia or tachypnea.

If the patient does not improve with neubulized beta-agonists, steroids, IM epinephrine, and NIPPV…

Intubation
Rapid Sequence Intubation: traditional way to intubate and ventilate in the emergency department involving rapid sedation, rapid paralysis and intubation. However, in the ill asthmatic, paralysis and sedation may cause hypoventilation and early desaturation.

Delayed Sequence Intubation:
DSI is employs the strategy of sedation, with a delay prior to paralysis. In rapid sequence intubation, sedation and paralysis occur simultaneously. In delayed sequence intubation, sedation is used to calm the agitated, tachypneic, distressed, and often altered patient. This gives the emergency team time to provide adequate oxygenation PRIOR to paralysis. It enables the patient to maintain airway reflexes while decreasing work of breathing. Using sedative medication prior to paralysis of airway reflexes or respiratory muscles prevents desaturation while obtaining a definitive airway. Sedative medications used can be ketamine or dexmetetomidine. Using ketamine 1-1.5mg/kg is similar to giving procedural sedation to obtain the optimal conditions for intubation- a calm (sedated) patient who is well oxygenated. Follow it up with paralysis and introduce the ET tube.

Post-Intubation Care

The sick, intubated asthmatic should be carefully monitored. Routine arterial blood gas sampling is NOT recommended in asthmatics who present to the ED. However, the intubated asthmatic with ongoing agitation, poor oxygenation, breath stacking should be monitored for increasing CO2 retention and acidosis.

Strategies to assist in ventilator management for the “difficult-to-ventilate” asthmatic:

1) increase the expiratory time for the patient, I:E ratio of 1:4.
2) external chest decompression for breath stacking
3) permissive hypercapnia
4) paralysis

Ventilation can prove challenging as the patient has tachypnea and airway obstruction causing retained volumes and increasing functional residual capacity. This is known as breath stacking. Ultimately it results in retained volume and increased airway pressure. Increased airway pressure puts the patient at risk for complications such as barotrauma (pneumothorax, pneumomediastinum) and inadequate volumes (worsening CO2 retention, acidosis). A strategy to decrease breath stacking is to increase the TIME that the patient has to exhale. This means having a short inspiratory phase of ventilation, and increasing the expiratory phase. The expiratory “E” interval should be lengthened to form a ratio of inspiration:expiration time (I:E) ratio to 1:4, rather than traditionally 1:3.

Breath stacking: When breath stacking occurs, we can reduce the retained volume manually. Disconnect the ventilator and externally compress the chest to remove extra volume.

Permissive hypercapnia

As breath stacking creates the problem of retained lung volumes, the compensatory ventilator response is to increase pressure to deliver volume to poorly compliant lungs. As discussed above, the increased pressure can cause pneumothorax and other barotrauma. Increasing I:E ratio decreases retained volume so that high airway pressures can be avoided. However, this also decreases minute ventilation of the patient, and they ultimately “blow-off” less carbon dioxide. While increasing plasma CO2 is undesirable, this “permissive hypercapnia” up to 80mmHg PCO2 or a pH of 7.15 is an acceptable trade-off for lower airway pressures and allowing the patient to exhale more completely. Naturally, patients to not “like” permissive hypercapnia and will continue to initiate ventilations at a high rate; therefore AGGRESSIVE sedation and even paralysis will be required. This is a critical aspect of managing the intubated asthmatic.

Paralysis: a controversy

Traditionally paralysis using neuromuscular blockade agents (NMBAs) is avoided because it can cause deconditioning of respiratory muscles, known as critical illness polyneuromyopathy (CIPM). This is especially the case when used with corticosteroids, as in all patients with acute asthma. However, the compensatory response to hypercapnia and hypoxia is tachypnea. This, as discussed above, leads to retained volume and the cycle of increased airway pressure. Paralysis can be used in a difficult-to-ventilate asthmatic for a SHORT TERM to allow for easier ventilation. Cisatacurium is the agent of choice as it has lower incidence of CIPM.

Beyond the ED....SALVAGE TREATMENT

Adjunctive Therapies when the patient is worsening despite maximal treatments:
– general anaesthesia in the OR
– bronchoalveolar lavage to remove obstructive mucous plugs

Limited evidence for:
-higher volatily, low-molecular weight gasses (helium/oxygen mixtures)
-aminophylline infusion
-ketamine by continuous infusion
-ECMO, extracorporeal membrane oxygenation – oxygenation of blood without the use of the lungs, thus allowing a pulmonary recovery.

By Dr. Sally Bogoch

References:

Brandao, D et al. Reversal of Bronchial Obstruction with Bi-level Positive Airway Pressure and Nebulization in Patients with Acute Asthma . Journal of Asthma, 46:356–361, 2009
Burburan, S et al. Anaesthetic Management in Asthma. Minerva Anestesiol. 2007;73:357-65
Carson, KV et al. Noninvasive ventilation in acute severe asthma: current evidence and future perspectives. Curr Opin Pulm Med 2014, 20:118–123
Cunnington D, et al. Oral versus intravenous vorticosteroids in adults hospitalized with acute asthma. Pulmonary Pharmacology & Therapeutics 18 (2005) 207–212
Keeney, GE et al. Dexamethasone for Acute Asthma Exacerbations in Children: A Meta-analysis. Pediatrics 2014;133;493;s
Kokotajlo, S et al. Use of Intravenous Magnesium Sulfate for the Treatment of an Acute Asthma Exacerbation in Pediatric Patients. J Pediatr Pharmacol Ther 2014;19(2):91–97
Melnick, ER et al. Current Guidelines For Management Of Asthma In The Emergency Department. EM Practice Guidelines Update 2010, www.ebmedicine.net,
Pallin, M et al. Noninvasive ventilation in acute asthma. Journal of Critical Care 29 (2014) 586–593
Weingart,S D. Preoxygentation, Reoxygenation and Delayed Sequence Intubation in the Emergency Department. J Emerg Med. 2011; 40(6):661-7.

Sally Bogoch

The views expressed on this blog are the author's own and do not reflect the views of their employer. Please read our full disclaimer here. Any references to clinical cases refer to patients treated at a virtual hospital, Janus General Hospital.