ACUTE SEVERE ASTHMA: Status Asthmaticus - in the ER and the OR
Jon Hooper, MD, FRCPC
Department of Anaesthesia
Ottawa Civic Hospital, University of Ottawa, Ottawa


After reading this review, you should:

1. be able to identify the patient at risk for or with life threatening asthma.
2. appreciate the indications for, the pharmacological approach to, and the complications of intubation and ventilation in the severe asthmatic.
3. be able to develop a strategy for ventilating the severe asthmatic that will minimize the risk of barotrauma.
4. have an understanding of the current recommendations for the pharmacological management of the acute severe asthmatic, as well as alternative therapies when standard treatment is unsuccessful.

[He} presents with a distressing sense of want of breath and a feeling of great oppression in the chest. Soon the respiratory efforts become violent, and all of the accessory muscles are brought into play. In a few minutes the patient is in a paroxysm of the most intense dyspnea.
Sir William Osler

Asthma is a lung disease that is characterized by inflammation, obstruction, and hyperresponsiveness of the airways.(1) Acute severe asthma is characterized by severe bronchospasm refractory to usual treatment.

In this review, the management of patients with acute severe asthma will be discussed. The review will not discuss the preparation of the stable asthmatic for elective surgery. For reviews of this topic the reader is referred elsewhere.(2)

Asthma affects 3-5% of North Americans and the incidence and severity of asthma appear to be increasing. American data for the years 1980 to 1987 show increased numbers of hospitalized and intubated patients. More disturbing is the 31% increase in mortality, with 4360 deaths reported in 1987.(3) Although Canadian data shows a similar rise in incidence and hospital admissions, the rise in mortality found in the late 1970s and early 1980s appears to have stabilized in the late 1980s at approximately 500 deaths/year.(4)

Over reliance on inhaled beta2 adrenergic agents, underuse of anti-inflammatory medi- cations, environmental conditions, and lack of appreciation of disease severity by both patient and physician are often cited as reasons for increasing morbidity and mortality. Population studies suggest that older age, black ethnicity, poor socioeconomic status, and psychological problems are risk factors for developing life threatening asthma.(5) Factors associated with those at risk for developing severe asthma include: previous severe attacks (i.e. previous intubation or respiratory acidosis without intubation), multiple or recent hospital admissions, recent steroid use, and deterioration while on steroids.(5)

Identification of High Risk Asthmatics

Historical Features
· previous life threatening attacks (increased CO2, intubation)
· frequent ER visits
· hospitalization in last year
· recent steroid use
· deterioration on steroids

Clinical Features
· heart rate > 130
· paradoxical thoracoabdominal motion
· silent chest
· confusion, lethargy, fatigue
· can't speak
· bradycardia

Clinical Features
Severe asthma is usually easy to diagnose. Patients will sit upright, have marked respiratory distress, may be diaphoretic, and are anxious. Physical examination shows hyperinflation, use of accessory muscles, widespread wheezes, tachycardia, hypertension and pulsus paradoxus. Decreased level of consciousness, the inability to speak, a silent chest, hypoventilation, bradycardia, and unremitting hypoxemia are ominous signs.

The degree of wheezing and dyspnea are not reliable indicators of the degree of obstruction.(6) Some patients will have minimal symptoms of dyspnea despite severe airflow reduction. The perception of breathlessness may be more related to the rate of change in airflow than the absolute degree of obstruction (temporal adaptation). Symptoms and signs of airflow obstruction may diminish after treatment despite minimal gains in FEV1 and PEFR. Spirometry is easy to do at the bedside and should be performed on all patients except those that are clearly life threatened. One of the frequently cited avoidable factors in asthma mortality is physician (and patient) underestimation of the degree of airflow obstruction!!! It has been estimated that anywhere between 25% and 89%(5, 7) of asthma deaths are avoidable!!!

ABG's usually show a respiratory alkalosis.(8) Normal or increased CO2 implies severe disease although the converse is not necessarily true. Hypercarbia is unlikely unless marked airflow obstruction exists (FEV1 < 20% OR 1 LPM, OR PEFR < 150 LPM).(5) Lactic acidosis is due to hypoxia, overworked respiratory muscles, and intracellular alkalosis from decreased CO2 and should be considered a marker of severe disease. However, beta2 agonists can induce lactic acidosis without the presence of cellular hypoxia.

A chest radiograph is rarely helpful.(5) However, an uncertain diagnosis, the question of barotrauma or pneumonia, and severe disease warrant that one be taken.
An ECG may show signs of right heart strain, myocardial ischemia, or dysrhythmias.
Monitoring should include continuous oximetry and ECG, respiratory rate, blood pressure, and level of consciousness. An arterial line is extremely helpful in the intubated asthmatic.

The differential diagnosis of wheezing includes: pulmonary edema, aspiration, pneumothorax, anaphylactic / anaphylactoid reactions, mechanical airway obstruction or compression (tumors, secretions, foreign bodies, laryngeal dysfunction, tracheal stenosis, tracheomalacia, congenital causes i.e. vascular ring), pulmonary embolism, and in the intubated patient, misplaced or obstructed ETT, and surgical compression.

Asthma has features of both bronchoconstriction and of inflammation. Numerous inflammatory mediators and neural mechanisms cause submucosal edema, plasma exudation, and subsequent mucous plugging. Patients with predominantly bronchospastic disease will usually respond to the aggressive use of bronchodilators. Those with more of an inflammatory obstruction may have minimal improvement from bronchodilators, and will take longer to improve.

Acute severe asthma may develop rapidly over a few hours (i.e. in response to ASA), or, more commonly, it develops over a number of days.(9) It is only the patients and physicians recognition of the severity of the attack that is acute! Prolonged attacks are more likely to have mucous plugging and bronchial edema.

In asthma, inspiratory muscles hold the lung at high volumes so as to maintain airway patency and to overcome increased resistance to airflow. Bronchial obstruction creates areas with low V/Q ratios (hypoxia). In other areas alveolar distension causes high V/Q zones and increased deadspace (hypercarbia). The respiratory muscles will have increased oxygen consumption and may eventually tire, leading to loss of lung volume, more obstruction, and frank respiratory failure. Alveolar distension and hypoxic pulmonary vasoconstriction increase pulmonary artery pressures which may impair RV function. Intraventricular septal shift to the left may impair LV function.

Oxygen should be administered to maintain normal saturations. Only those patients with chronic severe asthma and chronic hypercarbia are at risk for increasing hypercarbia with oxygen administration.
It is clear that the mainstays of acute asthma treatment are the beta2 agonists.(1,10,11) They relax bronchial smooth muscle and may inhibit the release of mast cell mediators. There is no apparent therapeutic advantage of parenteral over inhaled beta2 agonists.(10) Parenteral treatment consistently increases the incidence of side effects, such as tachycardia, hypokalemia, dysrhythmias, tremor, myocardial ischemia, and lactic acidosis.(5) In contrast to parenteral treatment the heart rate tends to decrease with successful inhalation therapy.(12) In almost all situations inhaled beta2 therapy should be given prior to parenteral.

In some severe cases however, there is so little airflow that inhaled therapy does not work. Parenteral therapy may be given SC, IV, or, in an emergency, via the ETT. Salbutamol or epinephrine are the most commonly used parenteral beta2 agonists Epinephrine may be given as an infusion (2-8 mg/min.), subcutaneously (0.3-0.5 mg q20-30 min.), or via the ETT (5 ml of 1:10,000). Salbutamol may given by metered dose inhaler (MDI) with a spacer (4-20 puffs/hour), by wet nebulization (WN) (5-10 mg q 15 min. prn), or intravenously (4 mg/kg load then 0.1-0.2 mg/kg/min. infusion).(1,5,9,10)
Inhaled bronchodilators can be given by MDI or by WN. MDI with spacers are as effective as WN even if the patient was using MDI prior to admission, and they are cheaper. MDI therapy is inspiration phased so more drug can be deposited in the lung per unit time as compared to WN. Appropriate MDI dosing is 4 - 20 puffs salbutamol per hour.

Considerable drug is wasted with WN as the predominant part of respiration is expiration hence as little as 1% of drug may actually reach the lungs. A large amount of drug (5-10 mg salbutamol) should be therefore be given frequently (q 15-30 min.).(10) Salbutamol may be given continuously by WN although this may increase risk for toxicity.(10)

The optimal delivery technique and appropriate dosing in ventilated patients has not been clearly established as considerable amount of drug is probably lost. If using MDI, use a spacer and increase the dose (? 6-15 puffs/treatment). Higher doses of WN drug are probably appropriate.(12)

Whether intubated or not, the dosing of beta2 agonists should be "titrated to effect" using objective and clinical signs of airflow limitation. Dosing cannot be standardized due to the heterogeneity of the disease process (spasm vs inflammation), and the heterogeneity of individual patients responses (? down regulation of beta2 receptors). Overaggressive dosing can cause severe side effects.

Anticholinergic agents, although not first line therapy may be of benefit in mild to moderate asthma, and should be used, in addition to beta2 agonists in severe asthma.(1,5,10) In the severely obstructed patient drug deposition tends to be in the more proximal airways which is where cholinergic receptors are located. Ipratropium may be given by MDI (4-8 puffs q15 min.) or by WN (0.25-0.5 mg). The maximum effect is probably reached with 0.5 mg, although more may be required in ventilated patients.(12) Glycopyrrolate and atropine both produce bronchodilation if given IV (atropine 20 mg/kg, glycopyrrolate 10 mg/kg), although there is a high incidence of side effects.(13) They may also be nebulized (glycopyrrolate 1.0 mg, atropine 1.2-2.0 mg) which diminishes the incidence of side effects, particularly with glycopyrrolate.(14)

Corticosteroids are invaluable in acute asthma but take 6-12 hours to show an effect - so give early! Methylprednisolone has less mineralocorticoid activity and is cheaper than hydrocortisone. Dexamethasone is cheaper again. Doses shown to be effective are 10-15 mg/kg/day of hydrocortisone or its equivalent (120-180 mg methylprednisolone/day, i.e. 40mg q6h).(15,16) There may be slight improvements with 125 mg q6-8h. Smaller doses may be as effective although firm data is not available.(15,16) There is no role for inhaled steroids during an acute severe asthma attack.

Aminophylline is second line therapy.(1,5,10) It is a weak bronchodilator, has a low therapeutic index, and a high incidence of potentially serious side effects. A recent meta anlaysis (17) and several subsequent studies (5,10) have not shown significant improvement in PFT's when aminophylline is added to conventional treatment (beta2 agents plus steroids). Although it has little additive bronchodilatory effect, its other possible actions including increased diaphragm contractility, diuresis, mucociliary clearance, and antiinflammatory action may offer some benefit.(18) If other first line therapy has been unsuccessfully tried, some clinicians will add aminophylline (loading dose of 3-6 mg/kg, infusion of 0.2-0.9 mg/kg/hr).

Magnesium Sulfate: There are several small studies that demonstrate improved bronchodilation with the addition of intravenous magnesium to conventional therapy.(19,20) Overall, most studies show only modest improvements in PFT's, and there are also some negative studies.(21) In the doses given (10-12 mmol/20 min) it appears to be a relatively safe agent and can be considered in those not responding to conventional treatment. Magnesium inhibits catecholamine induced arrhythmias.(41) In theory it may not only improve the efficacy of beta2 agonists, but also their safety.

Cromolyn and Nedocromil prevent the release of mediators from mast cells. They are of no benefit during an acute asthma attack although they may be of use in the preoperative preparation of a known asthmatic. They are devoid of any significant cardiovascular effects.(2)

Emergency Drug Doses
· MDI-SPACER 4-20 puffs/hour
· NEBULIZED 5-10 mg q15 min prn
· IV 4 ucg/kg load and 0.1-0.2 ucg/kg/min.

· SC 0.3-0.5 ml q20 min. prn
· IV 4-8 ucg/min.
· ETT 5 ml 1:10,000

· MDI-SPACER 4-20 puffs/hour
· NEBULIZED 500 ucg q30-60 min. prn

· Methylprednisolone 40-125 mg q6-8h
· Hydrocortisone 500 mg iv

· iv 3-6 mg/kg load and 0.2-0.9 mg/kg/hr infusion
· IV 2-4 grams over 20 min., and 1 gram/hour infusion.

With early and aggressive management the majority of asthma attacks can be managed without the need for intubation and ventilation. Ventilation can be life saving but there is an associated high incidence of morbidity and mortality. Williams has reviewed 28 publications on ventilation in asthma and found a range of mortalities from 0-38% (mean 13%).(22) Mortality and morbidity figures seem to be decreasing in recent years with the recommendation of controlled hypoventilation.(5,9,23)

The decision as to who and when to intubate is more of an art than a science. Progressive exhaustion, respiratory arrest, decreased level of consciousness, persistent respiratory acidosis (pH<7.2), AND UNREMITTING HYPOXEMIA (SATS<90) ARE CLEAR INDICATIONS FOR INTUBATION.(5,9,12,23)

Hypercarbia, although a marker of severe disease, is not an indication for intubation and ventilation. Studies show that the majority of patients with hypercarbia will improve with aggressive use of bronchodilators.(5,24)

Recommendations vary regarding the optimum route and technique of intubation. Intubation can be a marked stimulus for bronchospasm. This may be diminished with "deep" anesthesia rather than just "light" sedation. When positive pressure is initiated the markedly negative pleural pressures seen during spontaneous inspiration will become positive, venous return drops, and precipitous hypotension may occur. This can be aggravated by induction agents. Large bore IV's should be in place (some advocate fluid bolusing prior to intubation) and vasopressors should be immediately available. It would seem reasonable to avoid agents that may release histamine. A large ETT is preferred to facilitate suctioning and possible bronchoscopy. Once intubated, many patients will require sedation and paralysis.

Thiopental: Controversy exists over the ability of thiopental to constrict the airways when given in lower doses.(2) Large doses may block bronchospasm induced by an irritating ETT but increase the risk of hypotension. Although perhaps suitable for the elective intubation of a stable asthmatic, it may not be appropriate for a patient with severe status.

Ketamine: Ketamine causes bronchodilation predominantly due to its sympathomimetic effects. Inhibition of vagal pathways and direct relaxation of smooth muscle are other possible mechanisms of action. It has been used successfully for intubation of asthmatic patients and to improve bronchospasm in ventilated and non ventilated patients.(25,26,27) Exercise caution with regards to its cardiovascular effects when used with other sympathomimetics. Many would consider this the induction agent of choice.

Lidocaine: Intravenous lidocaine can reduce irritant induced bronchospasm by blocking airway reflexes (1-2 mg/kg). IV infusions of 1-4 mg/min. may also be helpful.(2) Topical application may induce bronchospasm.

Propofol: Propofol's effect on airway tone and reactivity are not clear. There are case reports of its successful use in decreasing bronchospasm in ventilated COPD patients (28) (? direct smooth muscle relaxation). It may be preferable to thiopental for induction and a good choice for sedation of the ventilated asthmatic patient.

Anticholinergics: As discussed above the anticholinergic agents (ipratropium and glycopyrrolate) may help block irritant induced bronchospasm via either the IV or inhaled routes (less side effects).

Benzodiazepines: Benzodiazepines are commonly used for intubation and sedation and appear to be safe.

Narcotics: With the usual caveat of avoiding histamine release there appears to be no major concern with the use of narcotics as an adjunct to intubation or sedation.

Neuromuscular Blocking Agents: NMBs can theoretically induce bronchospasm by inducing histamine release or by reacting with muscarinic receptors. It has been suggested that those NMBs that cause histamine release (dtc, atracurium), or that block M2 muscarinic receptors be avoided in the treatment of the acute asthmatic.(2) There has been recent concern over profound muscle weakness developing in asthmatic patients who have received both NMBs and corticosteroids. Although guidelines do not exist, it would be prudent to monitor CPKs, and to minimize the dose and duration of administered NMBs.(5)

Cholinesterase inhibitors may provoke bronchospasm by increasing acetylcholine at parasympathetic nerve terminals.(2) Muscarinic receptor antagonists can prevent this, although it may be advisable to avoid using cholinesterase inhibitors if possible.

The goals of mechanical ventilation in acute asthma are to oxygenate, rest the patient, rest the respiratory muscles, correct acidemia, and do no harm.(12) Most of the morbidity and mortality that occurs in ventilated asthmatics are related to the consequences of "dynamic hyperinflation" (DHI). This occurs as a consequence of severe airflow obstruction leading to excessive positive end expiratory pressure within the lungs (auto-PEEP). The result is barotrauma (pneumomediastinum, pneumothorax, air embolism, etc.), and volutrauma (decreased venous return and increased RV afterload leading to hypotension and shock).

Darioli and Perret (29) achieved 100% survival in their series of 34 patients using the concept of "controlled hypoventilation". Their goals of treatment were to keep peak inspiratory pressures (PIP) < 50 CM H2O (TO AVOID BARO/VOLUTRAUMA), MAINTAIN NORMAL OXYGENATION, AND TO ACCEPT HYPERCARBIA IF NECESSARY. THE SUCCESS OF THIS APPROACH HAS LED TO MANY RECOMMENDATIONS TO KEEP PIP BELOW 50 CM H2O.(9,23) Others feel that due to high airway resistance PIP was a poor predictor of alveolar pressures and of subsequent barotrauma, (5,22) and that controlled hypoventilation decreases barotrauma due to it's effect on DHI rather than PIP. If this is true, attention should therefore be paid to measures of DHI rather than PIP.

Hypercarbia and subsequent acidosis are usually well tolerated.(5,9,12,23) In theory, respiratory acidosis may cause myocardial depression and increased CBF (which may be inappropriate in a patient suffering from hypoxia brain injury). The acidosis can be treated with bicarbonate (? treat pH < 7.2). BICARBONATE ADMINISTRATION UNFORTUNATELY INCREASES CO2 PRODUCTION (? CLINICAL SIGNIFICANCE), INCREASES INTRACELLULAR ACIDOSIS, AND CAN POSSIBLY CAUSE METABOLIC ALKALOSIS WHEN THE CO2 IS CORRECTED.

Tuxen et al (30) have described a relatively simple way of estimating DHI. They measured the volume of gas that was exhaled during a prolonged apnea (40-60 sec) following a normal ventilator delivered tidal breath. This "volume at end inspiration" (VEI) appears to reflect the severity of DHI (composed of tidal volume and trapped gas). They found that VEI was more predictive of barotrauma than PIP. The most critical factor in determining DHI was minute ventilation (VE). Decreasing the inspiratory flow rate (VI) decreased PIP, but the subsequent obligatory shortening of expiratory time caused an increase in Pplat, VEI, and DHI. Slowing the respiratory rate, or increasing VI prolonged expiratory time (TE) and decreased DHI.(31)

It can be misleading to focus on I:E ratios rather than TE. For example, a patient with a VE of 15 lpm (VT1000 x 15) and VI of 60 lpm has an I:E ratio of 1:3. Increasing VI to 120 lpm will impressively increase the I:E ratio to 1:7 but only increase TE from 3 to 3.5 seconds. Decreasing the respiratory rate to 12 and maintaining the VI at 60 will "only" improve the I:E to 1:4 but will increase TE to 4 seconds.(5)

PEEP: The role of PEEP in acute asthma is controversial. There are both positive and negative case reports.(9,32) In theory PEEP will splint open airways during exhalation. If the applied external PEEP is less than auto-PEEP there should be little increase in alveolar pressure, and obstructed units could empty due to decreased dynamic airway compression. The risk is increased DHI. Overall there is little evidence to support use of PEEP in the sedated, paralyzed, mechanically ventilated patient. There may be an advantage to using low to moderate levels of PEEP in spontaneously breathing patients as it decreases WOB.(9,23,32)

Initial respirator settings may be as follows:
· FiO2 = 1.0
· Tidal volume = 6-8 ml/kg
· Rate = 6-8/min.
· Inspiratory flow = 60-100 lpm
· PEEP < 5 CM H2O
· Keep PIP < 50 CM H2O
· Square wave flow (increases VI)

On occasion profound hypotension will occur with ventilated asthmatic patients. This may be a result of barotrauma (pneumothorax) or volutrauma. If due to the latter, disconnecting the patient from the ventilator (apnea) may reduce the DHI and the BP should improve.

After intubation it may be physically impossible to ventilate a patient. The position and patency of the ETT should be determined and pneumothorax ruled out. If severe bronchospasm is the likely problem then adrenaline can be administered via IV or ETT. If related to extreme hyperinflation then repeated intermittent chest compression during expiration may increase exhaled gas volume and decrease DHI.(33)

Alternative Treatments

Volatile Anesthetics: Volatile anesthetics have been shown to dilate the unstimulated airway by decreasing vagal tone, and to prevent and reverse airway constriction induced by hypocapnia, vagal or antigen stimulation.(2) Conventional tests of airway resistance demonstrate little difference between the bronchodilation induced by halothane, isoflurane or ethrane. Using more sensitive tests Brown (34) has shown that halothane is a more potent bronchodilator than isoflurane. Obviously they are useful drugs in managing the asthmatic patient in the OR.
Volatile anesthetics have also been used in severe status asthmaticus unresponsive to conventional treatment.(35,36) Our local experience has shown that administration of isoflurane to patients refractory to inhaled and parenteral beta2 agents is extremely helpful. Isoflurane may be the most appropriate choice of volatile due to its minimal cardiovascular depressive and arrhythmogenic potential. There is a theoretical risk associated with the use of volatile agents in hypercapnic patients who may have suffered a degree of hypoxic brain injury (increased CBF and cerebral edema).

Heliox: Due to its low density, high kinematic viscosity, and low Reynolds number, Heliox should decrease airway resistance, flow resistive work, and hyperinflation. A recent report describes dramatic improvements in pCO2 and PIP in 7 patients ventilated with Heliox.(37) There are some logistical (type of ventilator, FiO2 delivered) and financial constraints to using Heliox.

ECMO: There are successful case reports of ECMO and ECO2R in severe intractable asthma.(38,39) However, as asthma will likely improve in a few days and hypercapnia is usually well tolerated there are few patients who would require this treatment.

Pulmonary lavage: Pulmonary lavage via a flexible bronchoscope has been used to remove mucous plugs in severe unremitting asthma. This is not without risk as DHI may increase during bronchoscopy due to the effects of diminished inspiratory and expiratory flows created by the bronchoscope; obviously a large ETT is required (> 8.0 mm) There is also a risk of hypoxemia, pneumothorax, and infection associated with pulmonary lavage.(40)

Suggested reading:
References 5 is an excellent review of Acute Asthma (although I disagree with their approach to intubation).
Reference 10 should hopefully be published soon. It will provide an up to date critical appraisal of current asthma management. Please see accompanying guidelines.
References 30, 31, 32 are interesting with regards to mechanical ventilation and DHI.


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Reprinted with permission of Jon Hooper, MD, FRCPC