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History of the present illness
Risk factors for death from asthma
Medical decision-making/treatment- albuterol
- steroids
- ipratropium bromide
- sc adrenaline
- aminophylline
- magnesium
- heliox
- hydration
- intubation
- mechanical ventilation
Inhaled steroids - recommended daily doses
Strategy for home management of asthma exacerbations
| Introduction |
Definition: Asthma is a chronic inflammatory condition of the intra-pulmonary airways, with a reversible obstructive component.
To establish a diagnosis of asthma, the clinician should determine:-
- that episodic symptoms of airflow obstruction are present
- that the airflow obstruction is partially reversible
- that alternative diagnoses are excluded
New NIH expert panel guidelines - 4 grades of asthma severity
| Days with
symptoms |
Nights with
symptoms |
Peak flow
|
||
| Step 1 | Mild intermittent
|
< 2x per week | < 2x per month | > 80% |
| Step 2 | Mild persistent
|
3 - 6x per week | > 2x per month | > 80% |
| Step 3 | Moderate persistent
|
Daily | > 1x per week | 60 - 80% |
| Step 4 | Severe persistent
|
Continual | Frequent | < 60% |
Suggested optimum treatment schedule for patients with asthma
| Mild intermittent | No daily medicines, but short-acting bronchodilators
or cromolyn before inciting exercise or allergen exposure
|
| Mild persistent | Daily low-dose steroid inhaler or cromolyn
use +/- anti-leukotriene agent
|
| Moderate persistent | Either medium-dose steroid inhaler or low-moderate-dose
steroid inhaler + long-acting bronchodilator +/- anti-leukotriene agent
|
| Severe persistent | High-dose steroid inhaler use + long-acting bronchodilator +/- po steroid +/- anti-leukotriene agent |
All patients should use ‘quick-relief’ short-acting beta-2 adrenergic bronchodilators prn (2 – 4 puffs q 20 minutes x 3 by MDI, or 0.05mg/kg albuterol by nebuliser)
| History of the present illness |
- identify the symptoms likely to be due to asthma (cough, wheezing, dyspnea, chest tightness)
(* specifically ask the patient whether his symptoms are typical of his usual asthma attack => any difference may suggest an alternative diagnosis eg. pulmonary embolism, upper airway disease)
- determine the onset and the duration of symptoms and whether the symptoms are episodic or continual
(* anticipate significant airway inflammation and secondary airway edema and mucus plugging in patients with ongoing symptoms lasting longer than 2 weeks)
- determine the severity of the asthma attack by asking the patient to compare the present asthma attack to previous asthma attacks and his habitual degree of respiratory difficulty
- inquire about the patient’s recent peak flow readings and inquire about the patient's "best" peak flow reading
- identify possible precipitating factors
- exercise
- recent upper respiratory infection
- contact with animals with fur and/or feathers
- contact with housedust mites in mattresses, pillows, furniture, carpets
- smoke exposure
- pollen exposure
- changes in weather
- strong emotional expression (laughing or crying)
- airborne chemicals or irritants
- drug exposure (aspirin, beta blockers)
- food additives/preservatives
(* patients often tend to under-emphasize the degree to which they have been using their ‘rescue’ short-term bronchodilator inhaler)
- review the patient’s previous asthma history for risk factors for death from asthma
| Risk factors for death from asthma |
- history of previous sudden life-threatening asthma exacerbations
- history of prior intubation for asthma
- history of prior ICU admission for asthma
- > 2 hospital admissions for asthma in the past year
- > 3 ED visits for asthma in the past year
- hospital/ED visit for asthma during the past month
- use of > 2 cannisters of short-acting bronchdilators per month
- current use of oral steroids or recent withdrawal from oral steroids
- complicating health problems (COPD, CHF)
- complicating psychiatric problems (marked depression, psychosis)
- illicit drug use
- poor patient perception of airflow obstruction and its severity
| Examination |
- first assess the patient’s degree of respiratory distress by evaluating the patient's respiratory rate, the degree of ‘active’ respiratory effort, the degree of accessory muscle use, the degree of retractions, and the patient's ability to speak fluently (sentences => phrases => words => cannot even ‘catch’ his breath long enough to be able to utter a word)
- listen for wheezing and determine the loudness and duration
- mild asthma - wheezing only during forced active breathing or only during the expiratory phase
- moderate asthma - wheezing during inspiration and expiration
- severe asthma - marked wheezing with markedly decreased or near-absent breath sounds
- very severe asthma - "silent" chest with no wheezing
(* unequal breath sounds is compatible with asthma, but consider the possibility of a pneumothorax => check for deviated trachea, unilateral chest asymmetry or hyperresonance and sc emphysema; also consider foreign body obstruction)
- determine the degree of pulsus paradoxus
(* the degree of pulsus paradoxus may reflect the degree of airway obstruction in mild-moderately severe asthma, but may then become inversely related to the severity of the asthma as the patient ‘fatigues’ and active respiratory muscle activity diminishes)
- look for physical signs that suggest alternative diagnoses (CHF, PE, COPD, croup, cystic fibrosis, bronchiolitis, bronchitis, or carcinoid syndrome)
| Diagnostic testing |
- always try and obtain a baseline peak flow reading prior to any treatment, because patients/physicians tend to clinically under-estimate the degree of airway obstruction
- the best of three readings should be determined
- the results are effort-dependent and physician participation/encouragement may be necessary to obtain usefully accurate readings
- peak flow measurements cannot reliably be obtained in children < 5 years
- the peak flow should preferably be determined immediately on arrival, 30 minutes after the initiation of treatment and then again after another 30 minutes, and prn thereafter
- usually of no value in assessing the severity or progression of an acute asthma attack because pulse oximetry readings do not correlate with the degree of alveolar hypoventilation
- however, a low initial reading (<90%) may have a high correlation with the subsequent need for hospitalization in pediatric patients
- the pulse oximeter reading often decreases temporarily after effective treatment - because of a temporary aggravation of the V/Q mismatch - and should not be misinterpreted as an indicator of worsening airway obstruction
- a disproportionately low reading, which is not concordant with the patient’s clinical status, suggests a possible complication (pnemothorax or pneumonia) or another diagnosis (CHF or PE)
- is usually not indicated (especially in mild-moderate cases)
- may be indicated if the peak flow remains < 25% of predicted after treatment, or if the patient’s clinical status worsens despite aggressive bronchodilator therapy
- a normal PaCO2 suggests very severe asthma (hypocarbia is expected)
- is not routinely indicated
- may be indicated in the new-onset asthmatic, or when alternative "asthma-mimic" diagnoses have not been adequately excluded by prior health-care providers (eg. extrinsic or intrinsic bronchial obstruction)
- also indicated when there is a strong clinical suspicion of pneumothorax, complicating pneumonia, foreign body aspiration, or a possible alternative diagnosis (CHF or PE)
- should be considered if the patient fails to respond to ED treatment + hospital admission is required
- a CBC is not routinely indicated if the patient is not febrile or coughing up purulent sputum
- a CBC may be indicated if superadded pneumonia is suspected
- an elevated WBC can be due to stress or steroids and does not imply infection
| Medical decision-making and treatment |
- treatment with short-acting inhaled bronchodilators should be initiated immediately after taking a very brief focused history and performing a quick focused examination
- a detailed history and complete examination should be deferred until treatment with oxygen and short-term inhaled bronchodilator therapy is well underway
- supplemental oxygen should be administered to keep the pulse oximeter reading >90%
- albuterol is the most widely used beta-2 adrenergic agonist aerosol-agent used in the ED treatment of acute asthma
- albuterol (or an equivalent beta agonist) is normally given by nebulization = 2.5 - 5.0 mg q 20 minutes x 3 for adults, and 0.05 - 0.15 mg/kg q 20 minutes x 3 for pediatric patients
- larger doses (given undiluted) can be used if the patient is unresponsive to standard doses
- high dose range in children = 0.15 - 0.3mg/kg up to 10mg every 1 hour prn
(* some asthma specialists believe that even higher doses/hour can be used - because albuterol is such a safe drug when used in controlled circumstances)
- albuterol (or an equivalent beta agonist) can also be given by MDI = 4 - 8 puffs q 20 minutes for a few hours in adults (4 - 8 puffs q 20 minutes x 3 in peds)
(* many physicians think that a MDI is a better alternative than nebulisation - because it easier and quicker to administer than nebulisation, and the use of a MDI in the ED allows the ED staff to assess the patient's skill in using a MDI + it also gives the ED staff an opportunity to educate the patient on better MDI technique prn)
- use a MDI spacer for children < 10 years, and spacer + mask for children < 3 years
- rough dose equivalencies:- 2.5mg albuterol by nebuliser = 4 - 10 puffs by MDI
- the advantages of nebulization therapy over MDI include:-
- it is easier to use in the elderly patient, or by the uncoordinated or severely agitated patient
- it is more readily usable in patients with severe asthma, who cannot effectively take a deep breath
- patient expectation - patients, who have been "over-using" their MDI at home, expect "something more" than repeated MDI use in the ED setting
- it does not require specialized staff to monitor MDI technique and can be administered to the drowsy patient
- there is a plateau beyond which side-effects (tremor, shakiness, palpitations) do not increase, but there is apparently no definite plateau for the beneficial bronchodilator effects => very high doses (10 - 40 mg per hour) can therefore be used in the hope that the patient will experience steadily increasing bronchodilation
- large doses do not usually increase the heart rate, and the heart rate may actually decrease secondary to the improvement in the degree of airway obstruction
- a second-in-line short-term inhalational bronchodilator, which can be administered by MDI or nebuliser
- may not be as effective for asthma (compared to its effect in COPD)
- a single dose may be added to the first dose of nebulised albuterol (0.5mg in adults, 0.25mg in children) in patients with severe asthma, or it can be given by MDI
(* some investigators recommend repeat doses by nebulisation or MDI)
- remember that "steroids treat the disease, while beta-aerosols treat the symptoms"
- prednisone is the most frequent oral steroid used in ED practice
- po adminstration of steroids is as effective as IV administration - even in severe asthma
(* some physicians prefer to use long-acting IM steroids, especially if the patient is likely to be non-compliant - dexamethasone or triamcinalone diacetate or depo-methylprednisolone - because it eliminates the need to use a short course of po steroids after ED discharge)
- standard dose of po prednisone = 1 - 2 mg/kg po
- an IV steroid (eg. 80 - 125 mg methylprednisolone IV for adults, 1mg/kg for peds) can be reserved for the severe asthmatic in extremis, or when the patient vomits up his po dose of prednisone within one hour of administration
- nebulised dexamethasone (1.5mg/kg to a maxiumum of 45mg) can be used as an alternative to po prednisone in children
- po prednisone (when indicated) should be given given immediately after initiating short-term bronchodilator therapy, because early therapy at the time of ED arrival may ? decrease the hospital admission rate
- there is a delay of 4 - 6 hours before steroids work and a delayed peak effect (12 - 18 hours)
- indications for po steroid administration include:-
- moderate-severe asthma attack
- worsening asthma over many days
- recent po steroid use
- mild initial asthma attack not responding promptly to the first bronchchodilator therapy in the ED
- not as effective as inhaled beta-2 adrenergic agonists
- should only be used when the patient is too dyspneic ("not moving air") or too uncoordinated/agitated to effectively use a MDI or a nebuliser
- sc adrenaline may be used as a "last-resort" treatment modality in the severe asthmatic, who is not responding to inhaled albuterol, just prior to proceeding with intubation
- the usual dose of sc adrenaline = 0.3 - 0.5cc sc in adults (0.01 mg/kg to a maximum of 0.3mg in peds) and sc terbutaline = 0.25 mg in adults (0.01 mg/kg to a maximum of 0.3mg in peds) given every 20 minutes x 3 doses max prn
- IV terbutaline can also be used as a last resort medication (10mcg/kg IV over 10 minutes as a loading dose, followed by an infusion of 0.4mcg/kg/minute => increasing by 0.2mcg/kg/minute to an expected use of 3 - 6 mcg/kg/minute)
- some investigators belief that IV adrenaline by infusion may actually be better than IV terbutaline or IV salbutamol (not available in the USA) because its alpha effect may decrease airway edema => however, this practice pattern is still investigational
- adrenaline is not contra-indicated in elderly patients or patients with CAD
- use terbutaline (and not adrenaline, which can cause uterine artery spasm) in pregnancy if sc adrenergic therapy is necessary
- no longer used in the treatment of acute asthma
- probably of no benefit in mild/moderate acute asthma, but some studies have shown that it may be useful in severe asthma
- safe to use
- dose = 2 - 4 g over 20 minutes IV in adults (30 - 70 mg/kg for peds)
- administered as a 80:20 or 60:40 combination of helium and oxygen
- can be used in the severe asthmatic, who is not responding to bronchodilators, to attempt to avert the need for intubation and mechanical ventilation; or as an aid to decrease peak airway pressures in mechanically ventilated patients
(* very few large studies => role ill-defined - may not be effective)
- over-emphasized in the past
- not been shown to affect pulmonary secretions
- the risk of over-hydration (pulmonary edema) probably outweighs any potential benefits
- is immediately indicated if the patient arrives in the ED comatose or near-apneic
- is also indicated if the patient clinically deteriorates (while being treated) in the ED
- the assessment of clinical deterioration is based on clinical criteria (degree of exhaustion + degree of altered LOC + degree of 'apparent' lung hypoventilation, which is based on a subjective clinical assessment of air entry into the lungs)
- an ABG is not needed to decide whether to intubate an asthmatic patient => however, an ABG showing normocarbia or mild hypercarbia suggests severe asthma; and a respiratory acidosis with marked hypercarbia is a definite indication for intubation
- anticipate the need for intubation in the clinically deteriorating patient => pre-oxygenate and get RSI drugs and airway equipment ready
- RSI using the orotracheal route is the optimum approach to intubation
- the blind nasotracheal route of intubation should probably only be used in extremely "difficult airway" conditions
(* attempted blind nasal intubation in the hypoxic asthma patient is associated with a high morbidity)
- RSI drug-of-choice = ketamine (1 - 2 mg/kg IV) + succinylcholine +/- pre-treatment with lidocaine
(* succinylcholine should always be used - because ketamine can rarely induce laryngospasm and also produce generalised hypertonia and jaw clenching)
- a surgical airway is obviously necessary if intubation proves to be impossible - because it is near-impossible to effectively BVM ventilate a very "tight" asthmatic patient
- the surgical airway technique must incorporate the use a cuffed tracheostomy tube in adults, because uncuffed tubes and cricothyrotome catheters are associated with too large an airleak when airway pressures are very high => inadequate lung ventilation
(* do not rely on rescue ventilatory devices that do not provide a tight airway seal, and do not use the technique of needle cricothyrostomy and jet insufflation)
- follow the principles of controlled hypoventilation and permissive hypercapnea to decrease peak airway pressures and the subsequent risk of barotrauma
- initial ventilator settings include a respiratory rate of 6 - 8 breaths per minute, a tidal volume of 6 - 8 cc/kg, an inspiratory/expiratory ratio of 1:3 - 1:6 and a peak inspiratory flow of 80 - 120 L/min
- monitor the peak airway pressures and change the ventilator settings so as to keep the peak airway pressure < 40 cm water
(* avoidance of high airway pressures and secondary barotrauma is more important than the avoidance of hypercarbia)
- vigilance is particularly necessary post-intubation re: barotrauma => tension pneumothorax and/or high intra-thoracic pressures => hypotension
(* some asthma specialists recommend a large IV infusion bolus of crystalloid just prior to intubation - to prevent the hypotension that may occur when mechanical ventilation of a patient with markedly increased airway resistance results in high positive airway pressures; use the "apnea" test if the patient suddenly becomes very hypotensive immediately after intubation => disconnect the patient from the ventilator for 30 seconds => immediate recovery from hypotension suggests auto-PEEP and lung hyperinflation +/- hypovolemia, while persistent hypotension suggests a tension pneumothorax)
- aggressive post-intubation sedation is required to ensure that the patient does not "fight" the ventilator => increased airway pressures and markedly increased risk of iatrogenic baro-trauma
(* heavy sedation may also be required to control any patient agitation that is secondary to the iatrogenic hypercarbia resulting from the deliberate use of controlled mechanical hypoventilation)
- useful sedating drugs include ativan by IV bolus (1 - 2 mg) prn or propofol by continuous IV infusion (2 mg/kg/hour and titrate up)
- use long-acting muscle relaxants prn if aggressive IV sedation is insufficient (eg. pancuronium - 0.1mg/kg)
- avoid an arterial pCO2 > 80mmHg, because a consequent respiratory
acidosis with ph < 7.2 will require bicarb => paradoxical CNS acidosis
and shift of the oxygen saturation curve to the left
Algorithm for the ED treatment of acute asthma - based on the NIH expert panel report
- a patient with a peak flow > 70% of predicted and no/little symptoms (after ED treatment) can be discharged to home if a good response is sustained for > 1 hour after the last bronchodilator treatment
- a patient with a peak flow < 50% of predicted and/or persistent respiratory difficulty should be admitted to the hospital
- note however, that there are no 'fixed' criteria for admitting patients with a post-treatment peak flow reading in the range of 50 - 70% of predicted + continued mild-moderate symptoms
- strongly consider hospital admission if there is:-
- a history of recent steroid use
- a recent ED visit for asthma
- poor asthma control in the 7 - 14 days prior to the present ED visit
- a history of frequent post-discharge relapses
- a history of poor medication compliance
- a poor home enviroment and social support system
- a 'sluggish' response to maximal ED treatment
Minimal instructions include:-
- sufficient medicines for home use
- arrange outpatient recheck in 3 - 5 days (1 - 2 days prn)
- instructions on inhaler use
- consider issuing a peak flow meter for home use
- consider starting inhaled steroids, or increasing the dose of inhaled steroids from low => moderate => high dose range to obtain better long-term control
Maximal instructions also include:-
- patient education on asthma triggers
- self-management 'home' plan for acute asthma exacerbations
Inhaled
steroids – recommended daily doses (pediatric doses in brackets)
| Inhaled steroid | MDI | Puffs | Low dose | Medium dose | High dose |
| Beclomethasone dipropionate
(Vanceril) (Beclovent) |
42 mcg
84 mcg |
200
120 |
4 - 12 puffs
(2 - 8 puffs) 2 - 6 puffs (1 - 4 puffs) |
12 - 20 puffs
(8 - 16 puffs) 6 - 10 puffs (8 - 16 puffs) |
> 20 puffs
(>16 puffs) > 10 puffs (> 8 puffs) |
| Triamcinalone acetonide
(Azmacort) |
100 mcg | 240 | 4 - 10 puffs
(4 - 8 puffs) |
10 - 20 puffs
(8 - 12 puffs) |
> 20 puffs
(> 12 puffs) |
| Flunisolide
(Aerobid) |
250 mcg | 100 | 2 - 4 puffs
(2 - 3 puffs) |
4 - 8 puffs
(4 - 5 puffs) |
> 8 puffs
(> 5 puffs) |
| Fluticasone
(Flovent) |
44 mcg | 60
120 |
2 - 6 puffs
(2 - 4 puffs) |
(4 - 10 puffs)
2 - 6 puffs |
|
| 110mcg | 120 | 2 - 6 puffs
(2 - 4 puffs) |
> 6 puffs
(> 4 puffs) |
||
| 220 mcg | 120 | > 3 puffs |
- prednisone po for 3 - 10 days (usually 5 - 7 days) without tapering
- adult dose = 40 - 60mg per day (standard dose)
- high dose = 120 - 180 mg/day in 3 - 4 divided doses for 48 hours, then 60 - 80 mg/day until PF > 70% of predicted value
- pediatric dose = 1 - 2 mg/kg/day (standard dose)
- high dose = 1mg/kg/dose qid x 48 hours => 1 - 2 mg/kg/day until PF > 70% of predicted
Strategy for home management of asthma exacerbations
