Asthma is a
common chronic affliction with wide clinical variability. Though most patients
have mild disease, asthma can be rapidly fatal. Patients with COPD often
present in distress, expending tremendous effort to combat hypoxia. Uncomplicated
medical or surgical disease will become more serious or life-threatening as the
impact of COPD is unmasked.
Clinical
Features:
Asthma is
defined as reversible airway obstruction, associated with hyper-responsiveness
of the tracheobronchial tree. An early component of an asthmatic attack is the
bronchial smooth-muscle contraction. Bronchial inflammation, edema, and mucus
hypersecretion become more prominent as the attack progresses. Increased airway
resistance leads to air trapping, increased airway pressures,
ventilation-perfusion imbalance, increased work of breathing, hypoxemia and, in
severe cases, hypercapnia. Although bronchospasm can be reversed within minutes,
mucus plugging and inflammatory changes do not resolve for days,
steroid-dependent patients, and those with prior attacks requiring intubation
are at higher risk for respiratory failure.
The most common
aetiology of COPD is cigarette smoking. Other causes include environmental
toxins, genetic aberrations, and sustained bronchospastic airflow obstruction. There
are two dominant clinical forms of COPD:
1. Pulmonary emphysema, characterized
by abnormal, permanent enlargement and destruction of the air spaces distal to
the terminal bronchioles.
2. Chronic bronchitis, a condition of
excess mucus secretion in the bronchial tree, occurring on most days for at
least 3 months in the year for at least 2 consecutive years. Elements of both
forms are often present, though one predominates. Airway resistance, especially
to expiration is the fundamental feature of either condition. Hypoxemia and hypercapnia
result from ventilation-perfusion mismatches and alveolar hypoventilation. As COPD
progresses, neuro-chemical and proprioceptive ventilatory responses become aberrant.
Pulmonary arterial hypertension develops leading to right ventricular hypertrophy
and cor pulmonale. Clinically, compensated patients present with exertional dyspnea,
chronic productive coughs (frequently with minor hemoptysis) and expiratory
wheezing. Coarse crackles are heard in patients with primary bronchitic
disease. An expanded thorax, impeded diaphragmatic motion, and diminished
breath sounds are noted in those with emphysema.
A Acute exacerbation of asthma / COPD are usually
due to increased bronchospasm, smoking an d exposure to other noxious stimuli,
adverse response to medication such as antihistamines decongestants, beta-blockers,
and hypnotic tranquilizers; allergic reactions, and noncompliance with prescribed
therapies. Respiratory infection, pneumothorax, myocardial infarction,
dysrhythmias, pulmonary edema, chest trauma, metabolic disorders, and abdominal
processes are triggers and complication s of asthma / COPD. Patients with
exacerbations of asthma / COPD present complaining of dyspnea, chest tightness,
wheezing, and coughs. Physical examination reveals wheezing with prolonged
expiration. Wheezing does not correlate with degree of airflow obstruction. A ‘quite
chest’ indicates severe airflow restriction. Patients and physicians often
underestimate the severity of attacks. Patients with severe attacks may demonstrate
sitting-up-and-forward posturing, pursed -lip exhalation, accessory muscle use,
paradoxical respirations, and diaphoresis. Pulsus paradoxicus of 20 mmHg or
more may be noted. Hypoxia is characterized by tachypnea, cyanosis, agitation,
apprehension, tachycardia, and hypertension. Signs of hypercapnia include
confusion, tremor, plethora, stupor, hypernea, and apnea.
Diagnosis
and Differential
ED diagnosis
of asthma / COPD usually is made clinically. The clinician should attempt to
determine the severity of the attack and the presence of complications.
Objective measurements of airflow obstruction, such as peak expiratory flow
rate, have been shown to be more accurate than clinical judgement in determining
the severity of the attack, and the response to therapy. Laboratory examinations
should be used selectively, chest w-ray is used to diagnose complications such
as pneumonia and pneumothorax, arterial blood gases should not be obtained routinely.
Arterial blood gases (ABGs) serve primarily to evaluate hypercapnia in moderate-to-severe
attacks. Hypoxia can usually be evaluated
by pulse oximetry. ABG results should be interpreted in light of the total clinical
picture. Compensated hypercapnia and hypoxia is common in COPD patients, therefore,
comparison with previous ABG’s is helpful. Normocarbia in the setting of an
acute asthmatic attack is an ominous finding if the patient is doing poorly. An
arterial pH below that consistent with renal compensation implies either acute
hypercarbia that consistent with renal compensation implies either acute
hypercarbia or metabolic acidosis. ECG are useful to identify arrhythmias or ischemic
injury. Measurement s of methylxanthine levels should be obtained.
The
differential diagnosis of decompensated asthma / COPD includes many of the
disorders listed above as complications.
In addition, interstitial lung diseases, pulmonary neoplasia, aspirated foreign
bodies, pleural effusions, and exposure to asphyxiants must be considered.
Managenment
and Emergency Care:
Although
patients with COPD often have more than underlying illnesses than asthmatic, therapy
for acute bronchospasm and inflammation is similar. Treatment should precede
history-taking in acute dyspneic patients, as the patient may decompensate
rapidly. These patients should be placed
on a cardiac monitor, noninvasive BP device, and have continuous pulse oximetry.
An intravenous line should be started in patients moderate and severe attacks.
The primary goal of therapy is to correct tissue oxygenation.
1. Hypoxemia is nearly universal during
asthmatic attacks. Therefore, empiric supplemental oxygen should be
administered. The need for supplemental oxygen with COPD must be balanced
against the suppression of hypoxic ventilatory drive. Arterial saturation should
be corrected above 90 %.
2. Beta-adrenergic agonists produce
prompt effects and are the drugs of choice to treat bronchospasm. Aerosolized
or parental forms should be used in critical settings. Aerosol therapy minimize
systemic toxicity and is preferred. Albuterol sulphate, 1.25 to 5 mg. and
metaproterenol, 10 to 15 mg are the most beta2 -specific agents. Iso-etharine,
2.5 to 5 mg or bitolterol mesylate, 0.5 to 1.5 mg can also be delivered by
nebulizer. Delivering doses in rapid succession maximizes results. Frequency of
dosing depends on clinical response and signs of drug toxicity =. Metered dose
inhalers with space devices may be reasonable to use in ill patients.
Subcutaneous terbutaline sulphate (0.25 – 0.5 ml) or adrenaline 1:1000 (0.1 –
0.3 mL) may also be administered. Adrenalin should be avoided in the first
trimester of pregnancy and possibly in patients with underlying cardiovascular
disorder. Beta -adrenergic agonists may inhibit uterine contraction when used
near term of pregnancy.
3. Systematic glucocorticoids elicit bronchodilator
response, facilitate the actions of concurrently given beta-agonists and
methylxanthines, and have anti-inflammatory effects. As the onset of action may
take hours, they should be given early in the course of treatment.
See my experience using reflexology on a young Malay girl with status
asthmaticus during the course
of my work in an isolated village here:
https://scientificlogic.blogspot.com/search?q=a+miracle+before+my+eyes
Once you get to this site, scroll right down to the paragraph on:
“Another Medical Emergency”
where I found natural therapy by merely
massaging the soles of her feet worked much faster and more efficiently in a
medical emergency than using any bronchodilators, e,g. beta 2-agonists, anticholinergics and theophylline
or other drugs described here.
Steroids should be given immediately to
patients with severe attacks, as well as patients who are currently taking, or
have recently taken, these drugs. The optimal daily dose is the equivalent of
60 to 180 mg of Prednisone day, with an initial dose being equivalent of 60 to
80 mg prednisone. The choice of steroid is not critical. If the patient is
unable to take oral medication, use methylprednisolone 125 mg IV.
Hydrocortisone should be avoided, however because of excess mineralocorticoid
effect. Inhaled steroids are extremely useful in the treatment of chronic asthma
/ COPD, but should not be used in the treatment of acute symptoms.
4.
Anticholinergics are useful adjuvants when given
with other therapies. Ipratropium bromide has recently replaced nebulized
atropine sulphate (1 – 3.5 mg) and glycopyrrolate (0.2 – 1 mg) as the agent of
choice. Nebulized iprotropium (500 mg = 2.5 ml) may be administered either alone
or mixed with albuterol. Iprotroprium is available as a metered dose inhaler.
The effects of iprotroprium peak in 1 in 2 hours and last for 3 to 4 hours. Dosages may be repeated every 1 to 4 hours
When used with beta-agonist agents, effects may be additive. The use of
nebulized anticholinergics has been reported to cause attacks of narrow angle
glaucoma due to tropical ophthalmic absorption.
5.
The role of methylxanthines in the treatment of
acute asthma has been seriously challenged. Theophylline produces less
bronchodilation than beta-adrenergic agents. In addition, studies have shown that
when used in combination with inhaled beta-adrenergic agents, theophylline
increases toxicity but not efficac7y of the therapy. Although methylxanthines
are no longer the first-line drugs, some patients not responding to
beta-agonists and steroids may benefit from the addition of theophylline. Methylxanthines
seem to have more of a role of theophylline in the treatment of chronic, stable
asthma. The efficacy of methylxanthines in COPD is still controversial. The
loading dose of theophylline is 5 to 6 mg / kg ideal body weight. In patients
previously medicated, a mini load should be given. The mini-load is calculated
as (target concentration – measured concentration ) x (0.5 x ideal body weight
in litres). The maintenance dose is 0.2 to 0.8 mg / kg ideal body weight. These
dosages should be used as guidelines. Metabolism of methylxanthines is highly variable.
Increased serum levels are associated with liver disease, CHF , cor pulmonale,
viral respiratory infections, advanced age, cimetidine, erythromycin, oral
contraceptives, and allopurinol. Decreased levels are seen with cigarette smoking,
phenobarbital, phenytoin, large consumption of charcoaled beef, and factors
that promote the hepatic P450 enzyme system. Toxicity can be severe and can
occur at drug level that fall within normal range. Serum levels should be
measured to guide appropriate therapy.
6.
Broad spectrum antibiotics such as TMP / SMX DS
bd, or doxycycline 100 mg bid, or others are indicated for the treatment of
bacterial respiratory infections. Preventive polyvalent pneumococcal and trivalent
influenza vaccination may be administered to stabile COPD patients.
7.
Although some authors have reported that 1 to 2
gm of intravenous magnesium sulphate reduces bronchospasm, no consistent clinical
benefit has been demonstrated.
8.
Sedatives, hypnotics, and other medication which
depresses respiratory drive are generally contraindicated. Beta-blockers may
exacerbate bronchospasms. Antihistamines and decongestants should also be
avoided as they diminish the ability to clear respiratory secretions. Mucolytics
may provoke further bronchospasm. The benefit of iodides and glyceryl
guaicolates in asthma and doxapram in COPD are unproven. Many asthmatics respond
poorly to ultrasonic nebulization and IPPB.
If all these standard Treatment fails,
what should we do?
Assisted mechanical ventilation
is indicated for inability to maintain oxygen saturation above 90 %, or severe
hypercarbia associated with stupor, narcosis, or acidosis. In selected patients,
non-invasive, positive-pressure ventilation (Bi-PAP) may avert artificial ventilation. Oral intubation is preferred as
large endotracheal tubes can be used. Large tubes facilitate suctioning, fibreoptic
bronchoscopy, and ventilator weaning. Initially, high inspired oxygen concentration
may be used. A volume -cycled ventilator should always be used. Excessive tidal
volume of over 15 mL / kg ideal body weight and air trapping due to bronchospasm can cause
barotrauma and hypotension. Utilizing high flow rates at a reduced respiratory
frequency allow adequate expiration. The goal of this approach, referred to as
controlled mechanical hypoventilation, is to maintain adequate oxygenation with
little regard to hypercarbia.
Therapy should be guided by pulse
oximetry and ABG results. Sedation and continued therapy for bronchospasm should
continue after the patient has been placed on artificial ventilation.
Source by Frantz R. Melio. For further reading and other references:
1. PH Feng, KM Fock. Philip Eng: Handbook of Acute Medicine
2. David M. Cline, O. John Ma, Judith E. Tintinalli, Ernest Ruiz, Ronald L. Krome: Emergency Medicine: Companion Handbook.
3. Richard Robinson & Robin Stott: Medical Emergencies: Diagnosis and Management
4. Sonke Mulle: Memorix Emergency Medicine
