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ACUTE ASTHMA

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					                                         ACUTE ASTHMA

Prof Salman Waris
Consultant Anaesthetist
Head of the Department,
Nishter Medical College Hospital
Multan


Asthma is an inflammatory disease of the airways characterized by episodic reversible bronchospasm
in which the initial phase of constriction of bronchial smooth muscle is followed by airway mucosal
edema and bronchiolar plugging. The word asthma is derived from a Greek word which is a synonym
for breathlessness. In 1698, Floyer defined it as a triage of three problems i.e. airway hyper
responsiveness, bronchospasm and reversible airway obstruction. In the hyper- reactive response,
smooth muscles in the airways constrict in response to inhaled allergens or irritants.

This stage is followed by the inflammatory response in which the immune system delivers white blood
cell and other immune factors to the airways. These inflammatory factors cause the airways to swell,
to full with fluid and to produce thick sticky mucus which results in wheezing, breathlessness,
inability to exhale properly and a phlegm producing cough. The pathophysiology of asthma involves
reduction in airway diameter due to smooth muscle contraction, vascular congestion & bronchial wall
edema leading to mucus plugging by thick secretions.

It also involves local release of various chemical mediators released by antigen-antibody interactions,
which activate membrane phospholipase and result in release of Arachidonic acid and its metabolites
like prostaglandins, leukotrienes, histamine or their precursors.

Another proposed mechanism for initiating bronchial hyper-responsiveness is over activity of
parasympathetic nervous system initiated by release of mediators of inflammation and other
environmental factors. Reflex vagal activation results in broncho constriction mediated by an increase
in cyclic AMP.

The physiological consequences of airway obstruction include.
    Increased airway resistance
    Decreased maximum expiratory flow rates
    Air trapping
    Increased airway pressures leading to baro-trauma and adverse haemodynamic effects
    Increased work of breathing causing pulsus paradoxus and respiratory failure due to respiratory
     muscle fatigue.

While taking the history, the patient classically presents with a triad of symptoms i.e. dyspnea,
wheezing & cough. In history also ask for key historical events including precipitating factor e.g. viral
upper respiratory infection, allergen exposure and smoke inhalation. Focus should be on current
medication and compliance. Past asthma related healthcare utilization also needs special attention.
Duration of present symptoms, degree of dyspnea, cough, wheezing are also important and must be
asked.

Symptoms include cough at night usually unproductive, episodic wheeze which worsens on expiration
giving feeling of tightness in chest and shortness of breath. Associated features include family history
suggestive of reactive airway disease, presence of eczema, rhinitis, hay fever, any history of atopy and
presence of any precipitating factors for wheezing like viral infection, exercise, allergen exposure or
any history of drug allergy need special emphasis.
In physical examination of the patient, level of alertness, ability to lie flat, ability to speak, presence of
stridor, use of accessory muscles of respiration, presence of central cyanosis, peripheral edema,
subcutaneous emphysema should be looked for. Auscultation of bilateral breath sound and peak flow
rate measurements needs special attention.

Additional findings on examination may include decreased breath sounds with poor airflow, pulsus
paradoxus, silent chest and presence of tachypnea & tachycardia. Lab studies include CBE showing
raised WBC count, eosinophilia, serum potassium levels, ABG, imaging studies like chest radiograph
have a pivotal role in establishing a diagnosis of asthma. ECG showing right ventricular strain, sinus
tachycardia or supraventricular tachycardia or arrhythmia may also be helpful in assessing the severity
of the problem. Pulse oxymetry is helpful in assessing the oxygenation and Spirometry is done to
assess the severity of the problem and the effectiveness o the treatment being offered to the patient..
Special concern is focused over measurement of peak expiratory flow rate.

A limitation in measurement of PEFR is that it is effort dependent. FEV1 can also be measured but it
is of limited value because of its effort dependence. MMEFR is the clear indicator of endurance and is
patient’s effort independent.

The goals of treating a patient with asthma are.
 Reverse the airflow obstruction
 Ensure adequate oxygenation
 Relieve inflammation


Treatment offered for treating asthma includes
 Beta 2 adrenergic agonists
 These are preferred initial rescue medication
 Causes bronchodilatation, vasodilatation, uterine relaxation and skeletal muscle tremor
 Produces effect by stimulating adenyl cyclase.
 Converts ATP to CAMP
 Binds intracellular calcium
 Reduces myoplasmic calcium concentration
 Relaxes bronchiolar smooth muscles
 Also inhibits mediators release
 Promotes mucociliary clearance
 Side elects include tremors, nervousness. Anxiety, hyperglycemia, palpitations, tachycardia and
    hypertension.
 Albuterol is the most commonly used agent
 Salmetrol is a long acting B2 stimulant but it is not indicated in acute exacerbations


Second line of Defence includes corticosteroids, which restore β adrenergic responsiveness and reduce
inflammation. The anti inflammatory effect reaches maximum in a short cause of time and might take
4-8 hours to achieve peak effect.


Drugs used include oral prednisolone 40-60mg or methyl prednisolone 60-125mg 1/v additional
dosing may be given 4-6 hour apart. Recommended continuation of treatment is 2-10 days after
discharge.
Class of drugs used in treating asthma includes anticholinergics which competitively antagonize
acetylcholine which in turn promotes bronchodilatation. These are particularly effective in
combination with β 2 agonists. Ipratropium bromide is the most commonly used agent. Side effects
include dry mouth, thirst, and difficulty in swallowing. Methylxanthine derivatives are not
recommended at present as first line agents, might be useful as adjuncts to first line drugs. While using
these drugs, plasma level should be monitored as more than 30 meg/ml increases the risk of seizures
and arrhythmias.


Most cell stabilizers like cromolyn sodium or nedocnomil are used as a membrane stabilizing agents
for mast cells which do not allow early degranulation and release of pro-inflammatory mediators. It
also blocks chloride channels which modulates mast cell mediator release and eosinophil recruitment.
These drugs are not indicated for acute attacks.


Another class of drug used in preventing acute exacerbations of asthma is anti-leukotrienes like
montelukast, zafirlukast etc. But unfortunately, their role in acute asthma is not defined. Another drug
magnesium sulfate has proven to have an important role in aborting acute attack of asthma. 1-2 grams
i.v. over 30 minutes is the recommended dose. In refractory cases, epinephrine may be considered as
an alternative to conventional therapy. It is administered either as intravenous infusion or by nebuliser.
Continuous ECG monitoring is mandatory as there is high risk of tachyarrhythmias during its
administration.


Ketamine has been reported to break refractory bronchospasm. It acts on cortex and limbic system.
Initial dose in 1-4.5mg/kg 1/V but it may cause intracranial hypertension, and increased bronchial
secretions. Heliox is a helium oxygen (80:20 or 70:30) mixture that may provide dramatic benefit for
emergency department patients with severe exacerbation. Helium is about 25% as dense as room air
and consequently it travels more easily down narrowed passages. It quickly decreases the work of
breathing and when used as a gas mixture to drive the nebuliser, it causes prompt relief in the
symptoms by better delivery of inhaled bronchodilators.


Another drug which has been recently approved by FDA for use in treating asthma is Omalizumab. It
prevents the IgE antibody from triggering the inflammatory events. It is given in the form of injections
every 2-4 weeks.

Therapies which are not recommended are
 Antibiotics
 Empiric aggressive hydration
 Chest physiotherapy
 Maculates
 Sedation


Now focusing the discussion over acute severe asthma
The features of acute severe asthma include
 Unable to finish sentence in one breath
 Respiratory rate > 25 /min
 Heart rate > 110/ min
 PEFR <50% predicted normal or recorded best



Features of life threatening asthma
Include.
    PEFR < 33% predicted normal or recorded best
    Silent chest, cyanosis, feeble respiratory effort
    Exhaustion, confusion, coma
    Bradycardia, hypotension
    Normal or rising PaCO2, acidosis, falling PaO2.



Management in emergency department include
 Proper history taking
 Any history of recent ER visit, current corticosteroid use
 Previous history of respiratory failure, progressive worsening of symptoms, seizures with asthma
    attacks.


Physical examination revealing
   Respiratory distress at rest, difficulty in speaking and completing a sentence in single breath,
    diaphoresis, agitation.
   R/rate > 28, HR > 110. Pulsus paradoxus of > 25 mm Hg.
   Use of accessory muscles of respiration
   Presence of sternocleidomastoid use or suprasternal retractions.


ICU management includes.
       Patient just requires additional time for respiratory function to improve earlier, mainstay of
treatment was intubation & ventilation but now alternatives to intubation have evolved.
    NIPPV
    Inhaled general anaesthetics
    Continuation of pharmacotherapy


Immediate ICU management includes
  Oxygen at highest available concentrative & flow
  Nebulized B2 against every 15 min.
  Salbutamol 5 mg (0.15 mg /kg)
  Terbutaline 10mg
  Nebulized Ipratropium bromide 0.1mg 6 hours.


Hydrocortisone 200mg I/V 6 hourly.
Intravenous bronchodilators
Aminophylline 3 mg /kg bolus followed by 0.5mg /kg/hour
Salbutamol 3-4 mg/kg bolus flowed by 5-50 mg /min

Mechanical ventilation is another mode of managing life threatening asthma. It does not relieve air
flow obstruction rather it allows the patient to rest while obstruction is relieved. Potential
complications include high peak airway pressure, barotrauma, air trapping & intrinsic PEEP
development
Ventilatory strategies include ventilation with
    Low tidal volume
    Low minute volume
    Long expiratory time


Non invasive positive pressure ventilation is potentially beneficial in following ways
   It reduces the work of breathing
    Causes a decrease in inspiratory threshold load
    NIPPV has proven to cause significant decrease early in patients with acute asthma.
    NIPPV has also reduced the number of hospitalization and improvement in lung function.


For employing NIPPV, first of all clear headed, conscious patient being able to incorporate his / her
breathing with ventilator cycling in mandatory
Initial ventilator settings include
     PEEP + 5 cm H2O
     Pressure support < 8 cm H2O


NIPPV should be instituted either with tightly fitting CPAP mask.
Pulmonary hyper inflation, hypovolemia, sedation and development of tension pneumothorax are
potential complications.


These are the few management guidelines which are gaining popularity in treatment of acute severe
asthma. Whatever the modality is selected, it is empirical to closely monitor the clinical response
frequently and emphasis should be laid down on the preferable avoidance of mechanical ventilation
until unless clearly indicated.

				
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