ACUTE EXACERBATION OF COPD

& STATUS ASTHMATICUS

MODERATOR – Dr.SHAGUFTA NAAZ

PRESENTER – Dr.MITHUN R
 COPD

 Is a common, preventable and treatable disease that is characterized by

persistent respiratory symptoms and airflow limitation that is due to
airway and /or alveolar abnormalities usually caused by significant
exposure to noxious particles or gases.
 ACUTE EXACERBATION OF COPD

 An exacerbation is an acute increase in symptoms beyond normal day to

day variation sufficient to warrant a change in management

 Generally includes an acute increase in one or more of cardinal symptoms

1. Cough (frequency and severity)

2. Sputum production ( volume and character)

3. Dyspnea
 INVESTIGATIONS TO CONSIDER
 Pulse oximetry

 Chest x ray

 ABG

 ECG

 Sputum c/s is of limited value because empirical therapy is effective

and prescribe if purulent

 Blood c/s if temp>37°C

 SPIROMETRY

 No demonstrated value in settings of COPD exacerbation

 Useful only in outpatient diagnosis of stable COPD

 Different for Asthma patients where spirometry is useful in

settings of stable asthma and status asthmaticus
 Diagnosis of COPD exacerbation relies exclusively on clinical
presentation of patient complaining of acute change of
symptoms that is beyond normal day to day variation.
 Criteria for ICU admission include:

 Patients with high-risk comorbidities (pneumonia, cardiac

arrhythmia, heart failure, diabetes mellitus, renal failure, liver
failure)
 Continued need for NPPV or invasive ventilation

 Hemodynamic instability

 Need for frequent nebulizer treatments or monitoring

 MANAGEMENT
Classification of hospitalized patients

No respiratory failure:

Respiratory rate: 20-30 breaths per minute

no use of accessory respiratory muscles

no changes in mental status

hypoxemia improved with supPlemental oxygen given via Venturi mask 28-
35% inspired oxygen (FiO2)

no increase in PaCO2
 Acute respiratory failure — non-life-threatening:

Respiratory rate: > 30 breaths per minute

using accessory respiratory muscles

no change in mental status

hypoxemia improved with supplemental oxygen via Venturi mask 25-30%

FiO2

hypercarbia i.e., PaCO2 increased compared with baseline or elevated 50-

60 mmHg.
Acute respiratory failure — life-threatening:

Respiratory rate: > 30 breaths per minute;

using accessory respiratory muscles;

acute changes in mental status;

hypoxemia not improved with supplemental oxygen via Venturi

mask or requiring FiO2 > 40%;

hypercarbia i.e., PaCO2 increased compared with baseline or

elevated > 60 mmHg or the presence of acidosis (pH ≤ 7.25).


 Provide supplemental oxygen to target a pulse oxygen

saturation of 88 to 92% or PaO2 of 60 to 70 mmHg.

 Provide combination of aggressive bronchodilator therapy

and ventilatory support (NPPV or invasive ventilation)
Noninvasive positive pressure ventilation (NPPV):

◦ Appropriate for the majority of patients with severe

exacerbations of COPD unless immediate intubation is
needed or NPPV is otherwise contraindicated

◦ Contraindications to NPPV include: Severely impaired

consciousness, inability to clear secretions or protect airway,
high aspiration risk
Tracheal intubation and mechanical ventilation

 Indicated for patients with acute respiratory failure,

hemodynamic instability (eg, heart rate <50/minute,
uncontrolled arrhythmia) and those in whom NPPV is
contraindicated or who fail to improve with NPPV and
aggressive pharmacotherapy
 MANAGEMENT – ABC APPROACH

 Antibiotics should be given to patients with

All 3 cardinal symptoms

2 of the cardinal symptoms if sputum is included

Severe exacerbation requiring mechanical ventilation

 Recommended length of antibiotic therapy is usually 5-10 days

 In complicated COPD with risk factors

 Amoxicillin/clavulanate

 Levofloxacin

 Moxifloxacin

RISK FACTORS
 Co – morbities

 Severe COPD (FEV1 <50% OF Predicted)

 >3 exacerbations/yr

 Antibiotic use in past 3 month

 At Risk of Pseudomonas infection
 High dose Levofloxacin (750mg) or ciprofloxacin

 Obtain sputum culture

RISK FACTORS
 >4 course of antibiotic in past year

 Severe COPD (FEV1 <50% of predicted)

 Isolation of pseudomonas during past hospitalisation

 GOLD GUIDELINE

 Although there is no high-quality evidence from RCTs, it is

recommended that short-acting inhaled beta2-agonists, with or without

short-acting anticholinergics, are the initial bronchodilators for acute
treatment of a COPD exacerbation.

 Theophyllines are used as second line therapy

SHORT ACTING

 BETA AGONIST  ANTICHOLINERGICS

Albuterol Ipratropium
Fenoterol
Terbutaline
CORTICOSTEROIDS

 Improve symptoms ,FEV1 and PaO2 in moderate/severe AECOPD

 Reduce treatment failure , Relapse

 Oral route is preferred

 Prednisolone 30-40mg for 10 -14 days

 SYSTEMIC CORTICOSTEROID

 Shorten recovery time,improve FEV1

 40mg Prednisolone daily for 5 days

 In patients with a COPD exacerbation presenting to the hospital , a

shorter course of systemic corticosteroids(5 days) was noninferior to
longer (14 days) course with respect to re-exacerbation within 6
months
Also known as STATUS ASTHMATICUS
 Formerly known as status asthmaticus
 Acute exacerbation of asthma that does not respond to standard
treatment (Bronchodilators, inhalers, steroids)

 Medical emergency
 50% due to URTIs
 Non adherence
 NSAID exposure in ASA-allergic patients
 Allergen exposure
 Irritant inhalation
 Chest tightness, wheezing, use of accessory muscles and dyspnea
that are often not or poorly relieved by their usual reliever inhaler

 breathless that they are unable to complete sentences

 cyanotic
 General appearance:
 alteration of consciousness

 fatigue

 upright posture

 diaphoresis
 Respiratory system
 tachypnea (>30\min)

 use of accessory muscles for breathing

 reduced respiratory excursion
 diffuse expiratory wheezing

 Cyanotic
 Cardiovascular system
 Tachycardia (>120/min)

 pulsus paradoxus
 SPIROMETRY
 PEFR< 120L/MIN

 FEV1< 1L
 Arterial blood gas analysis
 hypercapnia or normal
 CXR:
 over inflated lung
 Cardiac arrest

 Respiratory failure or arrest

 Hypoxemia with hypoxic ischemic central nervous system (CNS) injury

 Pneumothorax or pneumomediastinum

 Toxicity from medications

 Good prognosis if appropriate therapy is administered.
 …unless a complicating illness such as
 CHF

 COPD is present
 A delay in initiating treatment is probably the worst
prognostic factor
 High concentration of oxygen + High doses of SABA
 Severely ill patients with impending respiratory failure - IV β2-agonists
 Nebulized anticholinergic- if unsatisfactory response to β2-agonists
 patients who are refractory to inhaled therapies, a slow infusion of
aminophylline
 Magnesium sulfate given iv or by nebulizer with inhaled β2-agonists

 Prophylactic intubation for impending respiratory failure, when the PCO2

is normal or rises
 These patients may benefit from an anesthetic such as halothane
if they have not responded to conventional bronchodilators.
 Sedatives are C/I depress ventilation.
 Antibiotics not required unless there are signs of pneumonia.
 Corticosteroids
 Recommendation is to initiate steroid therapy within 48 hours

 Methylprednisolone 2-4 mg/kg/day divided every 6 hourly IV will

maintain plasma steroid concentration of 100 -150mcg cortisol/100 ml

 No special role of high dose corticosteroids

 Oral route is equally efficatious as IV or IM but not recommended in

severe cases
 Mechanism is still under study , proposed mechanism are

GENOMIC EFFECT (6-24 hours)

• Inhibition of pro inflammatory gene expression

• Up regulation of beta adrenergic receptors expression

NON GENOMIC EFFECT(immediately)

• Membrane stabilisation and effects on ion channels

 INHALED CORTICOSTEROID

 Not recommended in management of severe status

asthmaticus
 Severe airway obstruction and mucous plugging may limit
delivery of steroids to site of action
 Beta Adrenergic Agonists
 EPINEPHRINE

Subcutaneous 1: 1000 0.01ml/kg/dose every 15 – 20 minutes may be

repeated 3 times

Nebulised form not studied in status asthmaticus

once considered treatment of choice , nowadays not used frequently

because IV corticosteroids with newer beta agonist are very effective
 Subcutaneous epinephrine or subcutaneous terbutaline (0.01ml/kg of 1:1000
terbutaline or 1mg/ml max 0.3 – 0.5ml) is recommended in severe status
asthmaticus
 SALBUTAMOL

 Several studies have demonstrated superiorefficacy of inhaled beta 2

agonist as compared to subcut Epinephrine

 Fixed dose (2.5mg salbutamol in 2.5ml saline) is as efficacious as

calculated dose (0.1mg/kg) in moderate status asthmaticus

 In severe status asthamticus , “ High dose” (0.3mg/kg) salbutamol is

more effective than low dose(0.1mg/kg)
 NEBULISOR VS INHALERS
 Available evidence suggests that there is no difference between
MDIs with spacers compared with nebulizers, regardless of the
severity of acute Asthma and both options are reasonable in the
routine care in ER in mild to moderate cases. •

 However in acute severe Asthma continuous salbutamol

Nebulization is the most appropriate choice in critically ill child.
 IV Salbutamol
 Can be used as bolus (5-15mcg / kg) or continuous infusion (1 mcg /kg /
min to clinical improvement or greater than 20% increase in heart rate)

 One study suggested no clinical differences between IV sulbutamol and

IV Aminophylline in status asthmaticus

 IV Sulbutamol can casue tachycardia, tremors and cardiac arrhythmias.

 Ipratropium Bromide

 Parasympathetic nerve fibres are mainly supplied to larger central

airways and stimulate bronchoconstriction and mucous secretion.

 Sympathetic nerves are supplied to peripheral smaller airways and

cause bronchodilation.

 Studies have shown synergistic effect when Ipratropium bromide is

used along with salbutamol.
 Magnesium

 Exact mechanism of action in Status asthmaticus not known

 It may treat underlying hypo magnesemia (Hypo Mg can occur

due to continuous Beta agonist therapy,)

 Mg acts as Calcium antagonist reducing Ca uptake by muscles

and causing relaxation.
 doses:

IV 0.1ml/kg of 50% MgSO4 (50-75 mg / kg (Max 2 gram) over 20-

30 minutes, every 4 – 6 hourly

 Aim to keep Sr Mg above 4 mg% to have optimum broncodilatation

 Side effects: Nausea, facial flushing. When Sr Mg is > 12 mg% loss of

deep tendon reflexes, muscle weakness and respiratory depression.
Theophylline

 Although effective bronchodilator, its use has reduced as

Beta2 agonists are sufficient in most cases.

 It produces bronchodilatation without causing V/Q mismatch

 while Terbutaline infusion causes bronchodialatation along

with hypoxic vasoconstriction leading to some V/Q mismatch
 Theophylline’s diuretic effects may also reduce excess alveolar
fluid and microvascular permeability Theophylline also ..

 increases respiratory drive,

 improves mucociliary clearance,

 improves contractility of diaphragm

 and reduces pulmonary vascular resistance

 Decision to intubate should be based on clinical situation and NOT on
blood gas.

 Worsening acidosis,worsening hypoxia,deteriorating sensorium,

bradycardia etc are some indications.

 RSI should be by most experienced person

 More than 50% of complication in ventilated patients in Status

Asthmaticus occur at the time of intubation .
 Rapid sequence Intubation
 Preparation: of personnel, equipment & establish monitoring.

 Preoxygenation: for 2-3 min with 100% O2.

 Pretreatment: Ketamine 1- 2mg/kg

 Paralysis: Rocuronium, Vecuronium

 Positioning and pressure

 Placement and proof :Tracheal intubation

 Post intubation monitoring

THANK YOU