This document discusses the classification, pathophysiology, diagnosis, and treatment of status asthmaticus. Status asthmaticus is an acute severe exacerbation of asthma that does not respond to usual bronchodilator therapy. It can lead to respiratory failure if not treated rapidly. Treatment involves nebulized bronchodilators, systemic corticosteroids, magnesium sulfate, and sometimes noninvasive ventilation or intubation. The goals are to reverse airway obstruction, correct hypoxemia, and prevent complications. Proper follow-up care is important after discharge to ensure resolution and establish long-term management.

4. TRANSIENT NONATOPIC WHEEZING
 Common in early preschool years
 Recurrent cough/wheeze, primarily triggered by common respiratory viral infections
 Usually resolves during the preschool and lower school years without increased risk for asthma in later life
 Reduced airflow at birth, suggestive of relatively narrow AHR near birth; improves by school age
PERSISTENT ATOPY-ASSOCIATED ASTHMA
Begins in early preschool years
Associated with atopy in early preschool years:
 Clinical (e.g., atopic dermatitis in infancy, allergic rhinitis, food allergy)
 Biologic (e.g., early inhalant allergen sensitization, increased serum IgE, increased blood eosinophils)
 Highest risk for persistence into later childhood and adulthood Lung function abnormalities:
 Those with onset before 3 yr of age acquire reduced airtlow by school age.
 Those with later onset of symptoms, or with later onset of allergen sensitization, are less likely to experience airflow limitation in childhood.
ASTHMA WITH DECLINING LUNG FUNCTION
 Children with asthma with progressive increase in airflow limitation
 Associated with hyperinflation in childhood, male gender

5. ASTHMA MANAGEMENT TYPES
(From national and international asthma management guidelines)
Severity Classification*
 Intrinsic disease severity while not taking asthma medications
Intermittent
Persistent:
 Mild
 Moderate
 Severe
Control Classification*
 Clinical assessment while asthma being managed and treated
 Well controlled
 Not well controlled
 Very poorly controlled

6.  Status asthmaticus is an acute severe asthma attack that does not improve with usual doses of inhaled
bronchodilators and steroids.
 It is an extreme form of asthma exacerbation characterized by hypoxemia, hypercarbia, and secondary
respiratory failure.
 Despite advances in pharmacotherapy and access to early diagnosis and treatment of asthma itself, it
remains one of the most common causes of emergency department visits.
 Signs and symptoms include hypoxemia, tachypnea, tachycardia, accessory muscle use, and wheezing.
Wheezing may be absent when airflow is severely reduced. Rapid treatment is the key to preventing
cardiopulmonary arrest.

7.  Other symptoms of an asthma attack associated with status asthmaticus include:
 difficulty breathing
 heavy sweating
 trouble speaking
 fatigue and weakness
 abdominal, back, or neck muscle pain
 panic or confusion
 blue-tinted lips or skin
 loss of consciousness

8. PATHOPHYSIOLOGY
 At a physiological level, premature airway closure during exhalation
causes an increase in functional residual capacity and air trapping.
Heterogeneous distribution of air trapping results in ventilation-perfusion
mismatch and hypoxemia-triggering anaerobic metabolism and lactic
acidosis. It is offset initially by respiratory alkalosis and is compounded
once respiratory fatigue and respiratory acidosis ensue.

9. Physical Examination
 Tachypnea
 Wheezing in early stages
 Initially expiratory .
 Later in both phases, may have absent breath sound in advance stage
 Use of accessory muscles
 Inability to speak more than 1 to 2 words
 Decreased oxygen saturation
 Tachycardia and Hypertension
 Signs of complication, tension pneumothorax, pneumomediastinum
 Peak expiratory flow meter measurement

10. Risk factors for developing status asthmaticus
 Increased use of home bronchodilators without improvement or effect
• Previous intensive care unit (ICU) admissions, with or without intubation
• Asthma exacerbation despite recent or current use of corticosteroids
• Frequent emergency department visits and/or hospitalization
• Less than 10% improvement in peak expiratory flow rate (PEFR)
• History of syncope or seizures during acute exacerbation
• Oxygen saturation below 92% despite supplemental oxygen

11. Assessment of severity of asthma exacerbation
• Moderate asthma exacerbation:
• Increasing symptoms.
• PEFR >50-75% best or predicted.
• No features of acute severe asthma.
Acute severe asthma - any one of:
• PEFR 33-50% best or predicted.
• Respiratory rate 25 breaths/minute.
• Heart rate 110 beats/minute.
• Inability to complete sentences in one breath.
Life-threatening asthma - any one of the following in a patient with severe asthma:
• Clinical signs: altered conscious level, exhaustion, arrhythmia, hypotension, cyanosis, silent chest, poor respiratory
effort.
• Measurements: PEFR <33% best or predicted, SpO2, <92%, PaO2, <8 kPa, 'normal’ PaCO2, (4.6 6.0 kPa).

12. Workup
• Blood test
• CBC, ABG, Electrolytes, RBS, Theophillne level
• Chest X-ray
• To rule out pneumothorax, pneumomediastinum, heart failure,
pneumonia

13. Arterial blood gases
• If peak expiratory flow rate is less than 30% of predicted or patient best
• Signs of fatigue or progressive airflow obstruction
• Stages of progression

15. Electrolytes and glucose
 Hypokalemia as a result of medications
 Hyperglycemia and in infants hypoglycemia

16. Impulse Oscillometry Testing
• Almost independent of patient cooperation
• Valid for all ages from 4 years and older children, adult and geriatric
patients.
• Quite breathing i.e Tidal volume breathing for 30 seconds
• It measures impedance at different frequencies indicative of central and
peripheral airway resistance.
• Bronchodilator therapy often does not reach the peripheral airways. IOS
can provide objective response to drug therapy even when FEV1 can't.

18. Differential diagnosis
• In children
• Viral infections, bronchiolitis
• Foreign body
• Congestive heart failure
• Extrinsic compression, lymph node, tumor, blood vessel
• Tracheomalacia, primary or secondary
• Inhalational injury
• Other diagnosis, like cystic fibrosis, bronchiectasis etc

19. Treatment goals
• Reverse airway obstruction
• Correct Hypoxemia
• Prevent or treat complications like pneumothorax and respiratory arrest

20. Treatment
• Mainstay of treatment of status asthmaticus are beta 2 agonist, systemic
steroids and theophyllines.
• Pregnant and non pregnant are treated in the same manner
• Fluid replacement, hypokalemia and hypophosphatemia are important to
treat.
• Routine use of antibiotics is discouraged
• Oxygen monitoring and therapy
• Maintain Sato2 above 92% except in pregnant and cardiac patients
where maintain above 95%.
• Endotracheal intubation, ventilation and chest tube placement as needed.
• ECMO when needed.

21. Beta2 Agonists
• Albuterol neubulizer continuously 10 – 15 mg/hour or q5 to 20 min
• Albuterol MDI 4 puff with chamber 15 to 30 minute interval
• Endotracheal epinephrine has no role.
• Intravenous beta2 agonist when inhalation is not possible
• Epinephrine 0.3 to 0.5mg subcutaneously (caution in CHF and history of
arrhythmias)

22. Anticholinergics
• Ipratropium bromide every 4 to 6 hours
• Synergistic effect with beta2 agonist.
• Does not cross blood brain barrier like atropine

23. Glucocorticoids
• Most important treatment in status asthmaticus
• decrease mucus production
• Improve oxygenation
• Reduce beta-agonist or theophylline requirements
• Decrease bronchial hypersensitivity
• Help to regenerate the bronchial epithelial cells.
• Oral and IV have same onset of action
• No role of nebulized steroids
• Name any ten Adverse effects of steroids

24. Bronchodilators
• Methylxanthines theophylline, aminophylline
• bronchodilatation, increased diaphragmatic function, and central
stimulation of breathing
• Narrow therapeutic index, needs monitoring
• Smokers and patients on phenytoin need higher doses
• Side effects, nausea, vomiting, palpitation
• Omg/kg loading followed by 1mg/kg/hour

25. Bronchodilators
• Magnesium Sulfate
• relax smooth muscle and hence cause bronchodilation
• Usually 1 gm to 2.5gm is administered as a single dose.
• No studies on repeated doses
• More effective in children. 40mg/kg over 20 minutes

26. Stepwise approach to status
asthmaticus
1. Confirm the diagnosis(with severity of disease)
2. Oxygen inhalation
3. Nabulization with b2 agonist (salbutamol 3times for 5 min 15 min apart)
4. Intravenous corticosteroids if symptoms persists then
5. Inj Epinephrine subcutaneously if symptoms persists then
6. Magnesium sulphate if sypmtoms persists then
7. Inj Britanyl infusion if symptoms persists then
8. Intubation and ventilator care

27. NONINVASIVE POSITIVE-PRESSURE
VENTILATION
• Noninvasive positive-pressure ventilation improves airflow and respirations
compared with usual care.
• it is commonly used in clinical practice for acute life-threatening asthma.
• Noninvasive positive-pressure ventilation decreases the need for
intubation, results in clinical improvement, and decreases the need for
hospitalization.

28. Mechanical Ventilation and Sedation
• The decision to intubate a patient presenting with status asthmaticus is a
clinical one and does not unequivocally require a blood gas assessment.
• Immediate indications for intubation include:
• Acute cardiopulmonary arrest
• Severe obtundation or coma
• Frank evidence of respiratory fatigue with gasping or inability to speak at all
• "Intubation and Mechanical Ventilation") are necessary to prevent respiratory
arrest.
• Mechanical ventilation does not relieve the airflow obstruction—it merely
eliminates the work of breathing and enables the patient to rest while the
airflow obstruction is resolved.

29. Ketamine
 Ketamine has sedative, analgesic, anesthetic, and bronchodilatory properties
and has been increasingly recommended for emergency intubation in status
asthmaticus. The usual dose is 1 to 2 mg/kg given intravenously at a rate of
0.5 mg/kg per minute to provide 10 to 15 minutes of general anesthesia
without significant respiratory depression.
Potential risks to consider before deciding in favor of ketamine include:
 Ability to cause hypertension and tachycardia with sympathetic stimulation.
Thus it is to be avoided in patients with uncontrolled hypertension,
preeclampsia, or raised intracranial pressure.
 Lowering of seizure threshold
 Increase in laryngeal secretion Metabolism through the liver, thus causing
some accumulation with the continuous infusion in liver failure.

30. DISPOSITION AND FOLLOW-UP
• Disposition decisions should take into account a combination of subjective
parameters, such as resolution of wheezing and improvement in air
exchange, as assessed by auscultation and patient opinion.
• Objective measures, such as normalization of FEV1 or PEFR.
• Advise discharged patients to use a short-acting B-agonist on a scheduled
basis for several days and to complete any oral corticosteroids regimens.
• Add inhaled corticosteroids in patients with a history of persistent asthma
who are not already using this regimen.
• A good response to treatment resolves symptoms and results in a PEFR or
FEV1 of >70% predicted; these patients can be safely discharged home

31. • Arrange follow-up care to ensure resolution and to review the long-
term medication plan for the chronic management of asthma. High
previous relapse rates suggest the need for follow-up within 1 to 4 weeks
of the ED visit.
• Deliver an appropriate written discharge plan of action that addresses
routine care and care of worsening symptoms
• Educate patients on asthma triggers, and review all discharge
medications and the correct use of the inhaler and a peak flow meter
(for daily tracking).

32. Complications
• Slow compartments vs fast compartments
• Respiratory alkalosis vs hypercarbia
• Cardiac arrest
• Respiratory failure or arrest
• Hypoxemia with hypoxic ischemic central nervous system (CNS) injury
• Pneumothorax or pneumomediastinum
• Toxicity from medications

33. Prognosis
• Generally good except when combined with heart failure or COPD
• Poor prognostic factors include delay in starting treatment especially
steroids

34. THANK YOU
Dr. Zahid Ali
PG1