The document discusses status asthmaticus, focusing on its etiology, treatment goals, complications, and management strategies. It outlines the pathophysiology of acute exacerbation, the importance of early treatment, and various therapeutic approaches including bronchodilators and corticosteroids. Prognosis varies with risk factors, and specific assessments and hospitalization criteria are highlighted to guide treatment decisions.

1. Status Asthmaticus
Fakhir Raza

2. Background
• Acute Exacerbation
• Unresponsive
• Mild to Severe form
• Trend is towards less number of admissions in intensive care1
• Han P, Cole RP. Evolving differences in the presentation of severe asthma requiring intensive care unit
admission. Respiration. Sep-Oct 2004;71(5):458-62.

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

4. Etiology

5. Etiology
• Acute Bronchospastic component marked by smooth muscle
bronchoconstriction.
• Later inflammatory airway swelling and edema

6. Early bronchospastic response
• Exposure to allergen
• Mast cell degranulation
• Release of histamine, PGD2, LT-C4
• airway smooth muscle contraction, increased capillary permeability,
mucus secretion, and activation of neuronal reflexes
• Bronchoconstriction typically responds to bronchodilator therapy like beta 2
agonist

7. Later inflammatory response
• Inflammatory mediators prime endothelium and epithelium of
bronchial mucosa.
• Inflammatory cells like eosinophils, neutrophils and basophils attach
to primed endothelium and epithelium and later enter into the
tissues
• Eosinophils release ECP and MBP which induce desquamation of
airway epithelium and expose nerve endings
• It leads to further hyper responsiveness.

8. Later inflammatory response
• Airway resistance and obstruction
• caused by Bronchospasm, mucus plugging, and edema in the
peripheral
• Air trapping
• results in lung hyperinflation, ventilation/perfusion (V/Q)
mismatch, and increased dead space ventilation.

9. Later inflammatory response
• Increase in pleural and intra alveolar pressure and distended alveoli
leads to VQ mismatch, hypoxemia and increase in minute ventilation.

10. 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

11. Risk factors
• Genetic
• GERD
• Viral infections
• Air pollutants
• Medications
• Cold exposure
• Exercise

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

13. History
• Severe dyspnea or hours or days.
• Previous intubation and ventilation

14. 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

15. Asthma with No Wheezing
• Silent chest
• Severe obstruction
• fatigue

16. 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

17. 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).

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

20. Complete blood count
• CBC with differential to evaluate for pneumonia, ABPA, Churg-Strauss
vasculitis
• It could vary because of treatment as well with or without
neutrophilia
• Serum lactate level

21. 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

22. 4 stages of blood gas progression with status
asthmaticus
PaCO2 PaO2
Stage 1 Decrease Normal
Stage 2 Decrease Decreased
Stage 3 NORMAL Decreased
Stage 4 High Decreased

23. Electrolytes and glucose
• Hypokalemia as a result of medications
• Hyperglycemia and in infants hypoglycemia

24. Need for hospitalization
• If after treatment PEF and FEV1 is between 50% to 70%
• If less than 50% then intensive care admission is indicated
National Heart, Lung, and Blood Institute. Managing exacerbations of asthma. In: National
Asthma Education and Prevention Program (NAEPP). Expert panel report 3: guidelines for
the diagnosis and management of asthma. National Guideline Clearinghouse

25. Response to treatment
• Response to treatment is assessed by Pulse oximetry and spirometry

26. 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.

27. Impulse Oscillometry Testing

28. Histologic finding
• Autopsy of patients dying in few hours showed Neutrophil infiltration
• Those who die in days showed Eosinophilic infiltration.
• Extensive mucus production and severe bronchial smooth muscle
hypertrophy

29. 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.

30. 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)

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

32. 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

33. 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
• 6mg/kg loading followed by 1mg/kg/hour

34. 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

35. Sedatives
• Usually reserved for intubated patients
• In very agitated patients on high bronchodilator therapy a dose of
lorazepam 0.5mg to 1mg intravenous

36. Therapies for severe and resistant status
despite mechanical ventilation
• Ketamine
• Inhaled anesthetic agents
• NMBA
• Other treatments in case reports and personal experiences

37. Extracorporeal life support
• high risk of developing refractory status asthmaticus.
• Patients with a history of multiple incubations
• Respiratory failure requiring intubation within 6 hours of admission
• Hemodynamic instability
• Neurologic impairment at the time of admission
• Duration of respiratory failure greater than 12 hours despite maximal medical
therapy.
• Practiced in limited centers of the world
• references
1. Mikkelsen ME, Pugh ME, Hansen-Flaschen JH, Woo YJ, Sager JS. Emergency extracorporeal life support for asphyxic status
asthmaticus. Respir Care. Nov 2007;52(11):1525-9
2. Coleman NE, Dalton HJ. Extracorporeal life support for status asthmaticus: the breath of life that's often forgotten. Crit Care.
2009;13(2):136
3. Hebbar KB, Petrillo-Albarano T, Coto-Puckett W, Heard M, Rycus PT, Fortenberry JD. Experience with use of extracorporeal life
support for severe refractory status asthmaticus in children. Crit Care. 2009;13(2):R29

38. Non invasive ventilation
• Limited to weaning from ventilation
• Not effective in most of the acute cases unlike acute exacerbation of
COPD

39. Mechanical ventilation
• Indications --- already discussed
• Considerations
• Low volume, lower rate, I:E 1:3-4, addition of PEEP to prevent airway collapse
during expiration (cautiously)
• Heavy sedation
• Steroids and NMBA can cause prolong paralysis
• Monitor flow volume loop, exhaled tidal volume, autoPEEP
• Decreased cardiac output due to decreased preload, diastolic hypotension
• Fluid and judicious use of noradrenaline / phenylephrine
• Arterial line for repeated blood gases
• Replace electrolytes

40. Heliox
• Mixture of Helium and Oxygen
• Effective when percentage of Helium is at least 60%, so limiting its use
when FiO2 requirement is high
• It has more laminar flow and less turbulence in small airways so the
Oxygen reach to lower airways besides nebulized aerosols.
• No effect on caliber of bronchi.

41. A word about transfer, prevention and long
term care
• Features of stability
• Monitorting FEV1 and IOS

42. Comments and suggestion

43. Thank you and JazakAllah
• I am thankful to Medscape and internet to prepare this presentation
beside my teachers.