Status asthmaticus by Pushpa Raj Sharma

PushpaSharma 1,493 views 27 slides Aug 07, 2018
Slide 1
Slide 1 of 27
Slide 1
1
Slide 2
2
Slide 3
3
Slide 4
4
Slide 5
5
Slide 6
6
Slide 7
7
Slide 8
8
Slide 9
9
Slide 10
10
Slide 11
11
Slide 12
12
Slide 13
13
Slide 14
14
Slide 15
15
Slide 16
16
Slide 17
17
Slide 18
18
Slide 19
19
Slide 20
20
Slide 21
21
Slide 22
22
Slide 23
23
Slide 24
24
Slide 25
25
Slide 26
26
Slide 27
27

About This Presentation

severe bronchial asthma for MBBS


Slide Content

Status asthmaticus A severe form of asthma

Hypersecretion Epitheal damage with exposed nerve endings Hypertrophy of goblet cells and mucous glands Status asthmaticus : Pathophysiology

Pathophysiology Smooth muscle spasm Airway edema Mucous plugging Asthma is primarily an inflammatory disease

Risk factors for fatal asthma Medical Previous attack with rapid/severe deterioration or respiratory failure or seizure/loss of consciousness Psychosocial Denial ,non-compliance Family fear of inhalers

Lung Mechanics Hyperinflation Obstructed small airways cause premature airway closure, leading to air trapping and hyperinflation. Hypoxemia Inhomogenous distribution of the affected areas results in V/Q mismatch, mostly shunt.

Cardiopulmonary interactions Left ventricular load Spontaneously breathing children with severe asthma have negative intrapleural pressure as low as -35 cm H2O during almost the entire respiratory cycle. Negative intrapleural pressure causes increased left ventriculalr after load, resulting in risk for pulmonary edema Right ventricular load Hypoxic pulmonary vasoconstriction and lung hyperinflation lead to increased right ventricular after load

Cardiopulmonary interactions Pulsus paradoxus It is the clinical correlate of cardiopulmonary interaction during asthma. It is defined as exaggeration of the normal respiratory drop in systolic BP: Normally <5 mm Hg, but >10mmHg in pulsus paradoxus

Pathophysiology Severe air flow obstruction Incomplete exhalation Increased lung volume Expanded small airways Increased elastic recoil pressure Increased expiratory flow Decreased expiratory resistance Compenseted Hyperinflation, normocapnia Worsening airflow obstruction Decompenseted: Severe hyperinflation, hypercapnia

Metabolism VQ mismatch Increased work of breathing Dehydration Hypoxia Lactate Ketones Metabolic acidosis

Types of exacerbation Mild asthma exacerbation Dyspnea on exertion or tachypnea in young children. PEF< 70% predicted Prompt relief with inhaled with short acting beta agonist. Home management

Moderate asthma exacerbation Dyspnea usually limits activity PEF 40-69% Relief with frequent inhaled short acting beta agonists Hospistal/clinic management Anticipate 1-2 days of symptoms after treatment onset

Severe exacerbation Dyspnea at rest, limiting conversation PEF less than 40% predicted Only partial relief with inhaled short acting beta 2 agonists Emergency department management Hospitalization likely Systemic corticosteroids and ipratropium Anticipate > 3 days symptoms

Life threatening exacerbation Unable to speak, severe dyspnea with associated diaphoresis PEF <25% of predicted Minimal relief with inhaled short acting beta agonist Emergency stabilazation PICU admission Frequent or continuous salbutamol nebs Systemic Corticosteroid and ipratroprium ABC management.

Assessment: impending respiratory failure Altered level of consciousness Inability to speak Absent breath sounds Central cyanosis Diaphoresis Inability to lie down Marked pulsus paradoxus

Status asthmaticus

Status asthmaticus

Management Oxygen 100% warm, humidified Delver by non breather mask or high flow nasal canula Nebulized salbutamol with ipratroium continuously to hourly Systemic corticosteriod Adrenergic agonists: Epinephrine Terbutaline ( alterntive) Two intravenous line

Further management (Hypercarbia is a failure of ventilation not oxygenation) Hypotension Fluid bolus of normal saline Chest xray ? Tension pneumothorax (SIADH may be common in severe asthma) Magnesium 40-75 mg/kg Consider ketamine Consider non invasive ventilation: CPAP Heliox (helium to oxygen60:40) Avoid aminophylline or theophylline

Status asthmaticus

Status asthmaticus

Status asthmaticus

Status asthamaticus

Status asthmaticus Why hesitate to intubate the asthmatic child?

Case scenario 1 A 6 yr male with previous history of hospital admission for difficulty in breathing without fever and treatment with salbutamol MDI. Re admitted with severe respiratory distress. He is wheezing. RR is 40/min, HR 145/min. He sits upright, leans forward, has retractions and looks very anxious. He correctly tells you his name and phone#, but has to take breath after every few seconds. Discuss your initial therapeutic approach.

Case Scenario 1 Which of the following are mandatory in this child with severe asthma? (you may choose none, more than one or all) Arterial blood gas analysis (to detect onset of respiratory acidosis) Continuous pulse oxymetry Chest radiograph (to rule out penumomediastinum/ thorax Frequent determination of PFR Blood count to assess need for anesthetics

Scenario 2 When nebulizing drugs during status asthmaticus, the following statement about gas flow rate is correct: The higher is the gas flow rate through the nebulizer, the more particles will be deposited in the patient’s alveolar space. Most devices require a gas flow rate of 10-12 L/min to generate optimal particle size. Gas flow rates above 5L/min should be avoided to maintain laminar flow in the nebulizer output. The nebulizer device should not be driven by 100% oxygen.
Tags