Status Asthmaticus Treatment and Pathophysiology in Children
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Status Asthmaticus Treatment and Pathophysiology in Children
- 1. Status Asthmaticus in Children Heinrich Werner Pediatric Critical Care University of Kentucky Children’s Hospital
- 12. Irritable and damaged airway Hypersecretion Epithelial damage with exposed nerve endings Hypertrophy of goblet cells and mucus glands : Pathophysiology
- 16. Severe airflow obstruction Incomplete exhalation Increased lung volume Increased elastic recoil pressure Increased expiratory flow Expanded small airways Decreased expiratory resistance Compensated: Hyperinflation, normocapnia Decreased expiratory resistance Decompensated: Severe hyperinflation, hypercapnia Worsening airflow obstruction From text in : Tuxen. Am Rev Respir Dis 1992;146:1136 : Pathophysiology
- 21. Cardiopulmonary interactions Negative intrapleural pressure Pulmonary edema Pulsus paradoxus Hyperinflation Hypotension Altered hemodynamics : Pathophysiology
- 22. Metabolism V/Q mismatch Hypoxia Dehydration Lactate Ketones Metabolic acidosis Increased work of breathing : Pathophysiology
Notas del editor
- It appears that asthma incidence has been increasing especially in young children (0-4 years).
- The same goes for asthma morbidity
- Above are the known risk factors. It has to be remembered though that up to one third of children who die from asthma have only had mild asthma before, and had not been classified as “high risk” until then See: Robertson CF, Rubinfeld AR, Bowes G. Pediatric asthma deaths in Victoria: the mild are at risk. Pediatr Pulmonol 1992;13(2):95-100.
- The severe airflow obstruction in asthma results in incomplete exhalation already prior to intubation. Progressive dynamic hyperinflation (DHI) develops, and end-expiratory lung volume reaches a new equilibrium above functional residual capacity (FRC) . The increased lung volume increases pulmonary elastic recoil pressure (thus increasing expiratory flow) and expands small airways (thus decreasing expiratory resistance). Therefore, lung volume will rise until a point is reached where the entire inspired tidal volume can be expired during the available exhalation time . This process however becomes maladaptive in severe asthma, such that hyperinflation required to maintain normocapnia can not be achieved, as it would exceed total lung capacity . Hypercapnia and eventually respiratory failure ensue.
- Detailed, but nice reference for this can be found at Dolovich MA. Influence of inspiratory flow rate, particle size, and airway caliber on aerosolized drug delivery to the lung. Respir Care 2000;45(6):597-608.
- The traditional teaching has been to give ipratropium every 6 hours, due to its long duration of action (Goodman and Gilman). However, a recent study by Schuh seemed to suggest that several doses of ipratropium at 20 minute intervals caused greater improvement when compared to a single dose. In this double-blinded, three armed trial the investigators administered ipratropium to asthmatic children and compared between 250 micrograms given three times within an hour, 250 micrograms as a single dose and placebo. The group receiving three doses experienced the greatest improvement in pulmonary function. It has not been shown that higher doses than 500 micrograms are necessary. It may be beneficial to start treatment with three doses of ipratropium every twenty minutes, and then repeat it every four to six hours.
- Another, relative indication would be the child with massive increase in work of breathing, who is not improving and begins to tire out
- Should include immediate administration of high flow oxygen. Start inhaled beta agonist. Start intravenous access.
- ABG - Painful intervention, changes respiratory pattern and likely then will not reflect true baseline. How will the result alter therapy in the unintubated asthmatic? Arterial pCO2 is no longer an indication for intubating the asthmatic child - even the presence of hypercarbia does not dictate intubation. ABGs are not helpful in the unintubated asthmatic without clinical signs of respiratory failure. They are however mandatory in the ventilated asthmatic. Oximetry - no comment necessary. Essential. CXR - Not necessary unless clinical suspicion of air leak, or after intubation. Not very helpful in differentiating atelectasis from pneumonia. PFR - Frequent determination is probably not very helpful in the very acute presentation of the severely ill asthmatic. May be helpful to get a baseline, and then follow occasionally to assess treatment. WBC - not helpful. They all have elevated WBC, and WBC will not help to distinguish between stress, steroid effect, viral or bacterial infection
- Cardiac or respiratory arrest Severe hypoxia Rapid deterioration in mental state (Obvious exhaustion in the presence of severely increased work of breathing) Respiratory acidosis does not dictate intubation
- The correct answer is B The higher the gas flow rate, the smaller will be the particle size. Only particles between m are deposited in alveoli, this is achieved by a gas flow rate of 10-12 L/min for moist commercially available nebulizers.
- The correct answer is B Steroids should be avoided if the patient has recently been exposed to chickenpox and is non-immune, or currently has active chickenpox. All others can be considered, but are not first line treatments.
- Rapid change in mental state, as well as marked oxygenation failure, should be considered as indications to intubate. Ketamine plus anticholinergic is considered by many to be ideal induction drug. Strongly consider rapid acting NMB agent, such as rocuronium or succinylcholine. Anticipate hypotension after intubation, most often secondary to dynamic hyperinflation. Consider pneumothorax. Avoid rapid breaths. Use short inspiratory time, long expiratory time, low rate.
- Dynamic hyperinflation with marked decrease of venous return Pneumothorax/ Tension pneumothorax Obstructed ETT where plug is acting as valve Initial maneuver should be disconnection from ventilator circuit. If dynamic hyperinflation was the cause, disconnection will allow more complete exhalation with improvement in venous return and thus in arterial blood pressure. Hypotension due to tension ptx does not improve with interruption of mech ventilation. Give volume in either case.