Intra operative bronchospasm and its management

Introduction:

Today we are going to talk about one of the most common complications in anesthesia called bronchospasm.

The word bronchospasm is derived from the German language called bronchospasmus, which is a combination of two words: broncho, meaning bronchi, and spasmus, meaning spasm or constriction.

Definition:

A sudden contraction In the muscular wall of bronchi is called bronchospasm.

Pathophysiology:

Normally the muscular walls upon bronchi are relaxed and there is proper ventilation, but what happens in bronchospasm is that there is sudden constriction in these muscular walls as shown below, which causes narrowing of the bronchi, and hence there is resistance in ventilation, and according to the formula, when the cross-sectional area is decreasing, the resistance is increasing, which causes increased peak airway pressure at the tidal volume we have set.

Formula:R=ρ L/A

where;

R is the resistance 

rho is the resistivity constant

L is tube lengthning 

A is the cross-sectional area

So when the area is decreased, the resistance is increased and hence with the same amount of tidal volume, the resistance in the airway means the peak pressure will be increasing.

Causes/risk factors/triggers:

1. COPD 
2. Asthma (reactive airway)
3. ETT in light anesthesia
4. Pre existing reactive airway, like in upper respiratory tract infection 
5. Usage of pungent volatile anesthetics like desflurane or isoflurane
6. Smoking
7. Aspiration of secretions or gastric contents
8. Endobronchial intubation

Signs of bronchospasm:

Clinically the following signs can be seen in patient monitor, anesthesia workstation and patient monitor.

1. Increased peak airway pressure
2. Wheezing on lung examination because when the bronchi are constricted then upon air entry there will be a whistle-like sound production which is called as wheezing, but this wheeze will be absent, meaning no breath sounds will be there when the bronchospasm is severe.
3. Increased ETCO2 with upslping of capnography waveform giving it a sharkfin appearance
4. If you have set a PCV mode, then there will be decrease tidal volume
5. Rule out other causes of wheeze like pulmonary edema, pulmonary emoblus, and pneumothorax.
6. Severe bronchospasm is a diagnosis of exclusion. The quickest method of ascertaining the source of increased airway resistance is to connect a self-inflating bag/ambu bag directly on ETT, not HME, and manually ventilate. If the inflation pressure still feels too high, the problem is due to airway/ETT obstruction or reduced compliance
7. Decrease in SPO2
8. Hypotension due to autopeep development being the air trapping.

Management:

1. Increase Fio2 to 100%
2. Increase the inhalational agents as they are bronchodilators; especially use the sevoflurane because of having no pungenet effects 
3. Increase the expiratory time just because to remove the co2 and other gases inside the long and prevent the auto peep too
4. Decrease the respiratory rates too because of the air trapping
5. 1st line therapy:
6. Providing 6-8 puffs of slabuatamol via ETT (nebulized), each puff containing 100mcg
7. 2nd life therapy includes:
8. Ipratropium bormide 0.5 mg nebulized
9. Magnesium sulphate 2 g in adults slowly and 40mg/kg in paeds
10. Hydrocortisone 200 mg in adults and 4mg/kg in paeds
11. Aminophyline 250 mg in adults, 5 mg/kg in paeds
12. Ketamine, a bolus of 10-20 mg followed by infusion 1-3mg/kg/hr