Lma, laryngospasm and pulmonary edema
- 1. Laryngeal Mask Airway (LMA) Laryngospasm & Negative Pressure Pulmonary Edema. Block: Anesthesia Year: 2020
- 3. Laryngeal Mask Airway: • Is a type of supraglottic device. • Is used clinically as an alternative to both mask ventilation & ETT. – Introduced into clinical practice in the 1980s, predominantly used in OTs but have become widely used in the ICU, ED & field settings. • Usually placed & is less stimulating than ETT, but it does not provide complete protection against aspiration & does not prevent laryngospasm. • Easier to insert & has high rate of success. (95-99%) • Can use for short procedures. • Made in various sizes to suite neonates, children & adults. – Paeds. sizes formula: 1+BW/20 – NB: BW is rounded off to nearest whole number.
- 4. Supraglottic airway device (SAD) Mask Size Patient Size Weight (kg) Cuff Volume (mL) 1 Infant <6.5 2-4 2 Child 6.5-20 Up to 10 2½ Child 20-30 Up to 15 3 Small Adult >30 Up to 20 4 Normal Adult <70 Up to 30 5 Larger Adult >70 Up to 30 When properly placed, the mask rests on the hypopharyngeal floor. No suction in LMA removal.
- 5. Laryngeal Mask Airway (LMA):
- 6. Laryngeal Mask Airway (LMA):
- 7. LMA vs. face mask vs. ETT: Advantages Disadvantages Compared with face mask Hands free operation Better seal in bearded patients Often easier to maintain airway Protects against airway secretions Less facial nerve & eye trauma Less operating room pollution • More invasive • More risk of airway trauma • Requires new skill • Deeper anesthesia required • Requires some TMJ mobility • Multiple contraindications Compared with ETT Less invasive Very useful in difficult intubations Less tooth & laryngeal trauma Less laryngospasm & bronchospasm Does not require muscle relaxation Does not require neck mobility • Increased risk of GI aspiration • Less safe in prone positions • Limits maximum PPV • Less secure airway • Greater risk of gas leak & pollution • Can cause gastric distension.
- 8. Relative Contraindications for the LMA: • Patients with: – Pharyngeal pathology (e.g. Abscess) – Pharyngeal obstruction (glottic /sub) – Full stomachs (e.g. pregnancy, hiatal hernia) – Low pulmonary compliance (e.g. restrictive airway disease) requiring peak inspiratory pressures greater than 30 cm H2O. – Morbid obesity-(increased risk of sleep apnea) pts. may have a redundant tissue-difficult to seat device; increased ventilatory pressures required in obese patients may increase the likelihood of a leak. • The LMA has been avoided in patients with bronchospasm or high airway resistance, but new evidence suggests that ‘cause it is not placed in the trachea, use of an LMA is associated with less bronchospasm than a TT. • Stomach bulges up into chest through diaphragm • Risk of aspiration in anaesthesia induction
- 9. Complications: • Significant complications which may result from the utilization of an LMA include: – Complications associated with improper placement: Laryngospasm & obstruction. – N/V – Aspiration of gastric contents – Coughing – Local irritation – Pressure-induced lesions, nerve palsies.
- 10. LMA Supreme: • The new shape & stiffness of the device is intended to guide the airway into the correct position during insertion eliminating the need for placing the clinician’s fingers into pt.’s mouth. • Recommended for use in routine & emergency anaesthesia in fasted pts. Particularly when intubation may be challenging or delaying oxygenation. • Single use • Large inflatable plastic cuff, but no posterior cuff (PLMA) • Oesophageal drain tube • Preformed semi-rigid tube • Fins
- 11. Proseal LMA: • Passive regurgitation can occur unexpectedly intraoperatively. The LMA ProSeal enables the regurgitated fluid to pass up the drainage tube without leaking into the glottis. – Decrease risk of aspiration. • Reduces the likelihood of throat irritation & stimulation, & reduces PONV. • It achieves a high seal pressure
- 12. Laryngospasm: • Is a protective reflex mediated by the vagus nerve(CN X). • Stimulation of vagus nerve during light anaesthesia (Superior Laryngeal n, pharyngeal br of vagus, recurrent laryngeal below cords). • Reflex is an attempt to prevent aspiration of FBs into the trachea. • May be provoked by: movement of cervical spine, pain, vocal cord irritation by secretions, or sudden stimulation while patient still in a light plane of anesthesia. • Malposition, incorrect insertion of an LMA, secretions or blood in the airway, and inadequate depth of anesthesia during intubation/ extubation of the LMA or tracheal tube may induce laryngospasm. • Has potential to cause morbidity & mortality such as severe hypoxaemia, pulmonary aspiration & post-operative pulmonary edema.
- 13. Risk Factors(Laryngospasm): • Combination of anaesthetic, patient & surgery-related factors: Anaesthetic-related Patient-related Surgical-related Insufficient depth Age (young children more prone) Shared airway surgery – Tonsillectomy Airway irritation Airway hyper-reactivity (Asthma) Thyroid surgery –superior laryngeal n injury, hypocalcaemia Manipulation-laryngoscopy, suction catheter Tobacco-Chronic use, passive exposure Oesophageal surgery Airway device-LMA Airway anomaly –tracheal/ subglottic stenosis Others- appendicectomy, skin grafting, cervical dilatation. Volatile anaesthetics Gastroesophageal reflux Experience of anaesthetist Obesity with sleep apnea
- 14. Signs(Laryngospasm): • Inspiratory stridor/ airway obstruction • Increased inspiratory efforts/ tracheal tug • Paradoxical chest/ abdominal movements • Desaturation • Bradycardia (esp. in children) • Central cyanosis
- 15. Management (Laryngospasm): 1. Position patient supine. 2. Administer oxygen (terminate nitrous oxide) 3. Evaluate the airway- displace tongue, jaw thrust at the angle of the mandible. 4. Suction the airway-the oral cavity & posterior pharynx. 5. Reevaluate the airway-push down pt.’s chest, if no air heard/felt, proceed to step 7. Check saturation (desaturation will occur) 6. Positive-pressure oxygen (100%)-aim to mechanically break the laryngospasm by physically forcing oxygen through vocal cords. (Suctioning important) 7. Administer a muscle relaxant. (Succinylcholine 0.25-1 mg/kg iv) 8. Assess ventilation & control ventilation.
- 16. Succinylcholine: • Is a depolarizing NMBD. – It acts as Ach receptor agonist, generate AP. – Not metabolized by acetylcholinesterase, binding is prolonged resulting in an extended depolarization of the muscle end-plate. “persistent” depolarization leads to desensitization. – Phase I block often preceded by muscle fasciculation. – Probably result of the prejunctional action of succinylcholine, stimulating Ach receptors on the motor nerve, causing repetitive firing & release of NT. – Metabolized by plasma cholinesterase. – Desensitization- occurs when Ach-r are insensitive to the channel-opening effects of agonists, including Ach itself. • May be a safety mechanism that prevents over-excitation of the NMJ.
- 17. Negative Pressure Pulmonary Edema (NPPE): • Rare complication, usually occurs after extubation (anesthesia)-in some patients. • Onset usually rapid & without prompt recognition & intervention, outcome can be fatal (40%). • Incidence, as complications of all anaesthetics, is said to be 0.05-0.1% • Extubation-airway obstruction (laryngospasm) –patient under light-plane anesthesia • Can lead to life-threatening hypoxemia – Hypoxemia-defined as a condition where arterial oxygen tension (PaO2) is below normal (80-100mmHg) – Hypoxia-failure of oxygenation at the tissue level.
- 18. Mechanism of Negative Pressure Pulmonary Edema: The patient continues trying to inhale against the obstruction 2 An upper airway obstruction occurs 1 A high degree of negative intra- thoracic pressure develops 3 Venous return to the heart increases 4 Cardiac output decreases 5Pressure in the pulmonary capillary bed increases 6 A disruption in the alveolar membrane junction occurs 7 Fluid from the interstitial space floods into the alveoli 8 Airway obstruction is relieved 9 Pulmonary edema remains 10
- 19. Typical Signs & Symptoms (NPPE): • Respiratory distress • Hypoxia • Cyanosis • Frothy pink sputum • Hemoptysis
- 20. Management (NPPE): • Early diagnosis-careful monitoring • Reestablishment of the airway (maintenance) • Adequate oxygenation • Application of positive airway pressure – Via facemask or LMA – Endotracheal intubation with vent support • Although NPPE does not result from fluid overload, most authors recommend gentle diuresis using low-dose furosemide (1mg/kg) – And fluid restriction.
- 21. Guedel’s (1997) Signs & Stages of Anesthesia: • Stage I: Inducement, excitement, pupil constriction, voluntary struggling • Stage II: Obtunded reflexes, pupils start to dilate, still excited, involuntary struggling • Stage III: There are 3 planes; light, medium & deep – Light: More decreased reflexes, pupils constricted, brisk palpebral reflex, absence of swallowing reflex, lacrimation still present, no involuntary muscle movement – Medium: ideal plane for most invasive procedures, pupils dilated, loss of pain, loss of palpebral reflex/corneal – Deep: (early overdose) resp. depression, severe muscle relaxation, bradycardia, no reflexes, pupils dilated. • Stage IV (mainly dead): very deep anesthesia, respiration ceases, cardiovascular fxn. decreases & death ensues immediately.