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Fellow's Corner

This segment presents topics that should interest pediatric anesthesiologists of all levels written from a fellow's perspective. For this issue we have included an article review by one of the Pediatric Fellows from The Children's Hospital in Denver.

Fellow's Corner is an excellent opportunity for future pediatric anesthesiologist to present their viewpoint or ask question about articles, current controversies in anesthesia, or fellowship training. Additionally, it allows trainees an early exposure to the SPA. Questions, commentary or reviews can be sent to jeff@galinkin.net. Also include your name and hospital affiliation and whether you want these included if printed.

Jeffrey Galinkin, MD

Mechanisms and Treatment of Laryngospasm

Landsman IS, Int Anesthesiol Clin. 1997; 35(3):67-73.

This excellent article discusses the management and diagnosis of laryngospasm.

In the first portion of this article, the epidemiology of laryngospasm is discussed. Laryngospasm is most common in children age 0-3 years (28.2/1000) among normal patients and has a frequency up to 95.8/1000 in patients with URI or Asthma.

The anatomy, physiology and pathophysiology of the larynx and laryngospasm were reviewed next. The author notes that there is a multitude of mechano/chemo/thermal receptors over the whole larynx. Receptor concentration is particularly dense over the posterior portion of the larynx, which is relatively exposed to more secretions. Afferent stimulation of these receptors causes transient vocal cord adduction that differs from true laryngospasm. True laryngospasm is adduction of the vocal cords from superior laryngeal nerve stimulation. Animal models have shown central synaptic immaturity, transient reduction of central latency and reduction of central inhibition to be causative of laryngospasm. This article suggests that after vocal cord closure, redundant pharyngeal tissue collapse, creating a ball valve effect. Laryngeal closure tends to occur during expiration and is associated with stimulation of visceral nerve endings in the pelvis, abdomen and thorax.

To diagnose laryngospasm, bronchospasm and obstruction or the pharynx by the tongue should be ruled out. Cough often precedes laryngospasm and absent breath sounds with chest wall movement is a sign of severe laryngospasm. Marked negative pressure can precipitate negative pressure pulmonary edema. Predisposing factors of laryngospasm include light anesthesia, indwelling N/G tube, URI, pungent anesthetics, upper airway endoscopy, blood and secretion and hypospadias repair.

Treatment of incomplete laryngospasm is to remove airway irritants by deepening anesthesia and providing gentle positive pressure ventilation with 100% oxygen. Treating complete obstruction with positive pressure ventilation may result in distension of the pyriform fossa and cause further adduction of the vocal cords with air entering the stomach. Forcing the chin up with a jaw thurst may elongate the laryngeal muscles and may relieve laryngospasm. Otherwise muscle relaxants (succynlcholine) and atropine IV or IM may be needed.

Prevention by identification of risk factors, possible use of topical lidocaine (1/2 hour duration) and thorough suctioning of pharynx before extubation are important.

Zulfiqar Ahmed, MD #include ./footer_include.iphtml