Nasal foreign body, ketamine and laryngospasm

Alkaline button batteries should be removed because they can can cause chemical burns.

The complications of an intranasal button battery include:

• epistaxis
• purulent, malodorous unilateral nasal discharge
• necrosis of the nasal mucosa and septum
• dislodgement and subsequent ingestion or aspiration

Extraction using instruments:

• Direct extraction using forceps or a suction catheter to grasp the foreign body
• If the foreign body cannot be grasped, a blunt-tipped right-angled probe or a small Foley catheter may be used to dislodge it, or alternatively a ‘glue on a stick’ approach may be attempted

Extraction using positive pressure:

• Ask the patient to take a deep breath and blow hard through the nose while a parent occludes the unobstructed naris
• Administer a short burst of positive pressure via the patient’s mouth while the unobstructed naris is occluded – best performed as a ‘kiss’ by a parent (the proceduralist may get an ear full of snot!)

Procedural sedation should be performed with the use of appropriate monitoring equipment (e.g. baseline vital signs and continuous SO2 monitoring, and ETCO2 monitoring if available) on a fasted and consented patient by adequately trained and resourced staff who are able to manage an airway emergency .

Ketamine for procedural sedation can be given intravenously or intramuscularly. The dose of ketamine to produce profound dissociation is:

• 1 to 1.5 mg/kg IV
  This is given over 1-2 minutes, is effective within 1-2 minutes, results in effective sedation lasting 10-20 minutes, and if inadequate a further 0.5 mg/kg dose may be given
  or
• 4 to 5 mg/kg IM
  This is effective within 2 to 5 minutes, results in effective sedation lasting 15-30 minutes and a repeat IM dose (2-4 mg/kg) can be given after 10 to 15 minutes if the initial effect is inadequate

The IM route is useful when IV access is problematic, but the downsides include:

• a longer recovery time (mean of 120 minutes for IM vs. 80 minutes for IV)
• vomiting is more likely
• sedation doses are less easily titrated

Medication adjuncts:

• Traditionally, in older children (e.g. >5 years old), prophylactic administration of a low-dose benzodiazepine (midazolam, 0.02-0.05 mg/kg) is given to reduce the risk of emergence phenomena such as hallucinations and agitation. However, this is not supported by evidence from randomised controlled studies. Instead midazolam appears to be associated with more respiratory complications and less emesis.
• Atropine (0.02 mg/kg, up to maximum of 0.6mg) or glycopyrrolate are widely administered as a co-medication to reduce the hypersalivation caused by ketamine. The evidence-base for this practice is unclear.

March 2011 update:

A recent RCT (2011) in Annals of Emergency Medicine showed an NNT of 6 for pre-administration of 0.03mg/kg IV midazolam for reducing agitation from ketamine in adults. Reuben Strayer discusses this in Taming the Ketamine Tiger, and provides a good rationale for avoiding pre-medication and taking a prn approach.

There are risks associated with the procedure itself:

• • failure
  • local trauma resulting in bleeding
  • inadvertently advancing the foreign body to a more distant site in the aerodigestive tract

As well as the risks and side-effects of ketamine sedation:

• • Laryngospasm (see below)
  • Hypersalivation (~30%; ~10% with atropine in some studies)
  • Emesis (~5-15%)
  • Emergence phenomena such as recovery agitation (10-20%, with 1-2% clinically significant), dreams, hallucinations and depersonalisation
  • Transient respiratory depression (usually in the first 2-3 minutes following a large, rapidly administered IV dose)
  • Transient mild increase in heart rate and blood pressure
  • Evanescent patchy erythematous rash about the upper torso (5-20%)
  • Nystagmus and random purposeless movements while sedated
  • ketamine induces neuronal death in animal studies — the implication of this for clinical use is not yet known.

Laryngospasm is potentially life-threatening closure of the true vocal chords resulting in partial or complete airway obstruction unresponsive to airway positioning maneuvers.

Laryngospasm may be preceded by a high-pitched inspiratory stridor — some describe a characteristic ‘crowing‘ noise — followed by complete airway obstruction. It can occur without any warning signs. It should be suspected whenever airway obstruction occurs, particularly in the absence of an obvious supraglottic cause.

Complete airway obstruction is characterized by:

• No chest wall movement with no breath sounds on auscultation
• No stridor or airway sounds
• Sudden loss of carbon dioxide waveform
• Inability to manually ventilate with bag-mask ventilation

Management of laryngospasm includes the following:

• Tell the proceduralist to stop the procedure. 
• Call for expert help. Ensure equipment for difficult intubation is at hand.
• Administer 100% oxygen through a mask with a tight seal and a closed expiratory valve to try to force the vocal cords open with positive pressure. Hypoxia can occur rapidly in children when ventilation is inadequate.
• Use suction to clear the airway of blood and secretions – but only if the child is adequately oxygenated.
• Attempt manual ventilation while continuing to apply continuous positive airway pressure (CPAP).
• Attempt to break the laryngospasm by applying painful inward and anterior pressure at ‘Larson’s point‘ bilaterally while performing a jaw thrust. Larson’s point is also called the ‘laryngospasm notch‘.
• Consider deepening sedation/ anesthesia (e.g. low dose propofol) to reduce laryngospasm.
• If hypoxia supervenes consider administering suxamethonium. A dose of only 0.1-0.5 mg/kg may be sufficient, but in severe laryngospasm administer a full dose (1-2 mg/kg IV) and perform intubation. If there is no IV access administer the suxamethonium IM (3-4 mg/kg). Many experts advocate IM injection into the tongue.
  • Be prepared for bradycardia and cardiac arrest as a result of airway manipulation and/or suxamethonium administration in the hypoxic child. Correct hypoxia urgently and administer atropine (0.02mg/kg) for bradycardia.
  • Laryngospasm is usually brief and may be followed by a gasp – you may need to wait for this moment when attempting to pass a tracheal tube. A chest thrust maneuver immediately preceding intubation may temporarily open the vocal cords and allow passage of the tube.
• Laryngospasm may recur as neuromuscular blockade wears off.

Where is the ‘laryngospasm notch‘? According to Phil Larson:

“This notch is behind the lobule of the pinna of each ear. It is bounded anteriorly by the ascending ramus of the mandible adjacent to the condyle, posteriorly by the mastoid process of the temporal bone, and cephalad by the base of the skull.”

Larson’s point: the laryngospasm notch

Thanks to Dr. Bearamy for the image link.

Ketamine is known to preserve and exaggerate protective airway reflexes. Laryngospasm is a much feared complication — however, it is extremely rare.

From a 1990 meta-analysis of 97 studies including 11.589 children, Green and colleagues reported a rate of laryngospasm of 0.4% from ketamine sedation. In nearly all cases the laryngospasm was transient and responded to oxygenation and ventilation. Only two children (0.017%) required intubation for laryngospasm.

Laryngospasm is more common in children compared with adults.

Avoid ketamine sedation in children if:

• <3 months of age — Very young children have a higher risk of airway problems, laryngospasm and apnoea from all forms of sedation and anesthesia
• active URTI (RR 5.5)
• active asthma (RR 3.7)

Ensure adequate depth of sedation before commencing the procedure and avoid stimulation of the posterior pharynx.

Spraying the posterior pharynx with 1% lignocaine may reduce the risk of laryngospasm, but local anesthesia may also compromise airway protection.

Absolute contraindications:

• <3 months of age
  (higher risk of airway complications)
• Known or suspected psychosis, even if currently stable and controlled with medications

Relative contraindications:

• Age of 3-12 months
  (higher risk of airway complications)
• Procedures involving stimulation of posterior pharynx
  (higher risk of laryngospasm)
• History of airway instability, tracheal surgery, or tracheal stenosis
  (presumed higher risk for airway complications)
• Active pulmonary infection or disease, including upper respiratory infection or asthma in children
  (higher risk of laryngospasm)
• Known or suspected cardiovascular disease, including angina, heart failure, or hypertension
• Head injury associated with loss of consciousness, altered mental status, or emesis
  (elevated intracranial pressure with ketamine)
• Central nervous system masses, abnormalities, or hydrocephalus
  (elevated intracranial pressure with ketamine)
• Glaucoma or acute globe injury
  (elevated intraocular pressure with ketamine)
• Porphyria, thyroid disorder, or thyroid medications
  (enhanced sympathomimetic effect)

Note that elevated intracranial pressure due to ketamine is controversial — and probably a myth — but is still widely quoted as a complication/ contra-indication for ketamine use.