Book 5, Case 6 Pedi Laryngeal papillomatosis

Question 1

Are you allowing a child’s parents to come back to the OR?

Answer 1

If they are chill, then yes-they can come back

Question 2

Laser case where they’re removing a papilloma: what are you concerned about?
What damage can the CO2 laser cause
What about the KTP, Nd:YAG or ruby laser?

Answer 2

I would
also be concerned about potential complications associated with the surgical procedure and
the use of laser cauterization, such as airway fire, viral transmission to the operating room
staff, tissue injury, and eye injury (the limited tissue penetration of the C02 laser can result in
corneal injury, while the KTP, Nd:YAG, or ruby lasers can result in retinal injury). Another
concern would be determining the optimal mode of ventilation to provide adequate surgical
visualization, while at the same time, maintaining oxygenation.

Question 3

General issues you’re concerned about in pedi patients:

Answer 3

general issues associated with the pediatric patient, such as patient
cooperation, IV access, fluid management, intra-operative heat loss, and postoperative pain
management.

Question 4

Laryngeal papillomatosis: How would you evaluate this child’s airway?

Answer 4

Because lesions in or near the airway can result in life threatening airway
obstruction during the induction of anesthesia, I would perform a thorough history and
physical, focusing on the severity and progression of any airway obstruction. Specifically I
would ask about periods of apnea and assess the patient for noisy breathing, stridor, dyspnea,
tachypnea, use of accessory muscles of respiration, or nasal flaring. I would also examine
the airway anatomy including the size of tongue, mouth opening, dentition, Mallampatiscore, cervical range of motion, and thyromental distance. Finally, I would optimize the patient’s asthma and administer an anticholinergic to minimize oral secretions.

Question 5

What is the cause of respiratory papillomatosis? How is it treated?

Answer 5

Respiratory papillomatosis is a benign laryngeal neoplasm caused by the
human papillomavirus (HPV), a DNA virus that is also responsible for condyloma
acuminatum. It is a self-limited condition (spontaneous regression usually occurs at puberty)
associated with the growth of papillomas in the larynx that, if untreated, can lead to
progressive airway obstruction (hoarseness, stridor, respiratory distress), aphonia, right
ventricular hypertrophy, and cor pulmonale.

treatment: surgical removal or alpha interferon

Question 6

What form of expression is MH?

Answer 6

Autosomal dominant

Question 7

How can you test for MH susceptibility? What are some other tests you can do? Are they diagnostic?

Answer 7

Susceptibility to malignant hyperthermia may be determined by skeletal
muscle biopsies with in-vitro contracture testing, where the tissue is separately exposed to
both halothane and caffeine.

Other tests: THEY ARE NOT DIAGNOSTIC
elevated resting plasma creatine kinase concentration,
electromyography, and genetic testing for a DNA ryanodine mutation.

Question 8

If pt being treated with alpha interferon what labs could you get?

Answer 8

Hct as it can cause myelosuppression

Question 9

Are you premeditating an anxious child?

Answer 9

Only if I don’t think it would place my airway at jeopardy.

Question 10

Pt has asthma and laryngeal polyps-do you need IV access before going back?

Answer 10

Considering the risk for airway obstruction and bronchospasm during the
induction and intubation of this asthmatic patient with airway papillomas, I would prefer to
obtain prior IV access. Moreover, this patient’s potential susceptibility to MH further
complicates an induction without intravenous access, since volatile agents must be avoided.
However, if the patient remained uncooperative, despite my reassurances, I would proceed to
the OR, prepare for a difficult intubation and possible surgical airway (i.e. difficult airway
cart, rigid bronchoscope, tracheostomy/cricothyrotomy sets available, and a surgeon in the
room), place the standard ASA monitors, administer a fo-agonist, provide supplemental
oxygen, give a small dose of intramuscular ketamine ( 1-2 mg/kg), and attempt IV placement.
My goal would be to provide adequate sedation to obtain intravenous access while, at the
same time, maintaining spontaneous respirations and airway patency.

Question 11

During induction the patient develops laryngospasm and you are unable to ventilate.
The oxygen saturation falls to 80%. What would you do?

None of these interventions break the laryngospasm and her oxygen saturation is now
68%. Will you give succinylcholine?

Answer 11

I would immediately call for assistance, administer 100% oxygen, place an
oral airway, perform bimanual jaw thrust, and provide positive pressure ventilation by
facemask. If possible, I would avoid the administration of succinylcholine, a triggering agent
for MH, in this potentially MB-susceptible patient.

If alternative measures were unsuccessful and her condition continued to
deteriorate, I would give a small dose of succinylcholine (5-10 mg), recognizing that the
administration of this triggering agent places the patient at risk for developing a MH reaction.
While I could administer a non-triggering muscle relaxant, like rocuronium, I believe that the
increased reliability and faster onset of action provided by succinylcholine is required in this
emergent situation. Given the risk, however, I would closely monitor the patient for signs of
MH, such as tachycardia, hypercarbia, muscle rigidity, or metabolic acidosis, for at least 12-
24 hours.

Question 12

The surgeon complains that the endotracheal tube is in his way. What options do you
have for improving the surgeon’s view?

Answer 12

Given this patient’s preoperative stridor and the significant risk of airway
obstruction, my best option would be to maintain spontaneous respirations and exchange the current endotracheal tube for one of a smaller diameter. This may provide better
visualization while, at the same time, maintaining a secure airway. If the surgeon was still
having difficulty operating around the ETT, and assuming intubation and ventilation
following induction had not been difficult, I would consider utilizing a technique that
involved a less secure airway, such as intermittent apnea, spontaneous ventilation without an
endotracheal tube, or intermittent jet ventilation through the operating laryngoscope. Since***
the ability to fully exhale between jet ventilations is very important, the latter technique may
not be the best option for patients with significant lung disease. However, it would probably
be acceptable for this patient with mild asthma.

***I don’t like this because we literally just had laryngospasm and are at risk for bronchospasm in a patient with reactive airway disease-The surgeon will just have to work around the tube.

But…if we still had to do it, you could use intermittent apnea, or intermittent extubation:
reduces the risk of airway fire, since there is no combustible airway device in the field during surgical
ablation. However, there are limitations to this technique, including movement of the
surgical field with spontaneous respiration, the potential for inadequate ventilation, and
an unreliable depth of anesthesia when volatile agents are used.

Question 13

When would you NOT want to use jet ventilation?

Answer 13

However, this method of ventilation is not recommended for
those with decreased chest wall compliance (i.e. obesity, restrictive lung disease, and
gastric distention) or any condition that may inhibit full exhalation (i.e. severe COPD,
laryngospasm, glottic lesions, and interarytenoid scarring). Other potential limitations of
this technique include: 1) misalignment of the gas jet to the glottic inlet leading to poor
ventilation and/or gastric distention; 2) transmission of blood, smoke, and debris into the
distal airways (in this case, active virus could be transmitted to the distal airways); 3)
excessive vocal cord vibration; and 4) barotrauma (i.e. pneumomediastinum,
subcutaneous emphysema, pneumothorax).

Question 14

In a discussion with the surgeon, you determine that jet ventilation through the
suspension laryngoscope is the best option for this case. How would you deliver jet
ventilation?

Answer 14

For this already intubated patient, I would ensure the difficult airway
equipment was still in the room; ventilate with 100% oxygen until the surgeon was ready to
position the suspension laryngoscope with an attached jet injector needle; ensure adequate
muscle relaxation and depth of anesthesia to prevent bronchospasm or laryngospasm; remove
the endotracheal tube and position the suspension laryngoscope; and initiate jet ventilation
with a pressure of 5-10 psi, adjusting the pressure upward until adequate chest rise and fall
are noted (I would start with 15-20 psi for an adult patient). Given this patient’s
susceptibility to MH and the unreliable delivery of volatile agents with jet ventilation, I
would maintain anesthesia with an intravenous technique, using propofol and a short-acting

opioid. Moreover, I would continuously monitor the adequacy of ventilation using pulse-
oximetry combined with auscultation and observation of the chest (good chest excursion),

keeping in mind the potential complications associated with jet ventilation, such as
pneumothorax, pneumomediastinum, subcutaneous emphysema, gastric distention, and
aspiration of resected debris.

Question 15

During jet ventilation the oxygen saturation decreases to 82%. What do you think
might be going on?

Answer 15

Desaturation during jet ventilation is most commonly caused by inadequate
ventilation pressures or a malpositioned jet injector. However, I would also consider other
potential causes, such as pneumothorax, pneumomediastinum, subcutaneous emphysema,
significant gastric distention, aspiration, airway obstruction, bronchospasm, laryngospasm,
and decreased lung compliance. In managing this hypoxia, I would inform the surgeon,
confirm the position of the injector, ventilate with 100% oxygen, and auscultate breath
sounds over all lung fields. If the cause were not immediately identified, I would intubate the
patient, provide positive pressure ventilation, suction the trachea, deepen the anesthetic,
administer a -agonist, and consider a chest X-ray.

Question 16

After you intubate the trachea and increase the Fi02 to 100%, the oxygen saturation
improves and the case continues. Suddenly the endotracheal tube ignites. What would
you do?

Answer 16

I would immediately alert the operating room personnel, disconnect the
oxygen supply form the airway (disconnect the circuit), remove the endotracheal tube, and, if
the flame persisted, flood the surgical field with saline. Once the fire was extinguished, I
would ventilate with 100% oxygen and perform direct laryngoscopy and rigid bronchoscopy
to evaluate the airway for damage and remove any debris. If the fire had reached the interior
of the endotracheal tube (exposing it to relatively oxygen rich gas), resulting in a
“blowtorch” affect, I would consider bronchial lavage and a fiberoptic assessment of the
more distal airways. Given the risk of delayed airway edema formation with resultant airway
obstruction, I would reintubate the patient and delay extubation for a minimum of 24 hours.
Finally, I would examine the oropharynx and face for additional damage, order a chest.radiograph, consider a brief course of high-dose steroids, consider a pulmonary consult
(depending on the extent of the damage … i.e. a “blowtorch” type of fire), and monitor the
patient carefully.

Question 17

What measures can be taken to reduce the risk of airway fire during laser surgery?

Answer 17

Steps that can be taken to reduce the risk of airway fire include: 1) removal of
flammable materials from the airway by utilizing intermittent extubation with or without
apnea, or supraglottic jet ventilation with a metallic jet needle; 2) reducing the flammability
of the endotracheal tube by using a laser resistant ETT, a rubber ETT, or wrapping the ETT
with reflective foil; 3) minimizing the availability of oxidizing agent by reducing the Fi02 to
< 40%, avoiding nitrous oxide, using air to dilute the inspired oxygen concentration, and
protecting the ETT cuff so oxygen-rich gas does not flow into the surgical field with
inadvertent cuff rupture; 4) minimizing the intensity and duration oflaser treatment; and 5)
filling the ETT cuff with colored saline to rapidly identify a cuff puncture and, potentially,
quench a small fire.

Question 18

Assuming there were no clinical or bronchoscopic evidence of injury resulting from the
airway fire, would you extubate this patient at the end of this case?

Answer 18

Since inhalational injury can potentially progress from a lucid period with
mild symptoms and minimal evidence of mucosa} injury, to life threatening airway
obstruction secondary to rapidly developing airway edema, I would not extubate this patient
after an airway fire, regardless of the extent of injury evident by bronchoscopy. Rather, I
would keep this patient intubated, administer steroids to reduce airway edema, provide
humidified oxygen, and monitor her for a minimum of 24 hours with continuous pulse
oximetry and serial chest X-rays.

Question 19

When would you consider it safe to extubate someone following an airway fire?

Answer 19

Assuming there was no evidence of acute lung injury by chest X-ray, I would
consider extubation when the patient demonstrated adequate oxygenation and ventilation,
minimal ventilatory support, normal lung compliance, stable hemodynamics, and no
evidence of airway edema by bronchoscopy or laryngoscopy 24 hours following an airway
fire. Prior to extubation, I would make sure there was an appropriate leak around a properly
sized ETT, and make preparations for emergent re-intubation should it be required.

Question 20

After transfer to the ICU and initiation of mechanical ventilation, the patient becomes
hypoxic with increased airway pressures. What is your differential diagnosis? And what would you do?

Answer 20

Don’t forget about right mainstream intubation!! Hypoxia with increased airway pressures in an intubated patient is consistent
with airway obstruction or decreased lung compliance. Given this patient’s asthma, the
surgical procedure, and the recent airway fire, I would be concerned that her condition was
the result of bronchospasm, pleural effusion, pulmonary edema, or acute lung injury.
However, I would also consider the possibility of a plugged or kinked ETT, right mainstem
intubation, or a pneumothorax. In managing this patient, I would hand ventilate the patient
with 100% oxygen, suction the ETT, auscultate all lung fields, consider obtaining a chest X-
ray and/or ABG, and treat accordingly.

Question 21

Two hours following surgery the patient becomes tachycardic and hypercapnic despite
appropriate ventilator management. What do you think might be the cause?

Answer 21

Given this patient’s potential MH susceptibility and the decision to administer succinylcholine, and assuming appropriate ventilator settings, my primary concern would be that this tachycardia and persistent hypercapnia represent a MH reaction. Therefore, I would
look for additional signs and symptoms consistent with this diagnosis, such as tachypnea,
hypertherrnia (late finding), a mixed respiratory and metabolic acidosis, generalized rigidity,
changes in blood pressure, arrhythmias, peripheral mottling, rhabdomyolysis (tea colored
urine), hyperkalemia, elevated serum creatine kinase, sweating, and cyanosis. If after a brief
investigation I was still concerned that this may be MH, I would administer 2.5 mg/kg of
dantrolene and continue to monitor her closely.

Question 22

How long are you giving dantrolene after your initial 2.5 mg/kg?

Answer 22

continuing intravenous dantrolene, 1 mg/kg every 6
hours, for 24-48 hours to prevent relapse; and monitoring the patient for up to 72 hours in the
ICU for signs of disseminated intravascular coagulation, myoglobinuric renal failure, and
recrudescence (relapse).